Ian H. Gotlib

Ian H. Gotlib is an American psychologist. He received his Ph.D. of Clinical Psychology at University of Waterloo in 1981. Now he is a professor of psychology at Stanford University and the director of the Stanford Neurodevelopment, Affect, and Psychopathology Laboratory. His research mainly focuses on affective disorders and depression. He was awarded the APA Award for Distinguished Scientific Contributions to Psychology in 2013.


Brazilian Purpuric Fever


Inferior costal facet

The inferior costal facet (or inferior costal fovea) is a site where a rib forms a joint with the inferior aspect of the body of a thoracic vertebra.
In the adjacent picture, the arrow points to an inferior costal facet. The facets are named for their location on the vertebral body, not the rib. The inferior costal facet is located on the inferior aspect of the vertebral body, but has a superior location on the rib. Similarly, the superior costal facet is superior on the vertebral body but is inferior on the rib.


Cedric Garland

Dr. Cedric Garland is an epidemiologist known for his research in the field of vitamin D deficiency. He has written upwards of 150 articles and books on the subject. Garland partnered with his late brother Frank C. Garland in some of this research. Their most widely cited paper is Garland CF, Garland FC, Gorham ED, et al. "The Role of Vitamin D in Cancer Prevention." "American Journal of Public Health" 2006;96(2):252-261. doi:10.2105/AJPH.2004.045260, cited 829 times according to Google Scholar.


Julia Parsons

Julia Parsons (also McGuire) is a fictional character from the BBC soap opera "Doctors", portrayed by Diane Keen. She made her first appearance on 13 January 2003, and departed the show on 18 May 2012, after nine years of appearing in the series. On 21 November 2019, it was announced that Keen would be reprising her role as Julia in March 2020 for the 20th anniversary of "Doctors". She returned from 25 to 27 March 2020.
Storylines.
Julia begins working on reception at the Riverside Practice (later renamed to The Mill) in January 2003, alongside ex-husband Mac McGuire (Christopher Timothy). The two begin their relationship again, which leads to Mac proposing to Julia, which subsequently leads them to get married for a second time. Julia catches Mac kissing his ex-wife Kate McGuire (Maggie Cronin), and forces them to leave with their son to Ireland. Julia, now divorced in 2007, buys Mac's share of The Mill, and becomes the Practice Manager. In May 2007, Julia reluctantly dismisses her friend Donna Parmar (Martha Howe-Douglas) due to a breach of patient confidentiality. Donna is replaced with another of Julia's friends, Vivien March (Anita Carey). In May 2009, Julia persuades mentally ill colleague Ruth Pearce (Selina Chilton) to move in with her due to her instability, where Julia cares for her until Ruth returns to work. In 2010, Julia supports nurse Michelle Corrigan (Donnaleigh Bailey) when she chose to work as an army nurse in Afghanistan. Michelle's mother, Vera Corrigan (Doña Croll), was angry with Julia as Vera blames Julia for Michelle's enlisting. Months later, Julia falls ill with symptoms of delusions and confusion; later diagnosed as Lyme disease. Whilst at home recovering from the disease, she becomes the victim of sexual assault by colleague Charlie Bradfield (Philip McGough), who is later reported and dismissed from The Mill for misconduct.
In 2012, Julia meets garage owner Martin Millar (Miles Anderson). After parking her car in the way of his garage and therefore meeting, the two begin dating. After the couple begin not to trust each other through various acts, the two break up. They later get back together, but when Julia googles Martin and finds out that he was accused of arson, they end their relationship. Martin later reveals that he has had five wives, and that he had a daughter with his third, Sarah. Julia is stunned by this, and rejects Martin. She meets up with Martin again, but when Martin says that he wants to retire and move to Wales, she once again rejects him, as she does not want this. They keep arguing about this, and whilst they are, their car crashes with another vehicle, and they are both knocked unconscious. Martin and Julia survive, and the two embrace. Julia's son Patrick (Alan McKenna) arrives, wanting to take her to his house, so she can recover. However, after thinking about whether or not she wants a future with Martin, she decides she does, and goes to live with him in Wales.
Development.
Departure.
After Keen made the decision to leave the soap after nine years, Miles Anderson was cast, playing Martin, to coincide with the departure of Julia. Digital Spy said of her departure storyline; "Fans should also keep an eye out for a possible new love interest for Julia when she gets to know garage owner Martin Millar in a few weeks' time. It sounds like there's lots on the way for Julia in the next few weeks". Keen said of Martin's and Julia's relationship; "She's fighting it all the way, because she's had so many disastrous relationships in her life, so now she tends to take the negative point of view towards how something will turn out. Martin's really great because he won't take any nonsense and he's not taking no for an answer. He's forcing Julia to really give it a shot, and she needs that. She's obviously very attracted to him, too, so they could be very good together". Of the car stunt she said that it was filmed "on a mad, stormy, windy, rainy day". She called the stunt "phenomenal" and "amazing" saying, "In the end the scenes looked incredible because of that. It was very exciting for everybody, as we don't often get to do stunts like that on "Doctors"".
Return.
In November 2019, "Doctors" began filming for the 20th anniversary, and it was announce that as part of the celebrations for the milestone, Keen would return in March 2020.
Julia is reintroduced when a documentary is being made about The Mill, to film a segment. She also supports Jimmi Clay (Adrian Lewis Morgan) with adjusting to normal life after his release from prison.
Reception.
For her portrayal of Julia, Keen was nominated in the category of "Best Actress" at the 2005 and 2011 British Soap Awards. The character was selected as one of the "top 100 British soap characters" by industry experts for a poll to be run by "What's on TV", with readers able to vote for their favourite character to discover "Who is Soap's greatest Legend?" Julia's car crash was nominated for the "Spectacular Scene of the Year" award at The British Soap Awards 2013.


Stephen Malawista

Stephen Evan Malawista (April 4, 1934 – September 18, 2013) was an American medical researcher and Professor of medicine within the rheumatology department of Yale University. Malawista is credited as the co-discover of Lyme disease and led the research team which identified the disease.
In 1975, Malawista and his Yale colleague, researcher Dr. Allen Steere, began work which would reveal Lyme disease as a new, distinct illness. Malawista and Steere had been contacted by the Connecticut Department of Public Health, which had been concerned about a mysterious cluster of similar illnesses and symptoms which had begun afflicting patients within the southeastern region of Connecticut. Malawista and Steere identified the illness, as a new bacterial infection spread by the bite of a tick. In 1977, Malwista and Steere identified the illness as a new infection spread by tick bites. Malawista initially named the new disease "Lyme arthritis." The name was later changed to Lyme disease after the illness was later shown to encompass a wide range of symptoms which were not limited to joint pain.
Malawista and his colleagues initially hypothesized that Lyme disease was caused by a virus. However, was later disproved in 1982 by microbiologist Willy Burgdorfer, who correctly identified the "Borrelia burgdorferi" bacterium as the cause of Lyme disease in Connecticut and the eastern United States. Other scientists later determined that the deer tick was the carrier of the bacterium. Malawista and his colleagues contributed to the research the possible spread of Lyme disease by deer ticks by comparing the incidents of the disease along the eastern and western sides of the Connecticut River.
Another of Malawista's colleagues within the Yale rheumatology department, Dr. Linda Bockenstedt later spoke of his commitment to his research on Lyme disease, telling the "Hartford Courant" in 2013, "I think he recognized an opportunity when this was unfurling in 1975 that this was something different and unusual...It was this detective work that led to the discoveries that set the stage for the treatment that ultimately worked against it."
Malawista was born in New York City on April 4, 1934. His mother, Ann Marlowe Straus, was a theatrical producer and the head of the Berkshire Theater Festival. His father, Lawrence Malawista, was a real estate developer.
He was accepted to Harvard University when he was just 15 years old. Malawista studied under B.F. Skinner as an undergraduate student. He received a bachelor's degree in experimental psychology from Harvard in 1954. In 1958, he received a medical degree from Columbia University.
In 1994, the American College of Rheumatology awarded Malawista the Distinguished Investigator Award, calling him "one of the most creative investigators of our time." He was also the recipient of a Guggenheim Fellowship in 2001.
Malawista, died from metastatic melanoma at his home in Hamden, Connecticut, on September 18, 2013, at the age of 79. He was survived by his wife of 44 years, Tobé Miller Malawista.


