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|Why won't your hospital use DH's blod products? That's crazy! Even if he donates ahead of time and is screened appropriately? Our NICU was all about using my DW's blood for transfusion if necessary. She just had to wait three days for the screens to clear. Would you consider going to a different hospital that WOULD let DH donate to his own child?
|Haemolytic disease of the newborn
Murray, Neil A1; Roberts, Irene A G2
1Imperial College, Department of Paediatrics, Hammersmith Hospital, London W12 0NN, UK
2Imperial College Faculty of Medicine, Hammersmith Campus, Hammersmith Hospital, London W12 0NN, UK
Correspondence to: Dr Neil A Murray Senior Lecturer in Neonatal Medicine, Imperial College, Department of Paediatrics, 5th Floor, Ham House, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK; email@example.com
Competing interests: None.
The changing management of haemolytic disease of the newborn is reviewed
In the space of most paediatricians working lifetime, the spectrum of haemolytic disease of the newborn (HDN) has changed beyond recognition. Thirty years ago, HDN was almost synonymous with Rh D allo-immunisation and was a common neonatal problem. It was usually unmodified by antenatal therapy and caused overt fetal or neonatal haemolysis, leading to marked neonatal hyperbilirubinaemia and attendant anaemia. Affected neonates were commonly sick and unstable at birth, required multiple exchange transfusions, and suffered considerable neonatal morbidity and mortality. However, the introduction in the UK in the 1970s of routine postnatal prophylactic anti-D immunoglobulin for Rh D negative women has dramatically reduced this form of HDN, and as such this treatment ranks as one of the great success stories of modern perinatal care.
Although the clinical burden imposed on neonatal services by HDN has greatly reduced, it has not disappeared. Neonatal paediatricians continue to recognise a number of different presentations of neonatal haemolysis, many of which are considerably more subtle than the traditional "neonatal emergency" presentation of severe Rh D disease. In contemporary neonatal practice, HDN should be considered in the fetus or neonate where there is one or more of the following:
rapidly developing or severe hyperbilirubinaemia not predicted by maternal antenatal antibody screening;
positive maternal antenatal antibody screening and/or diagnosis of a severely anaemic/hydropic fetus;
a positive direct anti-globulin test (DAT);
haemolysis detected on blood film examination;
prolonged hyperbilirubinaemia.
In addition to these various presentations of HDN, the spectrum of the disease has altered as new treatments, particularly improved phototherapy and/or intravenous immunoglobulin (IVIG), are being evaluated and introduced to reduce the need for exchange transfusion in the reduced number of severe cases. This review will aim to place HDN in the context of contemporary neonatal services, systematically evaluate its various presentations, and review the evolving role of these new treatments.
This is now the clinical presentation that most often alerts neonatal paediatricians to newborns with HDN. All will be familiar with the relatively well term neonate presenting within the first 48 h of life with either early-onset jaundice or a total serum bilirubin that has already exceeded 300 µmol/l. By implication, the problem in such neonates has not been predicted by maternal antenatal antibody screening, as appropriate investigation, monitoring procedures and treatment would already have been started. Table 1 gives the most common causes of HDN presenting in this way.
ABO HDN occurs almost exclusively in the offspring of women of blood group O, although reports exist of occasional cases in group A mothers with high-titre anti-(group B) IgG. 1 In general, 15–25% of all maternal/fetal pairs are ABO-incompatible, but ABO HDN is confined to the roughly 1% of such group O women who have antenatal high-titre IgG antibodies. 2 Haemolysis due to anti- A is more common (1 in 150 births) than that to anti- B. Affected neonates will usually be DAT positive, but, in contrast with the clinical picture with anti-Rh antibodies, both anti-A and anti-B HDN usually result predominantly in hyperbilirubinaemia without significant neonatal anaemia. This is mainly because of the relatively few group A or B antigenic sites on neonatal red blood cells (RBCs), allowing the antibody-coated cells to remain in the circulation for a longer period than in Rh D disease. 3 As a reflection of this, the blood film in ABO haemolytic disease characteristically shows very large numbers of spherocytes, with little or no increase in nucleated RBCs (nRBCs), whereas in Rh D HDN there are few spherocytes and large numbers of circulating nRBCs. Management of ABO HDN is usually successful with phototherapy alone provided by modern equipment (see below). However, close monitoring of the affected neonate is essential, and exchange transfusion is occasionally required. This is particularly the case in ABO HDN due to anti-B IgG where racial differences in disease severity exist, severe cases being prevalent in mothers and neonates of black African origin. In such cases, severe anaemia as well as hyperbilirubinaemia 4 can occur and rarely antenatal hydrops fetalis has been described. 5
The main clues that a neonate with early-onset or rapidly progressive hyperbilirubinaemia has a RBC membrane disorder are a family history, non-immune (DAT negative) haemolysis and an abnormal blood film. Indeed, neonatal RBC membrane disorders can nearly always be recognised by the characteristic shape of RBCs on a blood film. However, the identification of the exact type of membrane abnormality is more complex and requires specialised investigations on both the neonate and the parents and close liaison with a haematologist. RBC membrane electrophoresis is the definitive investigation if the clinical pattern and appearance of the family blood films suggest a membrane disorder, as the osmotic fragility test is of limited value in neonates. It is essential to carry out these diagnostic investigations (RBC membrane studies) on pre-transfusion blood samples to minimise diagnostic confusion resulting from transfused cells. 6
Hereditary spherocytosis
This is the most common RBC membrane defect. It occurs in 1 in 5000 live births to parents of Northern European extraction, but is less often seen in other ethnic groups. 7 The usual presentation of hereditary spherocytosis in the neonate is with unconjugated hyperbilirubinaemia. Most affected neonates are not anaemic, but a small number develop anaemia severe enough to require transfusion. Hereditary spherocytosis is inherited as an autosomal dominant trait, but around 25% of cases occur as the result of new mutations. It is genetically heterogeneous; mutations in spectrin, ankyrin, protein 4.1 and protein 3 have all been reported. 7, 8 The blood film shows moderate numbers of spherocytes with an appearance identical with that of ABO HDN. However, (as above) the two disorders are distinguishable by the negative DAT in hereditary spherocytosis. Whereas some babies will require one or two transfusions during the first 1–2 months of life, very few remain transfusion-dependent after this time. In the on-going assessment of such neonates, it is important to pause "top-up" of a RBC transfusion programme to evaluate if steady-state clinical and haemoglobin (Hb) concentrations have been reached. All babies with hereditary spherocytosis should receive folic acid supplementation in the first year of life (500 µg/kg/day or a total weekly dose of 2.5 mg is recommended).
Hereditary elliptocytosis
This is a more complex disorder. It is caused by different mutations in the genes for spectrin, ankyrin or protein 4.1 than those seen in hereditary spherocytosis. 7, 8 In the common, autosomal dominant form of hereditary elliptocytosis, the heterozygotes have no clinical manifestations (ie no anaemia and no jaundice) apart from elliptocytes on the blood film. No treatment is required and folic acid supplementation is not necessary. However, neonates who are homozygous or compound heterozygotes for hereditary elliptocytosis mutations have severe haemolytic anaemia; the most important form is hereditary pyropoikilocytosis (HPP).
Hereditary pyropoikilocytosis
Neonates with HPP have more than one mutation in a RBC membrane protein (they may be homozygous or compound heterozygotes). 7, 8 Although HPP is not common, it is clinically important, as it leads to severe, transfusion-dependent, haemolytic anaemia in affected neonates and infants. The diagnosis of HPP can be made definitively by examining blood films from the neonate that show a high proportion of bizarre fragmented RBCs and microspherocytes. A further useful diagnostic clue is the low mean corpuscular volume at birth (<60 fl). Parental blood films normally show that one or both parents have RBC elliptocytosis. RBC transfusion is usually necessary until the child is old enough to undergo splenectomy, to which there is an excellent response.
The main RBC enzyme defects that present in the neonatal period are glucose-6-phosphate dehydrogenase (G6PD) deficiency and pyruvate kinase deficiency. They usually present with early-onset unconjugated hyperbilirubinaemia and can be distinguished from RBC membrane disorders in that there are usually no diagnostic changes on the blood film and by their inheritance pattern (G6PD deficiency being X-linked so rare in female neonates).
G6PD deficiency
G6PD deficiency is seen in all ethnic groups but has a high prevalence in people from central Africa (20%) and the Mediterranean (10%). In neonatal G6PD deficiency, jaundice usually presents within the first few days of life and is often severe. In contrast, anaemia is extremely rare and the blood film is completely normal. So the diagnosis must be made by assaying G6PD on a peripheral blood sample. 9 It is not clear why some, but not all, G6PD-deficient neonates develop neonatal jaundice. In addition, the pathogenesis of the jaundice is also unclear, as most babies with G6PD deficiency have no evidence of haemolysis. As severe hyperbilirubinaemia is common, close monitoring of the bilirubin concentration is essential, particularly when interactions with other risk factors for neonatal hyperbilirubinaemia are present, such as hereditary spherocytosis or Gilbert's syndrome, as kernicterus has been reported in this setting. 10, 11 Counselling for parents of neonates with G6PD deficiency about which medicines, chemicals and foods may precipitate haemolysis 12 is also an essential follow-up activity in such families. Certain uncommon variants of G6PD deficiency are associated with chronic haemolysis, and for these children folic acid supplements should be given. 9 However, for the vast majority of patients, there is no chronic haemolysis and no anaemia and therefore folic acid supplements are not indicated.