Bohr effect

The Bohr effect is a phenomenon first described in 1904 by the Danish physiologist Christian Bohr. Hemoglobin's oxygen binding affinity (see oxygen–haemoglobin dissociation curve) is inversely related both to acidity and to the concentration of carbon dioxide. That is, the Bohr effect refers to the shift in the oxygen dissociation curve caused by changes in the concentration of carbon dioxide or the pH of the environment. Since carbon dioxide reacts with water to form carbonic acid, an increase in CO2 results in a decrease in blood pH, resulting in hemoglobin proteins releasing their load of oxygen. Conversely, a decrease in carbon dioxide provokes an increase in pH, which results in hemoglobin picking up more oxygen.
Experimental discovery.
In the early 1900s, Christian Bohr was a professor at the University of Copenhagen in Denmark, already well known for his work in the field of respiratory physiology. He had spent the last two decades studying the solubility of oxygen, carbon dioxide, and other gases in various liquids, and had conducted extensive research on haemoglobin and its affinity for oxygen. In 1903, he began working closely with Karl Hasselbalch and August Krogh, two of his associates at the university, in an attempt to experimentally replicate the work of Gustav von Hüfner, using whole blood instead of haemoglobin solution. Hüfner had suggested that the oxygen-haemoglobin binding curve was hyperbolic in shape, but after extensive experimentation, the Copenhagen group determined that the curve was in fact sigmoidal. Furthermore, in the process of plotting out numerous dissociation curves, it soon became apparent that high partial pressures of carbon dioxide caused the curves to shift to the right. Further experimentation while varying the CO2 concentration quickly provided conclusive evidence, confirming the existence of what would soon become known as the Bohr effect.
Controversy.
There is some more debate over whether Bohr was actually the first to discover the relationship between CO2 and oxygen affinity, or whether the Russian physiologist beat him to it, allegedly discovering the effect in 1898, six years before Bohr. While this has never been proven, Verigo did in fact publish a paper on the haemoglobin-CO2 relationship in 1892. His proposed model was flawed, and Bohr harshly criticized it in his own publications.
Another challenge to Bohr's discovery comes from within his lab. Though Bohr was quick to take full credit, his associate Krogh, who invented the apparatus used to measure gas concentrations in the experiments, maintained throughout his life that he himself had actually been the first to demonstrate the effect. Though there is some evidence to support this, retroactively changing the name of a well-known phenomenon would be extremely impractical, so it remains known as the Bohr effect.
Physiological role.
The Bohr effect increases the efficiency of oxygen transportation through the blood. After hemoglobin binds to oxygen in the lungs due to the high oxygen concentrations, the Bohr effect facilitates its release in the tissues, particularly those tissues in most need of oxygen. When a tissue's metabolic rate increases, so does its carbon dioxide waste production. When released into the bloodstream, carbon dioxide forms bicarbonate and protons through the following reaction:
Although this reaction usually proceeds very slowly, the enzyme carbonic anhydrase (which is present in red blood cells) drastically speeds up the conversion to bicarbonate and protons. This causes the pH of the blood to decrease, which promotes the dissociation of oxygen from haemoglobin, and allows the surrounding tissues to obtain enough oxygen to meet their demands. In areas where oxygen concentration is high, such as the lungs, binding of oxygen causes haemoglobin to release protons, which recombine with bicarbonate to eliminate carbon dioxide during exhalation. These opposing protonation and deprotonation reactions occur in equilibrium resulting in little overall change in blood pH.
The Bohr effect enables the body to adapt to changing conditions and makes it possible to supply extra oxygen to tissues that need it the most. For example, when muscles are undergoing strenuous activity, they require large amounts of oxygen to conduct cellular respiration, which generates CO2 (and therefore HCO3− and H+) as byproducts. These waste products lower the pH of the blood, which increases oxygen delivery to the active muscles. Carbon dioxide is not the only molecule that can trigger the Bohr effect. If muscle cells aren't receiving enough oxygen for cellular respiration, they resort to lactic acid fermentation, which releases lactic acid as a byproduct. This increases the acidity of the blood far more than CO2 alone, which reflects the cells' even greater need for oxygen. In fact, under anaerobic conditions, muscles generate lactic acid so quickly that pH of the blood passing through the muscles will drop to around 7.2, which causes haemoglobin to begin releasing roughly 10% more oxygen.
Strength of the Effect and Body Size.
The magnitude of the Bohr effect is usually given by the slope of the formula_1 vs formula_2 curve where, P50 refers to the partial pressure of oxygen when 50% of haemoglobin's binding sites are occupied. The slope is denoted: formula_3 where formula_4 denotes change. That is, formula_5 denotes the change in formula_1 and formula_7 the change in formula_2.
Bohr effect strength exhibits an inverse relationship with the size of an organism: the magnitude increases as size and weight decreases. For example, mice possess a very strong Bohr effect, with a formula_3 value of -0.96, which requires relatively minor changes in H+ or CO2 concentrations, while elephants require much larger changes in concentration to achieve a much weaker effect formula_10.
Mechanism.
Allosteric interactions.
The Bohr effect hinges around allosteric interactions between the hemes of the haemoglobin tetramer, a mechanism first proposed by Max Perutz in 1970. Haemoglobin exists in two conformations: a high-affinity R state and a low-affinity T state. When oxygen concentration levels are high, as in the lungs, the R state is favored, enabling the maximum amount of oxygen to be bound to the hemes. In the capillaries, where oxygen concentration levels are lower, the T state is favored, in order to facilitate the delivery of oxygen to the tissues. The Bohr effect is dependent on this allostery, as increases in CO2 and H+ help stabilize the T state and ensure greater oxygen delivery to muscles during periods of elevated cellular respiration. This is evidenced by the fact that myoglobin, a monomer with no allostery, does not exhibit the Bohr effect. Haemoglobin mutants with weaker allostery may exhibit a reduced Bohr effect. For example, in Hiroshima variant haemoglobinopathy, allostery in haemoglobin is reduced, and the Bohr effect is diminished. As a result, during periods of exercise, the mutant haemoglobin has a higher affinity for oxygen and tissue may suffer minor oxygen starvation.
T-state stabilization.
When hemoglobin is in its T state, the N-terminal amino groups of the α-subunits and the C-terminal histidine of the β-subunits are protonated, giving them a positive charge and allowing these residues to participate in ionic interactions with carboxyl groups on nearby residues. These interactions help hold the haemoglobin in the T state. Decreases in pH (increases in acidity) stabilize this state even more, since a decrease in pH makes these residues even more likely to be protonated, strengthening the ionic interactions. In the R state, the ionic pairings are absent, meaning that the R state's stability increases when the pH increases, as these residues are less likely to stay protonated in a more basic environment. The Bohr effect works by simultaneously destabilizing the high-affinity R state and stabilizing the low-affinity T state, which leads to an overall decrease in oxygen affinity. This can be visualized on an oxygen-haemoglobin dissociation curve by shifting the whole curve to the right.
Carbon dioxide can also react directly with the N-terminal amino groups to form carbamates, according to the following reaction:
CO2 forms carbamates more frequently with the T state, which helps to stabilize this conformation. The process also creates protons, meaning that the formation of carbamates also contributes to the strengthening of ionic interactions, further stabilizing the T state.
Special cases.
Marine mammals.
An exception to the otherwise well-supported link between animal body size and the sensitivity of its haemoglobin to changes in pH was discovered in 1961. Based on their size and weight, many marine mammals were hypothesized to have a very low, almost negligible Bohr effect. However, when their blood was examined, this was not the case. Humpback whales weighing 41,000 kilograms had an observed formula_3 value of 0.82, which is roughly equivalent to the Bohr effect magnitude in a 0.57 kg guinea pig. This extremely strong Bohr effect is hypothesized to be one of marine mammals' many adaptations for deep, long dives, as it allows for virtually all of the bound oxygen on haemoglobin to dissociate and supply the whale's body while it is underwater. Examination of other marine mammal species supports this. In pilot whales and porpoises, which are primarily surface feeders and seldom dive for more than a few minutes, the formula_3was 0.52, comparable to a cow, which is much closer to the expected Bohr effect magnitude for animals of their size.
Carbon monoxide.
Another special case of the Bohr effect occurs when carbon monoxide is present. This molecule serves as a competitive inhibitor for oxygen, and binds to haemoglobin to form carboxyhaemoglobin. Haemoglobin's affinity for CO is about 210 times stronger than its affinity for O2, meaning that it is very unlikely to dissociate, and once bound, it blocks the binding of O2 to that subunit. At the same time, CO is structurally similar enough to O2 to cause carboxyhemoglobin to favor the R state, raising the oxygen affinity of the remaining unoccupied subunits. This combination significantly reduces the delivery of oxygen to the tissues of the body, which is what makes carbon monoxide so toxic. This toxicity is reduced slightly by an increase in the strength of the Bohr effect in the presence of carboxyhemoglobin. This increase is ultimately due to differences in interactions between heme groups in carboxyhemoglobin relative to oxygenated hemoglobin. It is most pronounced when the oxygen concentration is extremely low, as a last-ditch effort when the need for oxygen delivery becomes critical. However, the physiological implications of this phenomenon remain unclear.


Pospiviroidae

The Pospiviroidae are a family of viroids, including the first viroid to be discovered, PSTVd. Their secondary structure is key to their biological activity. The classification of this family is based on differences in the conserved central region sequence. The genome consists (in this order) of an LH terminal domain, a pathogenic domain, conserved central region (pospiviroid RY motif stem loop), variable domain, and an RH terminal domain. "Pospiviroidae" replication occurs in an asymmetric fashion via host cell RNA polymerase, RNase, and RNA ligase.


Joshua Henry Davidson

Joshua Henry Davidson FRSE PRCPE (1785–5 January 1847) was an eminent Scottish physician who was twice President of the Royal College of Physicians of Edinburgh and also First Physician to Queen Victoria when in Scotland.
Life.
He was born around 1785 in Edinburgh, the son of Hannah, sister to Henry Mackenzie, and John Davidson of Ravelrig, landowner south-west of Edinburgh. He attended Edinburgh High School 1793-8.
He studied medicine at the University of Edinburgh, and graduated with an MD on 24 June 1807. He worked partly from the New Town Dispensary.
He was elected a Fellow of the Royal Society of Edinburgh in 1813. His proposers were Henry Mackenzie (his uncle), Thomas Charles Hope and John Playfair. He served as President of the Royal College of Physicians of Edinburgh twice: from 1829 to 1831 and 1833 to 1834. He was also a member of the Medico-Chirurgical Society of Edinburgh and the Highland Society.
He died at home, 19 Abercromby Place in Edinburgh’s New Town on 5 January 1847.
Artistic recognition.
His father had been the subject of a portrait by David Martin.
A bust of Joshua Henry Davidson by Peter Slater is held in Royal College of Physicians of Edinburgh.
Family.
His daughter, Margaret Davidson (died 1904), married James Medlicott of Kildare (1828–1913) who at 84 was the oldest still-serving magistrate in Kildare.


Hybridoma technology

Hybridoma technology is a method for producing large numbers of identical antibodies (also called monoclonal antibodies). This process starts by injecting a mouse (or other mammal) with an antigen that provokes an immune response. A type of white blood cell, the B cell, produces antibodies that bind to the injected antigen. These antibody producing B-cells are then harvested from the mouse and, in turn, fused with immortal B cell cancer cells, a myeloma, to produce a hybrid cell line called a hybridoma, which has both the antibody-producing ability of the B-cell and the longevity and reproductivity of the myeloma. The hybridomas can be grown in culture, each culture starting with one viable hybridoma cell, producing cultures each of which consists of genetically identical hybridomas which produce one antibody per culture (monoclonal) rather than mixtures of different antibodies (polyclonal). The myeloma cell line that is used in this process is selected for its ability to grow in tissue culture and for an absence of antibody synthesis. In contrast to polyclonal antibodies, which are mixtures of many different antibody molecules, the monoclonal antibodies produced by each hybridoma line are all chemically identical.
The production of monoclonal antibodies was invented by César Milstein and Georges J. F. Köhler in 1975. They shared the Nobel Prize of 1984 for Medicine and Physiology with Niels Kaj Jerne, who made other contributions to immunology. The term hybridoma was coined by Leonard Herzenberg during his sabbatical in César Milstein's laboratory in 1976–1977.
Method.
Laboratory animals (mammals, e.g. mice) are first exposed to the antigen against which an antibody is to be generated. Usually this is done by a series of injections of the antigen in question, over the course of several weeks. These injections are typically followed by the use of in vivo electroporation, which significantly enhances the immune response. Once splenocytes are isolated from the mammal's spleen, the B cells are fused with immortalised myeloma cells. The fusion of the B cells with myeloma cells can be done using electrofusion. Electrofusion causes the B cells and myeloma cells to align and fuse with the application of an electric field. Alternatively, the B-cells and myelomas can be made to fuse by chemical protocols, most often using polyethylene glycol. The myeloma cells are selected beforehand to ensure they are not secreting antibody themselves and that they lack the hypoxanthine-guanine phosphoribosyltransferase (HGPRT) gene, making them sensitive to the HAT medium (see below).
Fused cells are incubated in HAT medium (hypoxanthine-aminopterin-thymidine medium) for roughly 10 to 14 days. Aminopterin blocks the pathway that allows for nucleotide synthesis. Hence, unfused myeloma cells die, as they cannot produce nucleotides by the "de novo" or salvage pathways because they lack HGPRT. Removal of the unfused myeloma cells is necessary because they have the potential to outgrow other cells, especially weakly established hybridomas. Unfused B cells die as they have a short life span. In this way, only the B cell-myeloma hybrids survive, since the HGPRT gene coming from the B cells is functional. These cells produce antibodies (a property of B cells) and are immortal (a property of myeloma cells). The incubated medium is then diluted into multi-well plates to such an extent that each well contains only one cell. Since the antibodies in a well are produced by the same B cell, they will be directed towards the same epitope, and are thus monoclonal antibodies.
The next stage is a rapid primary screening process, which identifies and selects only those hybridomas that produce antibodies of appropriate specificity. The first screening technique used is called ELISA. The hybridoma culture supernatant, secondary enzyme labeled conjugate, and chromogenic substrate, are then incubated, and the formation of a colored product indicates a positive hybridoma. Alternatively, immunocytochemical, western blot, and immunoprecipitation-mass spectrometry screening can also be used. Unlike western blot assays, immunoprecipitation-mass spectrometry facilitates screening and ranking of clones which bind to the native (non-denaturated) forms of antigen proteins.
The B cell that produces the desired antibodies can be cloned to produce many identical daughter clones. Supplemental media containing interleukin-6 (such as briclone) are essential for this step. Once a hybridoma colony is established, it will continually grow in culture medium like RPMI-1640 (with antibiotics and fetal bovine serum) and produce antibodies.
Multiwell plates are used initially to grow the hybridomas, and after selection, are changed to larger tissue culture flasks. This maintains the well-being of the hybridomas and provides enough cells for cryopreservation and supernatant for subsequent investigations. The culture supernatant can yield 1 to 60 μg/ml of monoclonal antibody, which is maintained at -20 °C or lower until required.
By using culture supernatant or a purified immunoglobulin preparation, further analysis of a potential monoclonal antibody producing hybridoma can be made in terms of reactivity, specificity, and cross-reactivity.
Applications.
The use of monoclonal antibodies is numerous and includes the prevention, diagnosis, and treatment of disease. For example, monoclonal antibodies can distinguish subsets of B cells and T cells, which is helpful in identifying different types of leukaemias. In addition, specific monoclonal antibodies have been used to define cell surface markers on white blood cells and other cell types. This led to the cluster of differentiation series of markers. These are often referred to as CD markers and define several hundred different cell surface components of cells, each specified by binding of a particular monoclonal antibody. Such antibodies are extremely useful for fluorescence-activated cell sorting, the specific isolation of particular types of cells.
In diagnostic histopathology.
With the help of monoclonal antibodies, tissues and organs can be classified based on their expression of certain defined markers, which reflect tissue or cellular genesis. Prostate specific antigen, placental alkaline phosphatase, human chorionic gonadotrophin, α-fetoprotein and others are organ-associated antigens and the production of monoclonal antibodies against these antigens helps in determining the nature of a primary tumor.
Monoclonal antibodies are especially useful in distinguishing morphologically similar lesions, like pleural and peritoneal mesothelioma, adenocarcinoma, and in the determination of the organ or tissue origin of undifferentiated metastases. Selected monoclonal antibodies help in the detection of occult metastases (cancer of unknown primary origin) by immuno-cytological analysis of bone marrow, other tissue aspirates, as well as lymph nodes and other tissues and can have increased sensitivity over normal histopathological staining.
One study performed a sensitive immuno-histochemical assay on bone marrow aspirates of 20 patients with localized prostate cancer. Three monoclonal antibodies (T16, C26, and AE-1), capable of recognizing membrane and cytoskeletal antigens expressed by epithelial cells to detect tumour cells, were used in the assay. Bone marrow aspirates of 22% of patients with localized prostate cancer (stage B, 0/5; Stage C, 2/4), and 36% patients with metastatic prostate cancer (Stage D1, 0/7 patients; Stage D2, 4/4 patients) had antigen-positive cells in their bone marrow. It was concluded that immuno-histochemical staining of bone marrow aspirates are very useful to detect occult bone marrow metastases in patients with apparently localized prostate cancer.
Although immuno-cytochemistry using tumor-associated monoclonal antibodies has led to an improved ability to detect occult breast cancer cells in bone marrow aspirates and peripheral blood, further development of this method is necessary before it can be used routinely. One major drawback of immuno-cytochemistry is that only tumor-associated and not tumor-specific monoclonal antibodies are used, and as a result, some cross-reaction with normal cells can occur.
In order to effectively stage breast cancer and assess the efficacy of purging regimens prior to autologous stem cell infusion, it is important to detect even small quantities of breast cancer cells. Immuno-histochemical methods are ideal for this purpose because they are simple, sensitive, and quite specific. Franklin et al. performed a sensitive immuno-cytochemical assay by using a combination of four monoclonal antibodies (260F9, 520C9, 317G5 and BrE-3) against tumor cell surface glycoproteins to identify breast tumour cells in bone marrow and peripheral blood. They concluded from the results that immuno-cytochemical staining of bone marrow and peripheral blood is a sensitive and simple way to detect and quantify breast cancer cells.
One of the main reasons for metastatic relapse in patients with solid tumours is the early dissemination of malignant cells. The use of monoclonal antibodies (mAbs) specific for cytokeratins can identify disseminated individual epithelial tumor cells in the bone marrow.
One study
reports on having developed an immuno-cytochemical procedure for simultaneous labeling of cytokeratin component no. 18 (CK18) and prostate specific antigen (PSA). This would help in the further characterization of disseminated individual epithelial tumor cells in patients with prostate cancer. The twelve control aspirates from patients with benign prostatic hypertrophy showed negative staining, which further supports the specificity of CK18 in detecting epithelial tumour cells in bone marrow.
In most cases of malignant disease complicated by effusion, neoplastic cells can be easily recognized. However, in some cases, malignant cells are not so easily seen or their presence is too doubtful to call it a positive report. The use of immuno-cytochemical techniques increases diagnostic accuracy in these cases.
Ghosh, Mason and Spriggs
analysed 53 samples of pleural or peritoneal fluid from 41 patients with malignant disease. Conventional cytological examination had not revealed any neoplastic cells. Three monoclonal antibodies (anti-CEA, Ca 1 and HMFG-2) were used to search for malignant cells. Immunocytochemical labelling was performed on unstained smears, which had been stored at -20 °C up to 18 months. Twelve of the forty-one cases in which immuno-cytochemical staining was performed, revealed malignant cells. The result represented an increase in diagnostic accuracy of approximately 20%. The study concluded that in patients with suspected malignant disease, immuno-cytochemical labeling should be used routinely in the examination of cytologically negative samples and has important implications with respect to patient management.
Another application of immuno-cytochemical staining is for the detection of two antigens in the same smear. Double staining with light chain antibodies and with T and B cell markers can indicate the neoplastic origin of a lymphoma.
One study has reported the isolation of a hybridoma cell line (clone 1E10), which produces a monoclonal antibody (IgM, k isotype). This monoclonal antibody shows specific immuno-cytochemical staining of nucleoli.
Tissues and tumours can be classified based on their expression of certain markers, with the help of monoclonal antibodies. They help in distinguishing morphologically similar lesions and in determining the organ or tissue origin of undifferentiated metastases. Immuno-cytological analysis of bone marrow, tissue aspirates, lymph nodes etc. with selected monoclonal antibodies help in the detection of occult metastases. Monoclonal antibodies increase the sensitivity in detecting even small quantities of invasive or metastatic cells. Monoclonal antibodies (mAbs) specific for cytokeratins can detect disseminated individual epithelial tumour cells in the bone marrow.


Sfiso Buthelezi

Sfiso Norbert Buthelezi (born 1961) is a South African politician and a member of the country's ruling party the African National Congress.
Buthelezi was appointed as the Deputy Minister of Finance after president Jacob Zuma reshuffled his cabinet and removed the Minister and Deputy Minister of Finance Pravin Gordhan and Mcebisi Jonas in April 2017. He was the first CEO of the National Gambling Board before joining Makana Investment.
When Jacob Zuma resigned as the President of South Africa on 14 of February 2018 there was much media speculation that Buthelezi would be removed from Cyril Ramaphosa's cabinet.
Ramaphosa reshuffled his cabinet and moved Buthelezi to the position of Deputy Minister of Agriculture.