Pyruvate kinase deficiency
Pyruvate kinase deficiency is the second most common RBC enzymopathy in neonates. It is autosomal recessive and clinically heterogeneous, with presentation varying from hydrops fetalis, through severe early-onset neonatal hyperbilirubinaemia requiring exchange transfusion, to a mild unconjugated hyperbilirubinaemia mimicking physiological jaundice. 13, 14 The diagnosis is made by measuring pre-transfusion RBC pyruvate kinase activity. In mild cases, the pyruvate kinase activity may be relatively modestly reduced, making the diagnosis difficult and it is often useful to assay levels in the parents for confirmation. The blood film is sometimes distinctive, but more often shows non-specific changes of non-spherocytic haemolysis, and therefore it is good practice to assay pyruvate kinase in all babies with unexplained haemolysis after the common causes have been excluded. After the neonatal period, some, but not all, children are transfusion-dependent, and folic acid supplements should be given to prevent deficiency due to chronic haemolysis.
Other RBC enzymopathies
The other RBC enzymopathies are rare. The most important to be aware of in the neonatal period is triosephosphate isomerase deficiency, which is autosomal recessive. 15 One third of patients present with neonatal haemolytic anaemia, and this may be the only presenting feature at this age. The devastating neurological features of this disorder only become apparent 6–12 months later, 15 emphasising the point that patients with persistent neonatal haemolysis should always be fully investigated and followed up appropriately.
The haemoglobinopathies, except for [alpha]-thalassaemia major, do not usually present in the neonatal period. Occasional non-thalassaemic, structural [alpha]-globin and [gamma]-globin gene mutations, which are clinically completely silent in adults and children, cause transient haemolytic anaemia in the neonate (see below). Symptoms and signs of the major [beta]-globin haemoglobinopathies (sickle cell disease and [beta]-thalassaemia major) are rare in neonates, although modern techniques (eg high-performance liquid chromatography (HPLC), isoelectric focusing) allow the diagnosis to be made on neonatal blood samples where family studies indicate that both parents are carriers. 16
[alpha]-Thalassaemia major
[alpha]-Thalassaemia major occurs when all four [alpha]-globin genes on chromosome 16 are deleted. 17 It predominantly affects families of south east Asian origin and presents with mid-trimester fetal anaemia or hydrops fetalis, which is fatal within hours of delivery (occasionally babies have lived a few days). It can occasionally cause diagnostic confusion if a fetus developing the marked anaemia and hydrops characteristic of the condition is delivered preterm and then rapidly develops hyperbilirubinaemia. Therefore, the diagnosis of [alpha]-thalassaemia major should be suspected in any case of severe fetal anaemia presenting in the second trimester and any case of hydrops fetalis with severe anaemia in which the parents come from south east Asia (it is also seen occasionally in families who originate from India, the Middle East or the Mediterranean). Checking the blood counts of the parents will immediately identify whether they are at risk of having a child with [alpha]-thalassaemia major: both parents will be carriers of a chromosome 16 in which both of the two [alpha]-globin genes are deleted and so they will have hypochromic, microcytic RBC indices (mean corpuscular volume usually <74 fl and mean corpuscular Hb usually <24 pg). The diagnosis of [alpha]-thalassaemia major is confirmed by Hb electrophoresis or HPLC (which shows only Hb Barts and Hb Portland; HbF and HbA are absent). The blood film shows hypochromic, microcytic RBCs with vast numbers of circulating nRBCs. Neonatal management of [alpha]-thalassaemia major has no impact on survival unless the baby has received a planned programme of intrauterine transfusions. For fetuses/neonates treated in this way, postnatal management is the same as for [beta]-thalassaemia—that is, life-long RBC transfusions or bone marrow transplantation after the age of 2 years. 18, 19
[alpha]-Globin and [gamma]-globin chain structural abnormalities
Most [alpha]-globin and [gamma]-globin gene variants are clinically silent. Occasional [alpha]-globin gene variants may cause haemolytic anaemia in the newborn because, when the abnormal [alpha]-globin associates with [gamma]-globin, the resultant Hb is unstable, whereas, when the variant [alpha]-globin associates with [beta]-globin, the resultant Hb is stable. An example of this is Hb Hasharon: [alpha]214Asp->His-[gamma]2 is unstable, but, as [gamma]-globin chain production is physiologically switched off and [beta]-globin chain production predominates, the [alpha]214Asp->His-[beta]2 produced is stable and the haemolytic anaemia completely resolves. 4 A similar principle occurs in the [gamma]-globin variant HbF-Poole which causes neonatal haemolytic anaemia, which resolves as the switch from [gamma]-globin to [beta]-globin occurs. 20 These variants can be identified by Hb HPLC and are worth considering when more common causes of unexplained haemolysis have been excluded.
Although most acute presentations of neonatal hyperbilirubinaemia/haemolysis now occur without antenatal warning, there continues to be a considerable number a cases of HDN predicted by antenatal screening. The principal allo-antibodies leading to these forms of HDN are those directed against Rh antigens (anti-D, anti-c and anti-E), anti-Kell, anti-Kidd (Jk), anti-Duffy (Fy) and antibodies of the MNS blood group system, including anti-U. Of these, anti-D remains the most common cause of significant haemolytic anaemia, affecting 1 in 1200 pregnancies. 21–23 Anti-Kell antibodies are less common, but can cause severe fetal and neonatal anaemia as they inhibit erythropoiesis as well as causing haemolysis. 24 The numbers of such cases are decreasing, but maternal/fetal pairs with these complications continue to represent a disproportionate part of the spectrum (and workload) of HDN as they require frequent antenatal monitoring and sometimes treatment—that is, repeated intrauterine RBC transfusion. Although beyond the scope of this review, important advances have been made in the monitoring of fetuses/neonates whose mothers carry significant allo-antibodies and who are therefore potential candidates for HDN. Antenatal blood group genotyping by polymerase chain reaction from fetal cells obtained by amniocentesis aids in the definitive identification of susceptible fetuses. 25 In time, this may also be possible as a routine by recovering fetal cells from the maternal circulation. 26, 27 In addition, accurate non-invasive assessment of the degree of fetal anaemia is now possible by using serial middle cerebral artery Doppler studies, thus helping to avoid repeated invasive procedures. For a more detailed overview of these advances, the reader is referred to two reviews. 28, 29
The antenatal diagnosis and postnatal management of fetuses/neonates affected by RBC allo-immunisation continues to require close cooperation between obstetric, neonatal and haematology teams. Not withstanding the results of antenatal investigations and management, all neonates at risk should have cord blood taken for measurement of Hb, DAT, and bilirubin (to confirm diagnosis, assess the effectiveness of any antenatal treatment, and predict the likely need for postnatal treatment). All potentially affected neonates should remain in hospital until hyperbilirubinaemia and/or anaemia have been properly assessed and managed and appropriate follow-up arranged. Trial evidence is lacking to support the use of prophylactic phototherapy in affected neonates, 30 but in busy postnatal wards this approach at least ensures that those who require effective phototherapy receive it in a timely manor and this may avoid exchange transfusion in a small number of neonates. Appropriate guidelines for exchange transfusion in neonates with HDN are becoming a more difficult area. Traditional guidelines suggest that exchange transfusion in HDN is required for:
severe anaemia: Hb <10 g/dl at birth (with the possible exception of anti-Kell, which, as outlined above, can cause considerable anaemia without appreciable hyperbilirubinaemia); and/or
severe hyperbilirubinaemia (total serum bilirubin >350 µmol/l) in the first 48 h of life or rapidly increasing hyperbilirubinaemia (total serum bilirubin increasing >10 µmol/l per hour).
However, these values are derived from clinical experience in preventing the development of kernicterus in sick neonates with untreated Rh D HDN (a progressively reducing clinical entity). As outlined above, the "typical" presentation of HDN is now the well term neonate with ABO incompatibility who presents with a total serum bilirubin already in excess of 300 µmol/l (sometimes as a re-admission from home) without clinically significant anaemia. Intensive phototherapy during the 4–6 h it normally takes to organise an exchange transfusion almost always results in a considerable fall in the total serum bilirubin and thereby almost always removes the clinical indication for exchange transfusion. This represents a modern clinical dilemma in neonatal practice, as blood products used for exchange transfusion in the UK are derived from highly restricted donors, they are in short supply, and potential wastage of these products represents an important issue for both the National Blood Service and neonatal paediatricians. Therefore, although the guidelines for exchange transfusion outlined above remain pertinent for untreated HDN associated with defined antenatally detected maternal antibodies, most cases must now be assessed on their individual merits, with particular attention paid to the general condition of the neonate (state of hydration, gestational and postnatal age), family history, rapid achievement of an accurate clinical/laboratory diagnosis, and initial response to modern intensive phototherapy (see below). Following this approach, most large maternity/neonatal services now perform only a handful of exchange transfusions per year without apparent detriment to the long-term health of neonates affected by HDN. 31