Freya Wilson (Doctors)

Freya Wilson is a fictional character from the BBC soap opera "Doctors", portrayed by Lu Corfield. She made her first appearance on 11 May 2011, and departed "Doctors" on 18 June 2012 after dying in a house fire. Following the character's death, Corfield went on to play the role of her sister, Lois Wilson, in 2014.
Storylines.
An open bisexual, Freya attends an interview at the Mill Health Centre and meets a fellow applicant, Kevin Tyler (Simon Rivers). The pair take an instant dislike to one another. Freya is mentored by Zara. Freya later starts a casual relationship with her friend Bobbie Greene (Gareth Jewell). Their romance soon becomes complicated when Freya decides that she would like more commitment. The pair later end their relationship.
Creation and casting.
Series producer Peter Lloyd asked his team to create two new characters. Dawn Coulson, who works as the serial's script editor was given the task of creating one of the roles. She decided that the character would be female and felt that the series needed a character who was quite different in comparison to their established set.
Corfield began filming on 18 February 2011, alongside fellow new cast member Simon Rivers who plays Kevin Tyler. She felt that it was great having someone else who was new by her side. Corfield and Rivers began shooting during triple banking and also had a documentary crew working with them. In early May, "Doctors" released a video on the serial's official website. This was to introduce their audience to the new characters. Lloyd said that when the series created new characters he worried about the casting stages. This was because he believed it can ruin the work put in during the creation process. However, Lloyd praised Corfield and Rivers' casting because he believed that they were just "right" and a "couple of corkers". Lloyd later told Daniel Kilkelly of Digital Spy that the introduction of Freya and Kevin had helped to "even things out" and create a "good cross section". Corfield's first scenes as Freya aired during the episode broadcast on 11 May 2011.
Character development.
Characterisation and Kevin Tyler.
The BBC initially described Freya as a "confident, career-hungry trainee GP". Corfield told Eden Carter Wood of "Diva" magazine that Freya made a big impact on her arrival and was instantly "pigeon-holed" by her colleagues. She described Freya as being a "passionate women's activist" who is not as together as she seems. Corfield felt that Freya hides behind her casual style. Freya sports a "eternal sloppy student" image complete with "jeans, trainers and baggy jumpers" which ultimately gives the impression that she makes no effort with her appearance. Freya does not feel the need to "conform to social conventions". While Corfield opined that she believes that Freya just does not believe she can find a meaningful relationship. Corfield told Rachel Mainwaring of the "Western Mail" that Freya is an exact opposite of her colleague Zara Carmichael (Elisabeth Dermot Walsh). Freya likes to help a "damsel in distress", something that Corfield said would ultimately land Freya into trouble. Danielle Henry who plays Freya's love interest, Mandy Marquez, told Digital Spy's Kilkelly that Freya "is the classic example of the road to hell being paved with good intentions". She always attempts to do "the right thing" and this leads to situations going wrong. Freya never has the intention of ruining her involvement in situations - but she never considers the eventual outcome.
Freya's development became more prominent in the latter half of 2011. Corfield stated that Freya had only been a catalyst in other character's storyline up until October 2011. She added that the scripts she had been given indicated that there would be a focus on discovering who Freya really is. She added that during November 2011, Freya's story "changes in a big way" where she is no longer the "reactor and an accomplice". Freya later begins a relationship with Kevin. Corfield told Digital Spy's Kilkelly that she and Rivers went on "a massive journey" together as they played their character's relationship. Initially the duo fought like "cat and dog" which eventually develops into a "fondness between them". Corfield added that "their default setting is to always snap at each other, but they care about each other a lot and they'll always look out for each other."
Relationship with Mandy Marquez.
Freya's following relationship is with a female character, Mandy Marquez (Danielle Henry). Lloyd told Katy Moon of "Inside Soap" that he believed Freya needed to grow up and have a "mature relationship" with meaning. He added that Freya's crush on Cherry Malone (Sophie Abelson) and her fling with Kevin were a direct result of Freya searching for stability. However, Mandy is left to contend with Freya's prevailing feelings for Kevin. Corfield opined that the dynamic of the three characters was "glorious" and that Mandy is not sure where she fits in. Freya reassures Mandy, but "there's still such a pull towards Kevin" which she fails to hide. Corfield revealed that Freya and Mandy's romance would face problems in future episodes. Freya is "useless" in relationships because she is "petrified" that something will go wrong as she has never been treated well. While Corfield felt that the pair setting up home was moving too fast, in the long-run it would benefit Freya. She added that Freya would mess things up "quite wonderfully" which sets the scene of the relationship that will not run smoothly. It was noted that a "Doctors" storyline never usually develops without problems. Like Corfield; Henry also believed Freya's "love-hate relationship" with Kevin could cause issues. Although, their relationship has positive traits which help Freya. Mandy is characterised as "honest" and "very upfront", which works out well for the indecisive Freya. Mandy's "straight-down-the-line" attitude and dislike to overcomplicate a situation; results in her just wanting to be with Freya. Mandy does not foresee the possible problems that Freya does. In one storyline, Freya promotes her blog on a radio station and gets ridiculed for her bisexuality. Mandy interrupts the broadcast to help Freya, which sets the theme of Mandy acting as her support network.
Henry later told Kilkelly that she thought "Doctors" did a "really good job" of making their character's sexuality incidental. She branded the realism of their lesbian relationship a rare occurrence on television - adding that they made a departure from the stereotypes and dramatisation associated with gay characters.
Freya has a "massive setback" when she fails her exams and Kevin wins the position they were competing for. She is forced to evaluate her life and contemplate why she has failed. For Corfield herself, this was a special and heart-breaking episode. Freya expects Kevin to be insensitive and boast about his promotion, but he actually "gutted" which shocks Freya. Corfield said that the support from two people that she loves "raises some questions for her". The character's career path is also affected by her obsession with online blogging. Instead of concentrating more on her career, she uses her blog as a "complete distraction". Freya is not getting the praise she wants from her online followers and not her work place. Corfield told Kilkelly, that Freya's online activities lead her into trouble when she meets one of her followers. However, she was not permitted to reveal any more details about the storyline.
Departure.
On 1 June 2012, Digital Spy's Kilkelly reported that "Doctors" would air an "unmissable" episode on 18 June prior to the series taking a three-week hiatus. He added that the episode would leave viewers with a "big and tragic cliffhanger". He later revealed that both Freya and Kevin would be involved in a fire storyline leading to them both being seriously injured. After an argument with Kevin she goes around to his house to find it on fire. Freya decides to enter the building in an attempt to save Kevin. Kilkelly added that there would be a "shock ending" to the episode which would leave an "agonising" three-week wait to see if they survive. He later reported that Kevin survives the blaze, but Freya dies in hospital leaving Mandy "grief-stricken".
Reception.
For her portrayal of Freya, Corfield received a nomination for Best Newcomer at the 2012 British Soap Awards. At the 2012 "Inside Soap" Awards, Corfield was nominated for Best Daytime Star. Alison Slade from "TVTimes" said that Corfield was a strong contender for the accolade because Freya had been a "breath of fresh air". A columnist for AfterEllen said that Freya's sexuality was true to life and not "likely to be straight-forward". They hoped that "Doctors" would explore Freya's sexuality, noting that it would be the "first time" the series had developed a bisexual character. Corfield received "a lot" of letters from viewers telling her that Freya is a positive role model. Henry said that she often received "really positive feedback" via Twitter regarding Freya and Mandy's relationship.


Thrissur Ayurveda Cluster

Thrissur Ayurveda cluster is an Ayurveda cluster situated in KINFRA Park in Koratty in Thrissur District. The cluster is meant for a comprehensive development of Kerala brand of Ayurvedic products and train the manufacturers of Ayurveda products on the importance of safety, quality and efficacy. The cluster have facilities for testing and analysis, process product validation, safety study and manufacture. The cluster is approved by the Department of Ayurveda, Yoga & Naturopathy, Unani, Siddha and Homoeopathy (AYUSH).
History.
The Government of India in 2005 sanctioned Rs 29 crore for setting up an Ayurveda cluster in Thrissur District to develop Ayurvedic products so as to compete in the international markets. The cluster is implemented by a consortium of 62 Ayurveda products manufacturers in Kerala known as Confederation for Ayurvedic Renaissance Keralam Ltd (CARe-Keralam), Kerala Industrial Infrastructure Development Corporation (Kinfra) and Kerala Industrial Development Corporation (KSIDC).
Infrastructure.
The cluster unit was set up on 5 acres of land at the Kinfra Park and started working in 2010. The cluster includes five buildings, one godown, one museum, one analytical laboratory, one process validation lab, one toxicology lab and one common production centre. The area of the buildings comes around 60,000 square feet. In the second phase of development, the production area will be increased. The Government of India and Department of Ayush, under Ministry of Health has also set up a Rs 20-crore quality testing facility in the cluster for exporters of Ayurveda medicine. The cluster has 53 manufacturing units as members and can be increased. About 20,000 direct job opportunities would be generated in phases.