Neonates with haemolytic disease who have received repeated intrauterine transfusions have a significantly altered neonatal course, as their fetal therapy substantially alters the underlying haemolytic disease process. The effect on fetal Hb of the first intrauterine transfusion is shortest-lived because of the continued presence of residual antibody-coated fetal RBCs. However, with subsequent intrauterine transfusions, fetal haemopoiesis is suppressed, and the fetal circulation is then maintained by compatible transfused RBCs that are not susceptible to the haemolytic process. As a result, in newborns that have been treated with a successful intrauterine transfusion programme until near term, neither neonatal jaundice nor immediate anaemia are major problems and few require postnatal exchange transfusion. 32 In contrast, late anaemia in such neonates is common, as the haemopoietic suppression induced by the intrauterine transfusion programme may last for many weeks after delivery. Management of such neonates is expectant, initially ensuring adequate nutritional support (including appropriate iron and vitamin supplementation). After discharge, monitoring of Hb concentration, blood film morphology, reticulocyte count and bilirubin is necessary to gauge when haemolysis has stopped and endogenous RBC production has re-commenced. The appropriate interval for this must be tailored to the individual neonate, taking into consideration the activity of the underlying haemolytic process and, most importantly, the general condition and growth and development of the affected neonate (simply bleeding such neonates weekly often only raises maternal anxiety without necessarily adding useful clinical information). RBC transfusions are only required in those with symptomatic anaemia (notoriously difficult to evaluate clinically 33), with most neonates requiring no RBC top-ups, although in some clinically well neonates the Hb concentration may fall as low as 5 g/dl before rising spontaneously (personal experience).
The DAT (Coombs test) is one of the cornerstones of diagnosis of HDN. It is a screening test for non-agglutinating antibodies present on an individual's RBCs. If maternal serum contains an IgG class, immunoglobulin directed against a fetal RBC antigen transplacental passage of this antibody will result in RBC antibody coating and a positive fetal/neonatal DAT. However, it should be appreciated that as a basic screening test, it has poor positive predictive value in identifying neonates who will require treatment of HDN by phototherapy. In a recent publication, Dinesh 34 reported that only 23% of neonates found to have a positive DAT on neonatal screening actually went on to develop hyperbilirubinaemia requiring phototherapy. Indeed it was only when the DAT was strongly positive (4+) that 100% of such neonates required phototherapy. This study also confirmed the preponderance of ABO incompatibility as the main cause of HDN in modern neonatal practice, with 87/93 cases of DAT positivity occurring in ABO-incompatible mother/neonate pairs. In addition, 21/145 neonates requiring neonatal phototherapy were both DAT positive and from ABO-incompatible mother/neonate pairs, with a further 17/145 neonates requiring neonatal phototherapy being DAT negative but also from ABO-incompatible mother/neonate pairs.
It must also be appreciated that, in a unit where Rh D negative women receive routine antenatal anti-D immunoglobulin in the third trimester, up to 15% of the resulting neonates will have a positive DAT simply from passive transfer of the prophylactic anti-D administered to the mother during pregnancy. 35 These antibodies do not induce fetal or neonatal haemolysis and so no special postnatal investigation or monitoring of such neonates is required (although it is all too easy for such neonates to be included in follow-up programmes for HDN). If doubt exists as to the cause of the DAT positivity in such neonates, blood film examination, by an appropriately experienced person, will give the correct diagnosis, as spherocytes, nRBCs and RBC fragments will not be present in unusual numbers.
As the recognised presentations of HDN become more varied and the number, and complexity, of identified causes increases, it becomes even more imperative for neonatal paediatricians to develop close working relationships with their local haematologists. In many cases, the first clinician who suspects/diagnoses HDN in a particular neonate will be the haematologist after a blood film examination for other reasons—for example, review for evidence of sepsis. This fact simply emphasises the importance of requesting blood film examination routinely on all neonates with non-physiological jaundice (table 1) and the importance of encouraging haematologists to develop skills appropriate to neonatal medicine.
All neonates with prolonged hyperbilirubinaemia should be thoroughly investigated to exclude the possibility of HDN (table 1). Persistent jaundice is a common presentation of HDN, and virtually all the conditions mentioned in this review may present with prolonged hyperbilirubinaemia. Achieving the correct diagnosis may well have implications not only for the jaundiced neonate but also for other family members.
Improved phototherapy
The changing clinical practice surrounding HDN is, in no small way, the result of improvements in both the understanding and delivery of phototherapy. Phototherapy was first introduced for the treatment of neonatal hyperbilirubinaemia in the late 1950s, 36 when white light was the mainstay of treatment. Since then, considerable advances have been made, and it is now appreciated more fully that the efficacy of phototherapy in reducing neonatal hyperbilirubinaemia is dependent on a number of factors:37
spectral qualities of the delivered light (optimal wavelength range 400–520 nm, with peak emissions of 460 nm);
irradiance (intensity of light)38;
surface area receiving phototherapy;
skin pigmentation;
total serum bilirubin concentration at the start of phototherapy;
duration of exposure.
Thus modern phototherapy devices are designed to maximise the efficacy of phototherapy to the neonate, and clinicians are more appreciative of the importance of ensuring that such devices are used correctly—that is, ensuring the correct distance between the device and patient, and ensuring proper maintenance and servicing of phototherapy units. As a result of this, phototherapy units have become smaller in size, more easy to use around a neonate's cot, more efficient, particularly high-intensity gallium nitride light-emitting diodes, 39, 40 and the total irradiance that can be applied to an individual neonate has vastly increased. In short, phototherapy is now a viable alternative to the planned use of exchange transfusion in the treatment of even moderate to severe HDN, 41 and, as devices continue to develop and improve, phototherapy will play an even greater role in the treatment of HDN. For a fuller description of developments in neonatal phototherapy since its first use, the reader is referred to two reviews. 37, 42
High-dose IVIG
In the last 10–15 years, a number of pilot studies have been published reporting the effect of high-dose IVIG as an adjuvant treatment to standard therapy for HDN. 43–48 Most of these studies have also formed the basis of two systematic reviews. 49, 50 Clearly, in the context of their applicability to modern neonatal practice, there are potential methodological difficulties with most of these studies: the studies have assessed a relatively small number of neonates; most patients studied have ABO HDN (and are therefore presumably clinically well); the protocols of the larger studies include exchange transfusion at relatively low concentrations of bilirubin, 290–340 µmol/l (concentrations that would not trigger automatic exchange transfusion for neonates with ABO HDN in most units); the timing of administration and dose of IVIG vary considerably between studies. Despite these problems, it seems clear that IVIG does confer benefit when administered to neonates with HDN. The published studies suggest that IVIG in this context reduces the number of neonates treated with exchange transfusion, the total length of phototherapy required, and the length of hospital stay. Late anaemia may be more prevalent in those treated with IVIG, presumably because fewer neonates have exchange transfusion and therefore removal of maternal antibody. No major side effects have been reported in the neonates treated with IVIG, but it should be remembered in this context that IVIG is a pooled blood product and so the potential for transmission of blood-borne infections will always be present. 51, 52
Given these facts, how should neonatal paediatricians approach the use of IVIG in patients with HDN? Clearly, one approach is to wait for results from a definite trial(s) with methodology that reflects modern clinical practice—that is, where the decision to carry out an exchange transfusion is based on the combination of bilirubin concentration, general condition of the neonate, rapid diagnosis of the likely cause of HDN, and response to intensive phototherapy—rather than a didactic approach based solely on bilirubin concentration or rate of rise of bilirubin. This approach is entirely justified given that IVIG can never be guaranteed to be 100% safe (although blood for exchange transfusion also cannot be guaranteed to be 100% safe, and, as clinical experience of exchange transfusion itself decreases, this procedure may well have increasing morbidity). Alternatively it may well be justified to electively use IVIG in a small number of selected patients with HDN where the likelihood of exchange transfusion is great—that is, neonates with Rh disease unmodified by antenatal treatment or neonates with potential ABO HDN where a previous sibling has suffered from severe disease requiring exchange transfusion. As a definitive trial reflecting modern practice recruiting sufficient patients to show a definite reduction in neonates who require exchange transfusion would need to be a large multicentre exercise, the latter option is likely to be followed by those swayed by the current evidence on IVIG for HDN.
The diagnosis, acute management, and follow-up of neonates with HDN still represent an important area of activity for maternity/neonatal services. Through the highly successful use of prophylactic Rh D immunoglobulin in Rh D negative women, Rh D allo-immunisation and its sequelae have greatly diminished. As a result, ABO incompatibility is now the single largest cause of HDN in the western world. However, with increasing knowledge at the molecular level, and closer liaison between neonatal paediatricians and haematologists, the diagnosis of non-immune causes of HDN is increasing. As these conditions have an inherited basis and therefore have implications for other family members (or future children), it must remain a high priority for all neonatal paediatricians to achieve an accurate diagnosis in all cases of HDN, and emphasises the point that patients with persistent neonatal haemolysis should always be fully investigated and followed up appropriately.