Bacterial stress response

The bacterial stress response enables bacteria to survive adverse and fluctuating conditions in their immediate surroundings. Various bacterial mechanisms recognize different environmental changes and mount an appropriate response. A bacterial cell can react simultaneously to a wide variety of stresses and the various stress response systems interact with each other by a complex of global regulatory networks.
Bacteria can survive under diverse environmental conditions and in order to overcome these adverse and changing conditions, bacteria must sense the changes and mount appropriate responses in gene expression and protein activity. The stress response in bacteria involves a complex network of elements that counteracts the external stimulus. Bacteria can react simultaneously to a variety of stresses and the various stress response systems interact (cross-talk) with each other. A complex network of global regulatory systems leads to a coordinated and effective response. These regulatory systems govern the expression of more effectors that maintain stability of the cellular equilibrium under the various conditions. These systems can include immediate responses such as chaperones, as well as slower responses like transcriptional regulation to control protein production, latency, and others.
Stress response systems can play an important role in the virulence of pathogenic organisms. Their stress response systems, such as entering into a latent state, can allow them to survive the stressful conditions inside of the host or other surroundings.
There are regulatory systems that respond to changes in temperature, pH, nutrients, salts, and oxidation. The response level is based on the amount of change that occurs in the environment. The response is highest when changes occur under stress conditions, in this case the control networks are called stress response systems. These systems are very similar within prokaryotes and some of the systems, specifically the heat shock response, are conserved in eukaryotes and archaea. While the systems are extremely similar, the conditions under which they are activated differ greatly from organism to organism. The systems that activate the response to environmental change have many control elements. These control elements can be specific to one gene or they can control a large group of genes. When control elements control a large group of genes it is called a regulon. A regulon is a group of genes that are all regulated by the same control pattern. A stimulon is all the genes who express responses to the same condition. The control elements also regulate the expression of genes during various environmental conditions including starvation, sporulation and others.
Types.
An initial stress response systems that will likely go into effect against situations that are damaging to the bacterial cell is chaperones. Chaperones are proteins that are responsible for keeping other proteins in their proper conformations by binding to them. Without the chaperones as a first line of defense, other stress response systems would not be able to react quickly enough to stop proteins from denaturing in time. While a protein is denaturing, it will produce intermediate conformations of itself, and these intermediates are what activate chaperone proteins. Another major stress response system is transcriptional regulation. Many transcriptional regulation systems are well defined, while others are less understood, but they can be activated by different pathways and stimuli, and is a general response to most stimuli. What this involves is proteins binding to promoter regions of DNA to regulate which sections are transcribed into RNA. The concentration of different RNA transcripts is then altered to favor the production of those that will produce proteins that will mitigate the effects of the stimulus. However, this system may be limited by the translational ability of the cell. The transcriptional changes can only be effective if ribosomal speed to translate mRNA to protein is quick enough. This can be a bottleneck in the capability of bacteria to react to stressors quick enough, and some stressors, such as oxidative stress, can inhibit the function of ribosomes.
A stress response that can occur under conditions that are non-advantageous, but also non-lethal, is the creation of a biofilm. In this response, bacterial cells can secrete extracellular polymeric substances to form a film that can provide support to the bacterial colony, such as by improving their ability to adhere to a surface. Another common stress response is latency. In a latent states, a cell will slow down its metabolism and become virtually dormant. This makes the cell much less affected by stressors such as antibacterial agents, starvation, hypoxia, and acidity. Some bacteria are able to enter a latent state and remain there for up to years before returning to an active state. A cell can also shift from production of unsaturated fatty acids to saturated fatty acids to decrease the fluidity of the cellular membrane. If the stressor is a molecule, this will make it more difficult for it to get into the cell. Overall cellular morphology can also be changed in response to a stressor.
In bacteria some other important stress response systems are:
Heat Shock Response.
Heat Shock Response helps to stop any damage to the cellular process in high temperature conditions. It is also caused because the heat allows for the proteins to be transcriptionally upregulated which also helps to protect the bacteria from protein denaturation. Heat proteins are created by factors of heat-shock promoters. Some heat proteins that are created are chaperones and proteases. This means that the protein will be folded the correct way as well as position in the right portions of the cell. It also ensures that any protein that is not folded correctly will be destroyed properly to ensure that the bacteria remains to function properly.
Envelope Stress Response.
The two-component signal transduction (2CST) system also allows the bacterial cell to be able to sense stress in the system. This is due to a histidine kinase that can be found in the cell's inner membrane, to detect the stress. It is able to detect the stress because of autophosphorylation that happens when the stress is detected. Once the stress is detected, the system moves to a cytoplasmic response regulator. This is due to the cell being in a phosphate group, but this new response regulator will start to act like a transcription factor. This means that it will start to change what is expressed when looking at the genes. This is especially true when looking at the Cpx proteins which help to prevent the protein from folding the wrong way or not at all. Cpx proteins also help to ensure that there will be no other damage when looking at other cellular processes.
Cold Shock Response.
When bacteria is in an area of very low and cold temperature, they will have a five hour long phase that will cause them not to grow at all. The way the bacteria tries to adapt is by creating child shock proteins that will be transcription factors that will be upregulated during the five hour phase. Once this five hour period ends, the bacteria will start to grow again, but it will be at a very slow rate. These proteins will help for the bacteria to continue to grow and survive at the lower temperatures. A protein called CspA was originally found in E. coli and is known to be one of the first cold shock proteins discovered and is known to be a single-stranded RNA. This will ultimately help with transcription and translation. With cold shock proteins, It is not just transcription and translation. You can also see that there can be condensation of the chromosome that occurs. This means that the cells will prematurely go onto the interphase stage of mitosis. There will also be an organization of the nucleoid which is when the intracellular and extracellular factors in the cell. And lastly, there is an enhancement when it comes to the survival of bacteria which helps the cell to get the food and nutrients it needs to survive.
Types of Stressors.
A stressor that can induce a stress response in bacteria can be any condition outside of the ideal conditions for survival. The stressors that inflict harm to the cell are the ones that illicit the strongest responses. One such stressor is exposure to reactive oxygen species and reactive chlorine species chemicals that are used as disinfectants. Included in this category is sodium hypochlorite(NaOCl), or household bleach. These chemicals inflict extensive cellular damage to different systems such as the bacterial membrane, denaturation of proteins, and interference with biomolecules such as amino acids, nucleic acids, and lipids. Another type of stressor could be the absence of an favorable electron acceptor for cellular respiration. The shift from a more favorable energy production to a less favorable one, such as nitrate, has been shown in a study to change cell morphology and composition of the cellular membrane. Other types of stressors include oxidants, nutrient deprivation, hypo/hyper-osmolarity, extreme pH, extreme temperature, and antimicrobial substances. This list of stressors is not comprehensive, as stressors by definition can be anything and everything that may not be favorable to a cell.


Tomasz Guzik

Tomasz Jan Guzik (born 8 March 1974 in Kraków, Poland) is a Polish physician scientist. Since 2012, he has been the Regius Professor of Physiology at the University of Glasgow.
He is a member of the American Heart Association and scientific societies of Poland, United Kingdom and the United States of America.
Early life and education.
Guzik graduated in Medicine from Jagiellonian University School of Medicine in Kraków, He continued his education in Oxford receiving a degree in molecular medicine from the University of Oxford where he studied under the guidance of Prof Keith M Channon. He received PhD degree in 2000 under the guidance of Prof Juliusz Pryjma and in 2004 became an Assistant Professor of Jagiellonian University.
Academic career.
His scientific work concerns vascular biology and pharmacology of endothelium. His research focuses on the mechanisms of oxidative stress in human vasculature and on the search for novel antioxidants which could be clinically more useful than vitamins currently available. Working in the Wellcome Trust in Oxford he found the possible relationships between genetic variation of human genome and free radical production and oxidative stress. He described selected mechanisms of oxidative stress in human diabetes mellitus.
Notable recognition that Guzik has received include the honorary Bernard and Joan Marshall Prize in Research Excellence from the British Society for Cardiovascular Research and the Corcoran Memorial Prize and Lecture from the American Heart Association in 2017.
Guzik is the current Editor-in-Chief of Cardiovascular Research, a high-impact academic journal produced by the European Society of Cardiology.
Honours.
He has received awards from the Polish Government, Crescendum Est Polonia Foundation, Wellcome Trust and others. In 2010, he was awarded the Prize of the Foundation for Polish Science.


Francis Wesley Lipsett

Francis Wesley Lipsett (October 25, 1850 – October 27, 1889) was a veterinarian and political figure in Manitoba, Canada. He represented Woodlands from 1879 to 1883 in the Legislative Assembly of Manitoba as a Liberal-Conservative.
He was the son of Robert Lipsett and Caroline Campbell and was educated at the Toronto Veterinary College. Lipsett practised in Woodlands, Manitoba and then in Portage la Prairie. He was defeated when he ran for reelection in 1883. He was an investor in the Portage la Prairie Street Railway Company.


Bacterial pneumonia

Bacterial pneumonia is a type of pneumonia caused by bacterial infection.
Types.
Gram-positive.
"Streptococcus pneumoniae" () is the most common bacterial cause of pneumonia in all age groups except newborn infants. "Streptococcus pneumoniae" is a Gram-positive bacterium that often lives in the throat of people who do not have pneumonia.
Other important Gram-positive causes of pneumonia are "Staphylococcus aureus" () and "Bacillus anthracis".
Gram-negative.
Gram-negative bacteria are seen less frequently: "Haemophilus influenzae" (), "Klebsiella pneumoniae" (), "Escherichia coli" (), "Pseudomonas aeruginosa" (), "Bordetella pertussis", and "Moraxella catarrhalis" are the most common.
These bacteria often live in the gut and enter the lungs when contents of the gut (such as vomit or faeces) are inhaled.
Atypical.
Atypical bacteria causing pneumonia are "Coxiella burnetii", "Chlamydophila pneumoniae" (), "Mycoplasma pneumoniae" (), and "Legionella pneumophila".
The term "atypical" does not relate to how commonly these organisms cause pneumonia, how well it responds to common antibiotics or how typical the symptoms are; it refers instead to the fact that these organisms have atypical or absent cell wall structures and do not take up Gram stain in the same manner as gram-negative and gram-positive organisms.
Pneumonia caused by "Yersinia pestis" is usually called pneumonic plague.
Pathophysiology.
Bacteria typically enter the lung with inhalation, though they can reach the lung through the bloodstream if other parts of the body are infected. Often, bacteria live in parts of the upper respiratory tract and are continuously being inhaled into the alveoli, the cavities deep in the lungs where gas exchange takes place. Once inside the alveoli, bacteria travel into the spaces between the cells and also between adjacent alveoli through connecting pores. This invasion triggers the immune system to respond by sending white blood cells responsible for attacking microorganisms (neutrophils) to the lungs. The neutrophils engulf and kill the offending organisms but also release cytokines that result in a general activation of the immune system. This results in the fever, chills, and fatigue common in bacterial and fungal pneumonia. The neutrophils, bacteria, and fluid leaked from surrounding blood vessels fill the alveoli and result in impaired oxygen transportation.
Bacteria can travel from the lung into the blood stream (bacteremia) and can result in serious illness such as sepsis and eventually septic shock, in which there is low blood pressure leading to damage in multiple parts of the body including the brain, kidney, and heart. They can also travel to the area between the lungs and the chest wall, called the pleural cavity.
Prevention.
Prevention of bacterial pneumonia is by vaccination against "Streptococcus pneumoniae" (pneumococcal polysaccharide vaccine for adults and pneumococcal conjugate vaccine for children), "Haemophilus influenzae" type B, meningococcus, "Bordetella pertussis", "Bacillus anthracis", and "Yersinia pestis".
Treatment.
Antibiotics are the treatment of choice for bacterial pneumonia, with ventilation (oxygen supplement) as supportive therapy. The antibiotic choice depends on the nature of the pneumonia, the microorganisms most commonly causing pneumonia in the geographical region, and the immune status and underlying health of the individual. In the United Kingdom, amoxicillin is used as first-line therapy in the vast majority of patients acquiring pneumonia in the community, sometimes with added clarithromycin. In North America, where the "atypical" forms of community-acquired pneumonia are becoming more common, clarithromycin, azithromycin, or fluoroquinolones as single therapy have displaced the amoxicillin as first-line therapy.
Local patterns of antibiotic resistance always need to be considered when initiating pharmacotherapy. In hospitalized individuals or those with immune deficiencies, local guidelines determine the selection of antibiotics.
Gram-positive organisms.
"Streptococcus pneumoniae" — amoxicillin (or erythromycin in patients allergic to penicillin); cefuroxime and erythromycin in severe cases.
"Staphylococcus aureus" — flucloxacillin (to counteract the organism's β-lactamase).
Atypical organisms.
People who have difficulty breathing due to pneumonia may require extra oxygen. An extremely sick individual may require artificial ventilation and intensive care as life-saving measures while his or her immune system fights off the infectious cause with the help of antibiotics and other drugs.