As the efficacy of phototherapy increases, the role of exchange transfusion in the acute management of HDN is rapidly decreasing. This represents a potential management dilemma for neonatal paediatricians, as the vast majority of neonates presenting with hyperbilirubinaemia, and presumed HDN, will respond to phototherapy-based management, thus avoiding any potential hazards associated with exchange transfusion. This makes gauging the appropriate time to intervene with exchange transfusion an increasingly difficult clinical decision. In addition, as the number of exchange transfusions undertaken by most maternity/neonatal services per year is now in single figures, few neonatal trainees can hope to develop practical competence in this technique. In view of these issues, all maternity/neonatal services must develop, maintain and teach appropriate written practice guidelines both for use of exchange transfusion in the management of HDN and for the performance of the procedure itself. Indeed this may be even more important in the future as the use of IVIG and/or metalloporphyrins 53 further reduces the need for exchange transfusion and continues to change the spectrum of HDN faced by neonatal paediatricians.
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23. Thompson J. Haemolytic disease of the newborn: the new NICE guidelines. J Fam Health Care 2002;12:133–6. Bibliographic Links [Context Link]
24. Vaughan JI, Manning M, Warwick RM, et al. Inhibition of erythroid progenitor cells by anti-Kell antibodies in fetal alloimmune anemia. N Engl J Med 1998;338:798–803. Ovid Full Text Bibliographic Links [Context Link]
25. Bennett PR, Le Van Kim C, Colin Y, et al. Prenatal determination of fetal RhD type by DNA amplification. N Engl J Med. 1993 26 329:607–10. [Context Link]
26. Al-Mufti R, Howard C, Overton T, et al. Detection of fetal messenger ribonucleic acid in maternal blood to determine fetal RhD status as a strategy for noninvasive prenatal diagnosis. Am J Obstet Gynecol 1998;179:210–4. Ovid Full Text Bibliographic Links [Context Link]
27. Bianchi DW, Avent ND, Costa JM, et al. Noninvasive prenatal diagnosis of fetal Rhesus D: ready for Prime(r) Time. Obstet Gynecol 2005;106:841–4. Ovid Full Text Bibliographic Links [Context Link]
28. Urbaniak SJ, Greiss MA. RhD haemolytic disease of the fetus and the newborn. Blood Rev 2000;14:44–61. Bibliographic Links [Context Link]
29. Harkness UF, Spinnato JA. Prevention and management of RhD isoimmunization. Clin Perinatol 2004;31:721–42. Bibliographic Links [Context Link]
30. Yaseen H, Khalaf M, Rashid N, et al. Does prophylactic phototherapy prevent hyperbilirubinemia in neonates with ABO incompatibility and positive Coombs' test?J Perinatol 2005;25:590–4. [Context Link]
31. Newman TB, Liljestrand, PJeremy RJ. et al Outcomes among newborns with total serum bilirubin levels of 25 mg per deciliter or more. N Engl J Med. 2006;4 354:1889–900. [Context Link]
32. van Kamp IL, Klumper FJ, Meerman RH, et al. Treatment of fetal anemia due to red-cell alloimmunization with intrauterine transfusions in the Netherlands, 1988-1999. Acta Obstet Gynecol Scand 2004;83:731–7. Bibliographic Links [Context Link]
33. Murray NA, Roberts IA. Neonatal transfusion practice. Arch Dis Child Fetal Neonatal Ed 2004;89:F101–7. Bibliographic Links [Context Link]
34. Dinesh D. Review of positive direct antiglobulin tests found on cord blood sampling. J Paediatr Child Health 2005;41:504–7. Buy Now Bibliographic Links [Context Link]
35. Cortey A, Brossard Y. [Adverse effects and patient information]. J Gynecol Obstet Biol Reprod (Paris) 2006;35 (1 Suppl):1S112–1S118. [Context Link]
36. Cremer RJ, Perryman PW, Richards DH. Influence of light on the hyperbilirubinaemia of infants. Lancet. 1958 24 1 (7030):1094–7. [Context Link]
37. Vreman HJ, Wong RJ, Stevenson DK. Phototherapy: current methods and future directions. Semin Perinatol 2004;28:326–33. Bibliographic Links [Context Link]
38. Hart G, Cameron R. The importance of irradiance and area in neonatal phototherapy. Arch Dis Child Fetal Neonatal Ed 2005;90:F437–40. Ovid Full Text Bibliographic Links [Context Link]
39. Vreman HJ, Wong RJ, Stevenson DK, et al. Light-emitting diodes: a novel light source for phototherapy. Pediatr Res 1998;44:804–9. Ovid Full Text Bibliographic Links [Context Link]
40. Seidman DS, Moise J, Ergaz Z, et al. A prospective randomized controlled study of phototherapy using blue and blue-green light-emitting devices, and conventional halogen-quartz phototherapy. J Perinatol 2003;23–7. Bibliographic Links [Context Link]
41. Thaithumyanon P, Visutiratmanee C. Double phototherapy in jaundiced term infants with hemolysis. J Med Assoc Thai 2002;85:1176–81. Bibliographic Links [Context Link]
42. McDonagh AF. Phototherapy: from ancient Egypt to the new millennium. J Perinatol 2001;21 (Suppl 1):S7–S12. [Context Link]
43. Miqdad AM, Abdelbasit OB, Shaheed MM, et al. Intravenous immunoglobulin G (IVIG) therapy for significant hyperbilirubinemia in ABO hemolytic disease of the newborn. J Matern Fetal Neonatal Med 2004;16:163–6. Bibliographic Links [Context Link]
44. Mukhopadhyay K, Murki S, Narang A, et al. Intravenous immunoglobulins in rhesus hemolytic disease. Indian J Pediatr 2003;70:697–9. Bibliographic Links [Context Link]
45. Alpay F, Sarici SU, Okutan V, et al. High-dose intravenous immunoglobulin therapy in neonatal immune haemolytic jaundice. Acta Paediatr 1999;88:216–9. Bibliographic Links [Context Link]
46. Dagoglu T, Ovali F, Samanci N, et al. High-dose intravenous immunoglobulin therapy for rhesus haemolytic disease. J Int Med Res 1995;23:264–71. Bibliographic Links [Context Link]
47. Voto LS, Sexer H, Ferreiro G, et al. Neonatal administration of high–dose intravenous immunoglobulin in rhesus hemolytic disease. J Perinat Med 1995;23:443–51. Bibliographic Links [Context Link]
48. Rubo J, Albrecht K, Lasch P, et al. High-dose intravenous immune globulin therapy for hyperbilirubinemia caused by Rh hemolytic disease. J Pediatr 1992;121:93–7. Bibliographic Links [Context Link]
49. Alcock GS, Liley H. Immunoglobulin infusion for isoimmune haemolytic jaundice in neonates. Cochrane Database Syst Rev 2002;3:CD003313. Bibliographic Links [Context Link]
50. Gottstein R, Cooke RW. Systematic review of intravenous immunoglobulin in haemolytic disease of the newborn. Arch Dis Child Fetal Neonatal Ed 2003;88:F6–10. Ovid Full Text Bibliographic Links [Context Link]
51. Hayakawa F, Imada K, Towatari M, et al. Life-threatening human parvovirus B19 infection transmitted by intravenous immune globulin. Br J Haematol 2002;118:1187–9. Ovid Full Text Bibliographic Links [Context Link]
52. Quinti I, Pierdominici M, Marziali M, et al. European surveillance of immunoglobulin safety--results of initial survey of 1243 patients with primary immunodeficiencies in 16 countries. Clin Immunol 2002;104:231–6. Bibliographic Links [Context Link]
53. Dennery PA. Metalloporphyrins for the treatment of neonatal jaundice. Curr Opin Pediatr 2005;17:167–9. Ovid Full Text Bibliographic Links [Context Link]
Keywords: haemolytic; hyperbilirubinaemia; jaundice; phototherapy
I thought this was nuts, too! Our NICU won't take my blood (me and DS are A positive). They said that (the truth is stranger than fiction) they won't take it because the baby builds up antibodies and if for some reason DS even needed a transplant from me he would reject it if he had my blood now. Wierd!!
I emailed my friend with the ABO incompatibility and her level of severity sounds similar to yours (the OP), as her baby #2 needed IVIg. Apparently it was her ped and neo that gave her this info. Anyway, this was her reply:
from what i understand, the mother makes more
antibodies as the pregnancy progresses (and more and
faster w/ subsequent pregnancies).. my pediatrician
said that if we had another, he would have my ob test
my blood for antibodies and deliver the baby as soon
as possible if they started going up too high...
so, i think that there is a point at which delivering
prematurely to limit the exposure (and increased
bilirubin) is better than going 40 weeks... i've also
read about intrauterine blood transfusions... but that
sounds scary too...
i don't think there is anything that can be done to
prevent it...
maybe she can talk to her pediatrician? my ob never
even brought it up to me...
i was led to believe that a 3rd kid would be worse if also type A...
hope that helps! i wish her well...
Well, I don't know the exact science behind it, so I can neither refute nor support any of your arguments. I wish I had the time to research it fully, but I do not, as I am in the middle of an intensive, fast-paced Pharmacology course while being a SAHM to toddler twins and taking another class as well. I am just trying to help out the OP by letting her know what my friend, who had a similar experience, was told by her doctors so that the OP can ask more questions of her own physicians.
To the OP: I wish you the best of luck with baby #3! Congratulations!
To the OP: I wish you the best of luck with baby #3! Congratulations!
OTF--at what gestational age was your baby born? My friend's doctor said that, depending on the severity of ABO incompatibility, they would consider deliving at 30 weeks! Having had 32 weekers myself, I told her to definitely check with a perinatologist prior to agreeing to that because, man, it was rough enough having 32 weekers!
GGirl--I wonder if they could use DH's blood for an exchange transfusion, rather than doing IVIg? Well, definitely keep us updated--I'll be thinking of you!
|Drabik-Clary K, Reddy VV, Benjamin WH, Boctor FN.
Department of Pathology, University of Alabama at **********, West Pavilion P230, 619 19th Street South, **********, AL 35249-7331, USA.
. . . The incidence of HDN ranges from one in 150 births to 1:3000 births, depending on the degree of anemia and level of serum bilirubin. The etiology of ABO hemolytic disease of the newborn (ABO-HDN) is complex because anti-A and anti-B antibodies are composed mainly of IgM. Since only IgG antibodies cross the placenta, those pregnant women with high levels of IgG anti-A,B, anti-A, or anti-B with an ABO incompatible fetus will be the ones to give birth to an infant with ABO-HDN. . .
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Hi, I have two questions about the stats collector during recovery. 1) Why does the stats collector need to wait for consistent recovery mode? The activity statistics which bgwriter may send before reaching the mode should be ignored? 2) Why doesn't ServerLoop() try to restart the stats collector when it's not in progress? Regards, -- Fujii Masao NIPPON TELEGRAPH AND TELEPHONE CORPORATION NTT Open Source Software Center
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subset: commoncrawl


text:
Resto Shaman vs. Karazhan – A Healing Guide Part 3
This is one in a series of posts covering resto-shaman-specific information for tier4 and tier5 boss fights. It will NOT be a boss kill strategy, rather a list of tips and tricks for your friendly neighborhood shaman to make these fights run a little more smoothly.
You can see other guides (includes Karazhan, Gruul's Lair and all of Serpentshrine Cavern) here.
Welcome to raiding! You're on your way to Karazhan, likely the first step into a raiding group of more than 5 people you've made since level 60… or at all, depending on when you started playing Warcraft! Karazhan is a large castle full of cool lore and cooler music… and about ten thousand bloodthirsty undead. This will cover the last three fights of Karazhan – that is the Chess Event, Netherspite, and Prince Malchezzar. Click for parts one and two!
Before we get started – Make sure you have your Consumables, and that you know enough about Totem Synergy to buff your group appropriately. Also – remember Earthshield and Heroism/Bloodlust!
Chess Event:
This is, by far, one of the most fun parts of Karazhan for me. There isn't any real strategy to this other than kill the other guy's king before your king dies. (Each faction controls the appropriate pieces, so for me, it's always King Llane). Most pieces move only one step in any direction, with the exception of the two Chargers/Worgs, that move like Chess Knights (two spaces up and one space diagonal, etc.) and the Human Conjurer/Orc Warlock that move like a Chess Queen – in any direction for up to 3 spaces.
Make sure you move enough of the Footmen/Peons to get the cooler pieces out of the way – you can drop them by clicking off the "Controlling Chess Piece" aura in your buffs, and make sure that both healers are being controlled and utilised. And have fun!
Oh – and Medivh cheats, but, as in all the old sayings, cheaters never prosper, and it doesn't often affect the outcome of the game.
Before you bother with reading any of my notes, the best Netherspite strategy I have *ever* read or encountered can be found here. Illithias used to raid with TRI and his explanations are fantastic and funny. (warning for some adult language)
Now that you know all about how Netherspite works, a few things to keep in mind.
- It is possible for one tank to take an entire red beam using what is called beam dancing. The "exhaustion" debuff does not apply for 5 seconds after you leave a beam, so the tank can hop in and out (3 seconds in, 3 seconds out, 3 seconds in, 3 seconds out) to keep some of the stacking debuff off of him/her, and take an entire beam.
- It is NOT POSSIBLE to beam-dance in ANY of the other two beams. DO NOT dance the green beam, just soak it.
- When you have to run away to the back of the room (if you are not healing the tank/melee who are staying to DPS the banished Netherspite), drop a searing totem. Hooray for DPS! When you get to the back of the room, drop a Mana Spring totem. Hooray for Mana!
- Make sure you earthshield whoever is tanking, and do not get caught in a Void Zone!
- If you have to soak a green beam temporarily, make sure to use Mana Tide afterwards, to recoup your healing.
Prince Malchezzar
During all three phases of this fight, Prince summons infernals. For the first two phases, they show up every 45 seconds. In phase three, every 15 seconds. These guys have a stationary hellfire AOE and cannot be killed or damaged. There is technically no limit to how many can be up at one time, but eventually they will make positioning the raid nearly impossible.
Infernal management is key. Bad infernal placement coupled with a raid that does not move well as a unit and has poor communication is a guaranteed wipe. Sometimes even raids that have good communication and movement skills will get pwnt by bad infernal placement.
Phase 1 – 100-60%
- Periodically Enfeebles a up to 5 characters that are not #1 on the aggro list. (not who are the tank. If you out-aggro the tank without actually pulling aggro (ranged) , the tank CAN GET ENFEEBLE). This causes no damage, but temporarily reduces your hit points to one.
- Casts a 24 yard AOE Shadow Nova that deals 3K damage and knocks players back. This should be avoided if possible, and absolutely MUST be avoided if Enfeebled. Shadow Nova is the enfeebled melee-killer.
- Periodically casts Shadow Word: Pain
Phase 2 – 60-30%
- Continues to Enfeeble and cast Shadow Nova
- Adds Thrash (two rapid fire melee attacks), Parry (which speeds up the next attack… including thrash), and Sunder Armor to his complement of tank-smashing moves.
- Phase Two is the Tankbuster – your tank is going to take spikes of damage, and you will have to continue to dodge Infernals while healing through it.
Phase 3 – 30-0%
- No more Enfeebles! Yay! But continues to Shadow Nova and cast Shadow Word: Pain.
- Summons his flying axes on random targets as separate (but not attackable) entities. You will have to heal through this damage. Earthshield is useful if you or another caster get axes.
- Casts a random, undispellable amplify damage.
What you need to keep an eye on: Enfeeble. If you get it, make SURE you're out of range. Also, watch the Infernals and move proactively – don't wait until you're boxed in, or it'll be too late.
This can be a long fight, so bring the standard complements of mana pots and mp/5 buffs. Totemically, anything that will help your tank is good on this fight, particularly Grace of Air during phase 2. Your Fire Elemental is a nice DPS boost during phase 3, when the raid will be trying to burn Prince down before they all get lit up with Infernals.
Congratulations! You have now beaten all the bosses in Karazhan! With luck, you and your raid will be able to team up with another raid (in your guild or not in your guild) and tackle the 25 man bosses soon! Welcome to Tier4!
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This product is no longer available.
You can try these similar gifts instead.
Mega Director Kit Gift Set
For amateurs and all film enthusiasts! Mega director's set includes a 'Director' t-shirt, embroidered 'Director' cap, an 11.5" x 11" clapboard, small megaphone, 'Director' license plate and a clapboard picture frame keychain.