J. Morton Howell

Joseph Morton Howell (March 17, 1863 Uniopolis, Ohio–1937) was a political appointee who served first as Agent/Consul General (appointed October 7, 1921) before being appointed Envoy Extraordinary and Minister Plenipotentiary to Egypt. While in Egypt, Howell "was one of four representatives of foreign nations present at the formal opening of the tomb of Tut-Ankh-Amen."
Howell graduated from Starling Medical College (now known as Ohio State University College of Medicine) in 1885.


Gustav Alexander

Gustav Alexander (1873 – 12 April 1932) was an Austrian otolaryngologist remembered for describing Alexander's law. He was the director of the Department of Otology of the "Wiener Allgemeine Poliklinik" from 1917 until his death. He was the father of Leo Alexander.
He was assassinated on the street between his home and the Poliklinik by Johann Sokoup, a Czechoslovakian former patient who had tried to assassinate him 22 years earlier.


Megan Gunnar

Megan R. Gunnar is an American child psychologist, currently Regents Professor and McKnight University Professor at University of Minnesota and an Elected Fellow of the American Academy of Arts & Sciences. In 2021, she will receive the James McKeen Cattell Lifetime Achievement Award for Applied Research from the Association for Psychological Science (APS). She is the main investigator for the International Adoption Project.
Education.
Gunnar received her PhD from Stanford University in 1978. She then did a postdoctoral fellowship at Stanford Medical School, in Developmental Psychoneuroendocrinology. She has a BA in psychology from Mills College.


Medsoc


Catherine Banfield

Catherine "Cate" Banfield is a fictional character in the American medical drama "ER", portrayed by Angela Bassett. She is an attending physician with a mysterious past with County General. Bassett's addition into the main cast opening credits was in the 2nd episode of season 15.
Life at County and Career.
Banfield was hired in 2008 to become the permanent Chief of the Emergency Department, replacing Dr. Skye Wexler who was serving as acting chief. The board had decided to offer the permanent position to Dr. Gregory Pratt, but with Pratt's death, Banfield was brought in as his replacement. She first appeared in the second episode of Season 15 and immediately puts the whole ER on edge with her tough attitude. It was mentioned that she flew to Indonesia to help that country deal with the 2004 tsunami disaster. On her first day, Nurse Haleh mentioned Banfield looked familiar as if she's been at County before, which Banfield immediately denies. Her first day as Chief tested her skills as an able and efficient leader when a bio-terrorist released a bag of weaponized Ricin in the ER, necessitating an evacuation and quarantine. She briefly met and clashed over a gunshot case with Abby Lockhart, who was finishing her last shift on her last day at County General. Nonetheless, Banfield made amends with her new acquaintance before Abby departed for Boston.
In the episode "Heal Thyself", the treatment of a little girl who almost drowned in the Chicago River triggered painful memories, yet in the end it helped Banfield figure out how to save the girl from a certain death, thereby in her mind redeeming herself from the mistakes she made with her son Darryl.
Later in Season 15, Cate and Archie Morris get snowed in at a conference in Omaha. Banfield ends up getting drunk and makes a wild scene of entertainment in the hotel lobby. She smiles and actually laughs for the first time (probably the first time since before the accident). The two end up having to share a room together before flying back to Chicago. Cate begins to open up more to Morris how they tried to have another baby a few years back but miscarried.
Early life.
In the Season 15 episode "Heal Thyself", the audience begins to learn about Cate Banfield's haunting past and how her experiences have damaged her emotionally. Set in 2002, 6 years earlier, the flashback episode revealed a happier Cate Banfield with her husband Russell (played by Bassett's real life husband, actor Courtney B. Vance) and their 5-year-old son Darryl. Banfield had a more youthful look with longer black hair. She is smiling, which was never seen by the show's audiences until this point. In this episode, she stated to Dr. Greene that she worked as an ER attending physician at the University of Chicago. She went to medical school at Johns Hopkins School of Medicine.
During a day out in the city park, Darryl was struck with a mysterious seizure. Cate at first didn't see it as anything serious and argued against calling 9-1-1, even though her husband Russell insisted. After Darryl began vomiting blood, Cate brought him to County General and was diagnosed by Dr. Mark Greene in Trauma 1. Darryl had acute leukemia, and died from advanced complications that arose with his illness. Cate's initial denial and delay contributed to one of the factors that led to Dr. Greene not being able to save Darryl. This explains how Nurse Haleh had recognized her before and the chilling moment Banfield had on her first day stepping into Trauma 1. In the last scene of the episode, Banfield and Greene talk about what happened near the Chicago River and how the ordeal proved to be completely damaging in Cate's mind and to her relationship with her husband.
Personal life.
In the present day in the episode "Heal Thyself" after Darryl's death, Cate lay in Darryl's empty room, where her husband Russell tells her how he never blamed her for what happened, and Cate cries for the first time over her son's death. Morris is stunned to learn that Cate is working at the hospital where her son died. Later in the season Cate has an appointment with Janet Coburn from O.B. since she and Russell decide they want to try for a baby one last time, even though Coburn tells them the chances are slim. Cate begins to take special injections of hormones to help with her chances in the process and tries to remain hopeful over all the odds, but she and Russell are devastated when the egg implantation process has zero success. Later in the season a mother abandons a baby at County with whom Cate bonds. She convinces Russell that they should adopt the baby. When in the penultimate episode the mother arrives to take him back, Cate convinces her to let her and Russell openly adopt the child.


Noakhali Medical Assistant Training School (MATS)

Noakhali Medical Assistant Training School provides 3 years course and 1-year internship Medical Assistant Training courses under Directorate General of Health Services (DGHS). Noakhali MATS is one of eight MATS along with Bagerhat, Kushtia, Sirajganj, Tangail, Comilla, Faridpur and Jhenaidah.


Rowan Nicks

George Rowan Nicks OBE FRACS FRCS AO (24 February 1913 - 26 May 2011) was a New Zealand surgeon. The Rowan Nicks Fellowships and Scholarships are awarded in his name by the Royal Australasian College of Surgeons.


NHS internal market

The NHS internal market was established by the National Health Service and Community Care Act 1990, to separate the roles of purchasers and providers within the National Health Service in the United Kingdom. Previously, healthcare was provided by health authorities which were given a budget to run hospitals and community health services (but not general practice) in their area. The Health and Social Care Act 2012 was intended to open up the internal market to external competition. The 2019 NHS Long Term Plan called for the establishment of integrated care systems across England by 2021, effectively ending the internal market.
Establishment.
Although the Thatcher government was slow to reform the NHS, following the 1983 Griffiths report, from 1988 it began to apply the principles of New Public Management vigorously across the welfare state. The plan was to decentralize decision making and introduce competition, with the state becoming a purchaser, rather than a provider, of welfare services.
The setting up of the market required the establishment of a system of Payment by Results and the formulation of a national NHS Tariff to complement the funding formula devised by the Resource Allocation Working Party. The Tariff includes a weighting system, the market forces factor, which pays providers in high-cost areas – principally in London – enhanced fees. In 2019 it was decided to reduce the London weighting.
The internal market initially established NHS trusts, in five annual waves, as separate bodies, splitting purchasers from providers. Until they became trusts the providing organisations were called directly managed units. The trusts had boards with non-executives, analogous to company boards, and business people were encouraged to serve on the boards. The Act also established GP Fundholding, a scheme whereby individual GP practices could take over the management of hospital services for their patients. Fundholding was abolished by the Labour Government in 1997/8. The Labour Party had campaigned against the internal market, but did not abolish it, though Tony Blair told the Labour Party conference in 1999 that the dreaded Tory internal market was finally banished for good. It introduced primary care groups, which were soon converted into primary care trusts—"thereby universalising fundholding while repudiating the concept."
Julian Le Grand was one of the chief proponents of quasi-markets influencing the Blair governments.
The fundamental concept was that patients would choose between different providers, money would follow the patients and so the best hospitals (there was never any choice of community health services) would prosper. It was never explained what would happen to the less successful institutions. As Kenneth Arrow explained in his famous 1963 paper, Uncertainty and the Welfare Economics of Medical Care "A competitive healthcare market is grounded in the expectation that some hospitals or surgeries will go bust". No hospitals did go bust, and only a minority of patients, mainly those needing elective surgery, were in a position to exercise choice between providers. Furthermore, as Arrow explained, “In practice, the theoretical advantages of choice are outweighed by the fact that people don’t do a good job of making these choices in a competitive environment—it’s almost impossible.”
In lieu of commercial failure, health and social care service regulators were established, first the Commission for Health Improvement, which was replaced by the Healthcare Commission and then the Care Quality Commission.
Cost.
Opponents of the internal market have regularly claimed that the introduction of the internal market increased NHS administration costs from 5% to 14% of total expenditure. As a report from York University pointed out "There are no agreed definitions of ‘administration’ and ‘management’ in health care between (and sometimes even within) countries’ health care systems." Nor is it clear which administrative functions are attributable to the market. Administrative costs in the NHS were generally thought to be lower than in other systems as there were no systems for billing patients, and indeed until the advent of the internal market there was little discussion of the costs of treatments. The number and cost of managers, administrative and clerical staff certainly increased significantly between 1988 and 1992, but Full Fact concluded that "No-one knows the exact cost or benefit of the NHS internal market in England".
The internal market was never introduced in Scotland, and was quickly abandoned in Wales, but there doesn't appear to be any evidence to suggest that the NHS is more efficient than in England. Such evidence is there is shows that performance across the UK is quite similar.
Political impact.
The internal market is no longer seen as a political asset by either of the main political parties. The Conservative manifesto in 2017 admitted that the NHS internal market could fail ‘to act in the interests of patients and creates costly bureaucracy’. Even right wing commentators concede that introducing the market into healthcare resulted in higher costs and clinicians complain that they have to collect data that is essential to services competing for contracts. Senior Conservative ministers said in 2014 that the Health and Social Care Act 2012 was biggest mistake they have made in government and that it undermined public trust of their stewardship of the NHS.
In 2016, Jeremy Corbyn repeatedly pledged that the Labour Party would re-establish "a modern health and social care service that is fully publicly provided and fully publicly funded".
Reform.
The reforms introduced in 2017 by Simon Stevens are regarded as the official abandonment of the policy of competition in the English NHS, the establishment of integrated care systems effectively ending the purchaser-provider split, although there has not yet been any legislative acknowledgment of the change in policy. In February 2019, NHS England called for the repeal of the regulations made under section 75 of the Health and Social Care Act 2012 which require competitive tendering.
From March 2019, with the effective merger of NHS Improvement and NHS England, there was no longer any real purchaser/provider split at a national level.
The move away from Payment by Results, which started in 2019, further undermines the principles of the internal market, as it is intended to reduce incentives for increases in hospital activity.
Karen James, chief executive of Tameside and Glossop Integrated Care NHS Foundation Trust, said in July 2020 that the NHS should aim to permanently scrap activity-based payment tariffs for acute care because block contracts – in which trusts are paid a set level of income – had encouraged "the right behaviours" in Greater Manchester during the COVID-19 pandemic in England.
In the financial allocations to local systems covering the second half of 2020–21, incentives and penalties depend solely on system-level performance, not performance of individual organisations.