text:
Michael Bay Is Ruining The Teenage Mutant Ninja Turtles
Look out! I'm letting my Geek Flag fly. The "Teenage Mutant Ninja Turtles" started as a comic book, became a kids cartoon and movie franchise. They are goofy, corny a little strange but most of all fun. TMNT has a cult following that knows the story like the back of their hands. So when Michael Bay of "Transformers" fame decided to change their origin he made many geeks VERY angry!


text:
Detail Information
- Computed tomographic colonography (CTC): a retrospective analysis of a single site experience and a review of the literature on the status of CTCMarcus Ghuman
Radiology Department, Auckland Hospital, Auckland, New Zealand
N Z Med J 125:60-7. 2012..To improve performance by identifying any deficiencies that need to be addressed, in relation to a literature review of the current status of CTC...
- Post-caesarean section surgical site infection: rate and risk factorsMarcus Ghuman
Auckland Hospital, Auckland, New Zealand
N Z Med J 124:32-6. 2011..To identify the incidence of surgical site infection (SSI) post-caesarean section, and important contributory risk factors...


text:
SEMINOLE — The City Council, firefighters, teen board and the Seminole Boy Scouts/West Central Florida Council are sponsoring the city's third annual canned goods drive. Can-It 2011 begins Nov. 1 and ends Dec. 15. All products will be donated to Aldersgate United Methodist Church, which will distribute them to area residents and church food pantries.
Canned goods can be dropped off at the following locations:
• Seminole City Hall, 9199 113 St. N (drop box in lobby)
• Seminole Chamber of Commerce, 8400 113th St. N
• Seminole Garden Florist & Party Store, 13030 Park Blvd. N
• Barnhorn Financials, 8338 Seminole Blvd., Suite C (in the back of the building)
• Seminole Gardens Apartments auditorium, 8324 112th St. N
• Hottin's Trophies, 9275 Park Blvd. N
• Dr. Sandra Lilo's dental office, 8300 113th St. N
• Ambrosia Spa & Salon, 10333 Seminole Blvd., Suites 1 and 2
• Centratel/Telephone Systems, 11193 Seminole Blvd.
For information, call Seminole council member Leslie Waters at 391-0204, ext. 102.


text:
November 12, 2013 BY Brendan Dunne
The Reebok Kamikaze II has been on quite a tear materials-wise as of late. Following up on the recent glow in the dark version was SNS's "Herringbone" re-working of the silhouette. By comparison this upcoming GS release almost seems tame with is playful palette of turquoise and purple. It's also worth noting that they're not quite working with the original material set, instead there's a slightly different leather cut a geometrically patterned shiny section. Continue reading for more on this Reebok release and then grab them early from ny_5thavenue on eBay.
Filed under: Reebok Upcoming Sneakers
Tags: Reebok Kamikaze II


text:
Brain Fitness in Parkinson's Disease
This study has been completed.
University of South Florida
Information provided by (Responsible Party):
Jerri D. Edwards, University of South Florida
ClinicalTrials.gov Identifier:
First received: June 29, 2010
Last updated: December 7, 2012
Last verified: December 2012
- Full Text View
- Tabular View
- No Study Results Posted
- Disclaimer
- How to Read a Study Record
No Study Results Posted on ClinicalTrials.gov for this Study
|Study Status:
|This study has been completed.
|Study Completion Date:
|May 2012
|Primary Completion Date:
|May 2012 (Final data collection date for primary outcome measure)


text:
And here we go to Candy Crush Level 349! For those of you that can't pass it, you just need to carefully watch our video:
Patricia Frederick's Tips for Candy Crush Level 349
Try to avoid the bomb dispensers when creating the color bombs if you can—they are 10 move bombs. Keep the chocolate from closing off both sides at the top or you won't have any candies to work with. Lastly, when you match your color bomb with a color, pick one that won't open the bomb dispensers in the lower outer columns.


text:
Great luxirious spacious rooms with good food friendly personel and very close to the major sites in beijing
- Official Description (provided by the hotel):
- The Red Wall Garden Hotel is a cultural oasis of tranquillity in the very heart of the vibrant city of Beijing. It is located in Shijia Hutong, one of the city's most historic neighbourhoods and is within walking distance of the Forbidden City and the famous shopping and food streets of Wangfujing and Jinbao in DongCheng. A traditional Chinese courtyard hotel invoking the past, yet replete with modern facilities. All 40 individually appointed guest rooms feature ultra-luxury DUX beds, wooden flooring, en-suite bathrooms and amenities such as large flat screen TV, complimentary WI-FI throughout the hotel and private in-room bar. All rooms have air-conditioning & heaters. Located within the central courtyard of the award-winning Red Wall Garden Hotel, The Courtyard Bistro serves great value dishes that are inspired by the eight main culinary areas in China. The Courtyard Bistro also features open stage Cultural Entertainment nights as well as indoor and outdoor Noodle Stations and daily special chalkboards to further enhance the guests' dining experiences. The Lounge Bar invites guests to kick back in an armchair with a drink, a snack and a book. The Courtyard Bistro's full service bar serves up classic and specialty cocktails as well as traditional afternoon tea and features an excellent selection of wines, beers and other alcoholic or non-alcoholic drinks. Situated just off the west lounge of the hotel, The Courtyard Bistro Tea House offers daily tea ceremonies where the in-house tea master guides patrons through Chinese tea history that looks back on over 4000 years of tea excellence. The Private Dining and Event Rooms at The Red Wall Garden Hotel can accommodate up to 200 people for Meetings, Weddings or Events. The tailor-made menus offer an array of traditional Chinese Cuisine to suit either a formal or an informal Meeting, Wedding or Event. The "Red Wall Garden Boutique Hotel Experience" emotionally connects our guests with the intense Historical, Cultural and Artistic life of Authentic and Historic Beijing. ... more less
- Reservation Options:
- TripAdvisor is proud to partner with Booking.com, Expedia, Hotels.com, Travelocity, Orbitz, Ctrip TA, Cancelon, Cheap Tickets, Agoda, TripOnline SA, Priceline, Hotwire, getaroom.com and Evoline ltd so you can book your Red Wall Garden Hotel reservations with confidence. We help millions of travelers each month to find the perfect hotel for both vacation and business trips, always with the best discounts and special offers.


text:
Jack Osbourne is on the mend.
Hospitalized recently to have his appendix removed, the engaged father-to-be, 25, kept his Twitter followers up to date on his health over the weekend in a series of messages on the micro-blogging site.
"This is what you look like when you have had your appendix removed," Ozzy Osbourne's son posted Sunday, along with a photo of himself clad in a hospital gown with pregnant fiancee, Lisa Stelly, by his side.
Later, Osbourne shared more about his recovery process.
"Man, high powered pain killers + Radiohead = dangerous territory for me," he wrote. "I gotta get outta this hospital. This is getting [too] good."
Confirming their engagement in September, Osbourne and Stelly will become first-time parents later this year.


text:
This the GTK+ port of Euler, a program for quickly and interactively computing with real and complex numbers and matrices. It features advanced graphical capabilities and a simple programming language.
|Scientific/Engineering Mathematics
Release Notes: This version was ported to GTK2. The autoconf tools are now used. Some bugs were fixed. New functions were added for degree and rad.
Release Notes: Bug were fixed. The GUI has been improved (wheel mouse support and drag and drop to load the notebook files). Events are handled better so that animations are now usable. Logplots have been enhanced. gcm, lcm, primes, isprime, and factor functions have been added. The documentation has been updated and translated partially into French and German.
Release Notes: Bugfixes were made in the scan_dir, input, and lineinput functions. New figure, animate, and rotate functions were added. An antialiasing function for density plots was implemented.
Release Notes: A deep reordering of source code to ease future enhancements, a more portable scandir function which will prevent compiling errors on Solaris, a "delete outputs" menu item to delete all the outputs in a notebook (the first lines as well), and addition of the GPL license text with the distribution.
Release Notes: Clipboard management, a color scheme for 3D graphics, a demo menu for quick demo access, a few bugfixes were added. Minor changes were made to enable the forthcoming Debian package.
Great math tool!
This application rocks! I may throw away my ti-89
A Fluent OpenStack client API for Java.
A TWiki appliance that is easy to use and lightweight.