Franz Kaspar Hesselbach

Franz Kaspar Hesselbach (27 January 1759 – 24 July 1816) was a German surgeon and anatomist who was a native of Hammelburg.
He was a pupil, and later Prosector under Karl Kaspar von Siebold (1736–1807) at Würzburg. Later Hesselbach was a lecturer at Würzburg, where one of his students was Konrad Johann Martin Langenbeck (1776–1851). His son, Adam Kaspar Hesselbach (1788–1856) was also a surgeon.
As a surgeon, Hesselbach is best known for his work with hernia operations. He was the first to describe a handful of anatomical structures, such as the cribriform fascia (Hesselbach's fascia), interfoveolar ligament (Hesselbach's ligament) and the inguinal triangle (Hesselbach's triangle).


Ear Research Foundation

The Ear Research Foundation, located in Sarasota, Florida, is a center for research and development and medical education. Herbert Silverstein, M.D., is the president and founder of the non-profit corporation.
Significance.
A division of the Silverstein Institute, the Ear Research Foundation is one of the largest centers in the world for:
Facilities and equipment.
The Ear Research Foundation maintains a complete microsurgical laboratory, and an audiovisual and scientific library for ear physicians and surgeons. In 2004, Gloria and Louis Flanzer donated $100,000 to the Temporal Bone and Research Laboratory in the Ear Research Foundation wing. This donation enabled the Ear Research Foundation to purchase microscopes, flat screen monitors and video equipment which visiting physicians use to learn minimally invasive surgical techniques.
Academic opportunities.
The Ear Research Foundation also offers a Clinical Fellowship for board eligible or board certified otolaryngologists. The Fellowship provides training in the diverse field of otology. Thirty two fellows have been trained as of 2007.
The Ear Research Foundation offers lectures and symposia, including a Ménière's Symposium, Minimally Invasive Otologic Surgery course, Non-Invasive Cosmetic Facial Rejuvenation and many others. They also host several support group meetings including Tinnitus and Cochlear Implant Support Group Meetings.
Treatment of ear and sinus disorders.
The Ear Research Foundation also provides medical care, treatment, and rehabilitation of ear diseases and hearing and balance disorders. Primarily for the low-income sector, Ear Research Foundation provides some treatment funding for children and adults referred from such agencies as children's Medicaid Children's Medical Service, Early Learning Coalition, County Health Department, public schools and service agencies. Ear Research Foundation doctors donate 10 hours each week to provide medical and surgical care.
The Flanzer Children's Hearing Outreach Program, which is run by the Ear Research Foundation, was established in 2004 by a donation from Gloria & Louis Flanzer. The program travels to local pre-schools and daycare facilities to test children's hearing. It offers a free children's clinic to diagnose and treat all ear, nose and throat problems. The Ear Research Foundation clinic has treated 35,000 children and has performed over 8000 surgeries including many cochlear implant surgeries for indigent children.


John Nyathi Pokela

John Nyathi "Poks" Pokela (1922 or 1923 – 30 June 1985) was a South African political activist and Chairman of the Pan Africanist Congress (PAC). Born in Herschel in the Transkei region, he was educated at Healdtown Comprehensive School and the University of Fort Hare. Originally a member of the African National Congress Youth League, he left the African National Congress and helped found the PAC in the late 1950s.
Incarceration on Robben Island.
In 1966, he was sentenced to 13 years in prison on Robben Island on charges of sabotage related to the Azanian People's Liberation Army (APLA), the militant wing of the Pan Africanist Congress; he had helped found the APLA (originally known as Poqo) in 1961, along Z. B. Molete and Clarence Makwetu.
While incarcerated, Pokela worked towards uniting the various factions of the PAC. In 1980, having served his sentence, Pokela was released from Robben Island. In February 1981, he was appointed to succeed Vusumzi Make, (who had resigned after the Chunya massacre in March 1980 when APLA troops refused to accept his leadership), to become head of the Tanzanian backed faction of the PAC. His leadership was rejected by the survivors of the 500 strong APLA Chunya force as well as the Maoist PAC factions in Zimbabwe, Libya, Ghana, and Kenya but Tanzania persuaded the Mugabe government to deport or imprison the major opponents (Leballo, Leeman, Gaelisiwe, Buqwana) .
Chairmanship of the Pan Africanist Congress.
Attempts at intra-party reconciliation.
Once he assumed the position of chairman, Pokela set to work reuniting the PAC, which had been fractured since the 1979 Tanzanian-backed deposition of Chairman Potlako Leballo, leader of the party from 1962 to 1979. He held talks with the 70 member Azanian People’s Revolutionary Party (APRP), a short-lived offshoot of the PAC formed by members expelled by 1978 PAC National Executive meeting in Arusha. Because of this reconciliation effort, they rejoined in 1982 and the APRP disbanded.
Support for Iraq.
During the Iran–Iraq War, Pokela visited Baghdad, Iraq with a PAC delegation, and stated his support for Iraq. However, this was contrary to the position of the PAC, which was to not pick sides in a conflict between members of the Non-Aligned Movement, and Pokela was criticized for this action by other members of the party, including Henry Isaacs and Mike Muendane. Iraq later sent 50,000 dollars to the PAC.
Reorganization of the party.
Pokela also attempted the reorganization of the party itself, which was suffering from both differences between various Central Committee members and differences between the leaders and the party members. He appointed outgoing Chairman Make to the position of Deputy Chairman, even though Make was being investigated for misuse of funds at the time, and increased the power of the Chairman. Pokela also encountered more opposition from Isaacs about his organizational changes (Isaacs eventually resigned.)
Under Pokela, the use of funds was set, with 50% set aside for military operations, 30% going to administration, and 20% used for propaganda; the idea of members submitting annual financial reports about their use of PAC funds was also floated. Nevertheless, money went missing at various points in time, and the PAC ran out of funds between March and November 1981.
Death.
Pokela died in Parirenyatwa Hospital in Zimbabwe in June 1985. He was buried in a state funeral in Zimbabwe officiated by Dr. Stanley Mogoba, a Methodist bishop, and was praised by Zimbabwean president Robert Mugabe for reuniting the PAC. Pokela was succeeded as chairman by Johnson Mlambo.


Friedrich Boerner

Friedrich Boerner or Börner (June 17, 1723 – June 30, 1761) was a German physician.
Boerner was born in Leipzig. His father, Christian Friedrich Boerner, wanted him to study theology and he started to study theology at the University of Wittenberg, but eventually he finish medicine. He was a professor of this university until he had to come back to Leipzig the raising of Seven Years' War (1756–63). He died in Leipzig in 1761.


Sheldon Gilgore

Sheldon Gilgore (February 13, 1932 – February 12, 2010) was an American physician and executive who served as president of Pfizer and CEO of G.D. Searle. He also served as chairman of the board of Clark University and was a member of the founding family of the Connecticut Grand Opera.
Gilgore was trained as an endocrinologist. Gilgore retired from Searle in 1995.


Phil Northrup

Philip M. Northrup (c. 1904c. 1963) was an American track and field athlete. He won the NCAA javelin championship in 1925 and 1926 and tied for the NCAA championship in the pole vault in 1925.
Biography.
Northrup grew up in Detroit, Michigan where he attended Northwestern High School. In 1923, he won the state high school championship in the long jump with a distance of 21 feet, 7 inches.
After graduating from high school, Northrup enrolled at the University of Michigan where he competed in track and field for the school's famous track coach, Stephen Farrell.
As a sophomore in 1925, Northrup won the javelin throw event at the Penn Relays, the Big Ten Conference championship, and the NCAA championships. He also competed for Michigan in the long jump and pole vault. His versatility led the press to report:"In Philip Northrup, Michigan has a most versatile athlete. He stars in the broad jump, javelin throw and pole vault. ... Coach Steve Farrell of the Maize and Blue school rates Northrup one of the best all-round men he has had in some time, with the possible exception of Hubbard, the great colored ace."
Northrup's performance at the 1925 Big Ten outdoor meet held in Columbus, Ohio helped lead the Michigan track team to the conference championship as he accounted for 9-1/2 points. At the meet, Northrup won the javelin and set a new conference record in the event. He also finished fourth in the long jump and tied with three others for third in the pole vault.
At the 1925 NCAA Men's Track and Field Championships, he helped Michigan take second place as the Wolverines narrowly lost the team title to Stanford. At the NCAA championships, Northrup won the event championship in the javelin throw (201 feet, 11 inches) and tied for first in the pole vault (12 feet, 4 inches).
As a junior in May 1926, Northrup led Michigan to another Big Ten track and field championship. Northrup accounted for 12-1/2 points at the conference championship by winning the javelin throw, tying for first in the pole vault and finishing third in the long jump. Northrup's javelin throw of 207 feet, 7-3/8 inches, set a new conference record. Northrup's Big Ten record in the javelin throw stood until 1933 when Duane Purvis of Purdue recorded a distance of 208 feet, 5-1/4 inches.
Northrup also retained his national title in the javelin at the 1926 NCAA track and field championships with a winning throw of 200 feet, 10 inches.
In 1927, Northrup was selected by his teammates as the captain of Michigan's track team. At the 1927 Penn Relays, Northrup won the javelin throw and finished second in the long jump to 1928 Olympic gold medalist Ed Hamm of Georgia Tech. At the 1927 Big Ten meet, Northrup finished third in the javelin as his Michigan teammate Lovette won the event with a throw of 181 feet, 1 inch.
Northrup graduated from the University of Michigan School of Dentistry in 1928 and became an oral surgeon. He also served on the faculty of the University of Michigan from 1935 to 1963. He died in 1963 at age 59.
In 2007, Northrup was selected for the University of Michigan Track & Field Hall of Fame.


Shape of Training review

The Shape of Training was a review of postgraduate medical education and training in the United Kingdom, which reported in 2013. The review was undertaken to consider workforce issues, such as the balance between specialisation and generalism in medicine. The review was supported by a range of organisations concerned with medical education and had an independent chair, Professor Sir David Greenaway.
Background.
In 2005, Modernising Medical Careers (MMC) had launched, introducing a new style of specialist training across the UK. The independent inquiry into these changes led by John Tooke in 2007 had commented on some of the issues. In 2011, Medical Education England (MEE) scoped themes that could be considered as part of further restructuring of medical training.
The relative lack of generalist training had been highlighted by another advisory group, the NHS Future Forum, who pointed towards the review that would follow.
The review.
The Independent Review of the Shape of Medical Training was launched in March 2012 with economist David Greenaway, Vice-Chancellor of The University of Nottingham, appointed as the chair.
The review was jointly sponsored by Academy of Medical Royal Colleges (AoMRC), The Conference of Postgraduate Medical Deans of the UK (COPMeD), the General Medical Council (GMC), Health Education England (HEE), the Medical Schools Council (MSC), NHS Scotland, NHS Wales and Northern Ireland Department of Health, Social Services and Public Safety. Greenaway met with representatives of these organisations on 22 March 2012 and the terms of reference were agreed.
Twelve people were selected to be part of an advisory group, which had the opportunity to consider written and oral submissions from stakeholders, research evidence, site visits, feedback from focus groups and other events. The GMC provided the secretariat.
The initial intention was for the review to report by June 2013. A report was published in October 2013.
The report.
The report suggests an argument for changing the structure of training is that there are more patients with a complex mixture of conditions.
This means doctors need to have a greater breadth of knowledge, rather than specialising early in their careers, it says.
Proposals.
The final report of the review listed 19 recommendations. There were a number of suggestions for the UK governments, including that :
Responses.
Peter Rubin, the chair of the GMC, acknowledged that moving the point of full registration would need further discussion. He also said that there would need to be "some stability in a system that has already been subject to a great deal of change and pressure in recent years."
There were questions raised about transparency and political independence of the review, after details emerged of meetings between the GMC and civil servants from the Department of Health which were not mentioned in the final report.


Jesse Bullowa

Jesse Godrey Moritz Bullowa (October 19, 1879 – November 9, 1943) was an American medical researcher, and an early proponent of controlled clinical trials. From 1928 until his death he was a clinical professor at New York University College of Medicine.
Early life and education.
Bullowa was born in New York City on October 19, 1879 to Moritz and Mary (née Grunhut) Bullowa. He graduated from the College of the City of New York (now part of New York University) in 1899 and then received his MD from the College of Physicians and Surgeons in 1903. Bullowa was married on September 24, 1907 to Sadie Nones, with whom he had five children.
Career.
In the late 1920s, he was appointed a clinical professor of pulmonary medicine at New York University College of Medicine and joint director of the pulmonary service of Harlem Hospital with Milton Rosenblüth, where he also worked with William Hallock Park. He later consulted at several other New York hospitals. He was a member of the American Trudeau Society and the Society for Experimental Biology and Medicine, and a Fellow of the New York Academy of Medicine.
He conducted a controlled trial of serum treatment of lobar pneumonia, with funding from Lucius Littauer. He used a study design with alternation of patients to serum vs standard treatments, established inclusion criteria and severity scales, approximated an intention-to-treat analysis, and included nearly 800 participants. His work was published in the "Journal of the American Medical Association" in 1928; this work "reveals a knowledge and use of statistics which was still unusual among medical researchers at that time" and "stands out as one of the most sophisticated invocations of the controlled clinical trial in the 1920s, and as a self-conscious attempt to justify and promote the methodology". Bullowa acknowledged statistician Louis Israel Dublin for help, and introduced a measure of the "ratio of outcome differences between the two groups divided by the square root of the sum of the squares of the two groups' standard errors", arguing that once the ratio was above 2 then the beneficial treatment should be administered to all patients. He later tested sulfa therapy, serum therapy, and combined therapy in 1939, but despite the results favoring sulfa monotherapy he made post-hoc arguments for the benefit of his serum treatment in sub-stratified patient groups.


Pierre Masson

Claude L. Pierre Masson (November 12, 1880 – May 11, 1959) was a Canadian doctor. He was considered one of the leading histopathologists of his era.
He was born in Dijon and studied medicine at the University of Paris and the Pasteur Institute. Originally, Masson planned a career in clinical medicine, but, after suffering poor health, decided to change his area of interest to biology. Masson was offered the chair of pathology at the University of Strasbourg. He is credited with first describing neurocrine secretion and his work led to the development of modern neuroendocrinology. He was also known for his research into brain tumours. Masson developed at three-stain protocol used in histology known as "Masson's trichrome stain". In 1927, he left Strasbourg to become chair of the Pathology department at the Université de Montréal. Masson reworked the pathology curriculum at the university and reorganized the pathology laboratories there. He retired from that position in 1954.
He died at the age of 79 and was buried in the Notre Dame des Neiges Cemetery.
Masson was named to the Canadian Medical Hall of Fame in 1997.


Georg Joachimsthal

Georg Joachimsthal (8 May 1863 – 28 February 1914) was a German orthopedist who was native of Stargard in Pommern.
In 1887 he earned his medical doctorate from Friedrich Wilhelm University with a dissertation on scoliosis titled "Zur Pathologie und Therapie der Skoliose", and afterwards remained in Berlin as an assistant to Julius Wolff (1836-1902). He received his habilitation in 1898, and two years later founded a private clinic. In 1908 he became an associate professor and director of the orthopedic university polyclinic in Berlin.
In Berlin, Joachimsthal performed important experimental studies involving the physiological effects of orthopedic procedures. He was a founding member of the Deutschen Orthopädischen Gesellschaft (German Orthopedic Society), and in 1910 founded the Berlin Orthopedic Society.
In 1905 he published a highly regarded textbook on orthopedic surgery called "Handbuch der Orthopädischen Chirurgie". In 1907 became an editor of the "Zeitschrift für Orthopädische Chirurgie".


Galvanic vestibular stimulation

Galvanic vestibular stimulation is the process of sending specific electric messages to a nerve in the ear that maintains balance. There are two main groups of receptors in the vestibular system: the three semi-circular canals, and the two otolith organs (the utricle and the saccule). This technology has been investigated for both military and commercial purposes. The technology is being applied in Atsugi, Japan, the Mayo Clinic in the US, and a number of other research institutions around the world. It is being investigated for a variety of applications, including biomedical, pilot training, and entertainment. Not much is known about galvanic vestibular stimulation, but more scientists are continuing to research the topic.
A patient undergoing GVS noted:
I felt a mysterious, irresistible urge to start walking to the right whenever the researcher turned the switch to the right. I was convinced—mistakenly—that this was the only way to maintain my balance.
The phenomenon is painless but dramatic. Your feet start to move before you know it. I could even remote-control myself by taking the switch into my own hands.


Preureteric vena cava

A preureteric vena cava, also known as a retrocaval ureter, is a rare congenital malformation of the right human ureter, in which the ureter passes behind the inferior vena cava, causing compression possibly leading to hydronephrosis. The prevalence of this condition is approximately 1 per 1,000 persons, with males 2-3 times more likely than females to develop the condition. Symptoms often do not manifest until those with the condition are aged in their 20s or 30s.


CDC National Prevention Information Network

The Centers for Disease Control and Prevention's National Prevention Information Network (CDC NPIN) is a source of information and materials for both international and American HIV/AIDS, Viral Hepatitis, Tuberculosis, and Sexually Transmitted Disease education and prevention organizations.
NPIN is located on the Corporate Square Campus of the Centers for Disease Control and Prevention in Atlanta, Georgia and includes a small resource library, a call center, training facilities, and educational materials. The CDC NPIN project also supports/manages GetTested.cdc.gov, the national HIV and STD testing site locator web site and FindTBResources.cdc.gov, a site dedicated to partners in TB education.


Amniotic band sequence


John Lilleyman

Sir John Stuart Lilleyman FRCP, FRCPE, FRCPath, FRCPCH, FMedSci (born 9 July 1945) is a British paediatric haematologist. He specialization is the childhood leukemia.
In 1991, the Royal College of Pathologists awarded him its first Distinguished Service Medal for establishing the United Kingdom's system of pathology laboratory accreditation.He greatly contributed to the testing of leukemia treatment methods and conducted the unique
researches on "thiopurine metabolism" which was made on children suffered with leukemia. Other branch of medicine that is of great interest to him is childhood ITP, where he feels qualms about the early treatment of this disease with the help of immunoglobulin.
He served as President of the Royal Society of Medicine from 2004 to 2006.
Being the President of the Royal College of Pathologists he has also the role of Vice-Chairman of the Academy of the Medical Royal Colleges.
In 2004 with the difference of three months he became medical director of the National Patient Safety Agency (NPSA) and the president of the Royal Society of Medicine
At the moment he works as strategic Advisor to the National Research Ethics Service.