text:
LondonUnited Kingdom
May 1, 2012
My name is Adriana. I am from Brazil, but I live in Uk for a very long time. I am a back to university and this time I am studying Social Sciences with Social Anthropology. It is hard to restart..
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Zyxel iCard SSL for ZyWALL USG 1000 - Upgrade license - 50 concurrent sessions - upgrade from 25 concurrent sessions - (SSL25TO50USG1000)Item#: 7512067 | Model#: SSL25TO50USG1000
- Price:
- $435.99
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- Temporarily out of stock. Order today and we'll deliver when available. (Details)
ZYWALL SSL VPN TUNNEL-UPG 25 TO 50-USG1000 Product Details
Remote access has never been so easy. Utilizing only a standard web browser, users can easily and secure access email, files, applications, web servers and any resources on the corporate network from any location. With industry strength security and encryption algorithms, the ZyWALL's SSL VPN feature ensures your privacy of data.
Related Items
Manufactured by: Zyxel
Warranty provided by: Zyxel
UPC No: 0760559115685
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- Zyxel logos are registered trademarks of Zyxel. All others trademarks and copyrights mentioned herein are the property of their respective owners.


text:
Bridge set for Sunderland medical
Manchester City defender Wayne Bridge is heading to Sunderland for a medical ahead of a loan move to Wearside.
Sunderland manager Martin O'Neill wants to bolster his injury-hit squad with the addition of Bridge, 31, on the final day of the January transfer window.
O'Neill moved for the hugely experienced former England left-back after his defensive resources were further stretched by the loss of Wes Brown to a suspected medial ligament injury at the weekend.
Bridge has played just 78 minutes of senior football this season after slipping down the pecking order at Eastlands. His only appearance of the campaign to date came in a 2-0 Carling Cup third-round victory over Birmingham on September 21.
Bridge joined City from Chelsea in a £12 million move in January 2009, but has managed only 58 appearances in his three years with the club.
He began his career with home-town club Southampton and hit the big time when he was snapped up by Chelsea in a £7 million deal in July 2003.
Bridge, who has 30 senior England caps, would fill a position which has been vacant for some time at the Stadium of Light.
Either right-back Phil Bardsley or midfielder Kieran Richardson have more often than not played on the left side of defence for the last two seasons.
O'Neill's predecessor Steve Bruce chased Wigan's Maynor Figueroa for much of his time at the club, but was never able to plug the gap with a specialist.
It is understood npower Championship Reading had more than a passing interest in Bridge, but the offer of Premier League football appears to have eased Sunderland ahead of the Royals.
Use a Facebook account to add a comment, subject to Facebook's Terms of Service and Privacy Policy. Your Facebook name, photo & other personal information you make public on Facebook will appear with your comment, and may be used on ESPN's media platforms. Learn more.


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The subscription fee for delivery of the Oregonian newspaper includes unlimited access to the daily Oregonian digital newspaper. The delivery fee also includes access to any app offered from the Oregonian.Continue Reading
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This went so well! I cant thank those who helped out enough! Trick comp had 10 solid riders in it looking to get some pretty decent prizes. Some with the race and aside from one cop confrontation [sorry squirrel!] all went well with that too. Party at the house was probably the best for me [as it was what i got to participate in :)]. Lots of people came through, some i dont see very often, so that was real swell. I so wish someone had taken a picture of me in my get up…if you were there you know what im talking about. Bahaha. Definitely seemed like everyone had a good time and were really positive on the event. You can bet on more stuff like this in the future!
Big thanks to all the sponsors…we seriously had some nice prizes for this!
– Eighthinch
– Leader Bikes
– Lucky Lefty's
– Nemesis Project
– Ikon Cycles
– Sub Q Body Piercing
– Trick Track
– Redbull
I was too busy yelling stupid things at the riders to take pictures…luckily Tim had the time (with some help) in between getting second place! Check the rest here!
I also have some video that ill be going through to try getting and edit together…we'll see how that turns out.
Soooo…finally releasing the location and specific details for the trick comp and race.
– Meet at 7th and T st for start of event…
– $2 for either the trick comp or race…free entry to the other for one. Party be freee. (Any money left over from entry and not covering costs will be donated to our friend Jason who had his Fuji Track Pro recently stolen. There will also be donations accepted for him at the event…everything helps!)
– Trick comp sign ups will be between 4:30 and 4:45…comp starts at 5.
– Minicat will leave from trick comp location. Sign ups at 6:10 with race starting at about 6:30.
– Afterparty location will be on the manifests and everyone is welcome from the end of the minicat till the break of dawn! Bom bom ba bom.
Prizes!…with a few more expected.
Provided by…
– Eighthinch
Gold drop bars.
Gold cranks.
– Leader Bikes
– Lucky Lefty's
Mash/Benny Gold sprints, Fuct and 10 Deep tees.
Mishka and Lucky Lefty's hats.
– Nemesis Project
Tioga neon green and black toe clips.
Nemesis Project X Cup Noodles lunch.
– Ikon Cycles
Knog Skink front and rear lights.
Ikon Cycles water bottles.
– Sub Q Body Piercing
$50 Gift cert.
Kitty cat tee.
– Trick Track
Moral support.
– Redbull
Well DUH! On location at the event…
Thanks for all the support over the last year everyone! Look forward to seeing you this weekend if you make it out!


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Nashville, TN – Jamey Johnson has received two nominations from the Academy of Country Music Awards, including Album of the Year for The Guitar Song, the most-lauded country album of 2010.
"The triumph of a gold-selling double album is shared by my family, my friends/bandmates/producers, my staff, my label, my booking agents, my publishers, my management, my publicists, my handlers, my wranglers, my fans, my dog, Willie's braids and that beautiful brunette in Toledo," Jamey says. "Thanks all for the hard work and dedication. You all deserve each
accolade. And thanks to the Academy voters for the recognition." Jamey also received an ACM nomination in the category of Vocal Event of the Year for his performance with Colt Ford of "Cold Beer." "If working with Colt in the studio was a ball, touring with him on the road with the Grascals and Hank Williams, Jr. was several balls," Jamey says. "He's a unique artist in a day where uniquity is not usually rewarded. I'm proud to be nominated alongside my friend."


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I think the whole country is ready for spring. We are actually having spring here, but I am still ready for warmer temps. To be able to go outside without a jacket one would be nice. I can't wait to be able to open up the windows and let some fresh air in. We are in for a nice weekend here, so I am excited to maybe get outside and enjoy the weather. One thing I am becoming a little obsessed with this spring is citrus. If you know me, you know this is not normal, but I am loving it!
I don't think I have ever made a lemon bar before. I made Lemonade Pie a couple years ago, but that is the only lemon dessert I have ever made. I am a chocoholic to the core. Don't worry, chocolate will still take up prime real estate on this blog, but I am starting to see the draw of lemon desserts. Sweet, tangy, tart, and just plain good! My husband is not a fan of chocolate, so he might like this new trend.
My husband was having a team outing at work, a couple weeks ago. They were heading up to the mountains to go snowshowing for the afternoon. I took the opportunity to bake these bars, and send them along. They needed fuel for the hike, right? They disappeared very quickly. Lemon is just perfect for spring; these bars would even make a great dessert to have for Easter. So even if you are as obsessed with chocolate as I am, you really do need to make these. I could not stay away from them!
- 2 cups flour , sifted
- 1/2 cup powdered sugar
- 1 cup butter , cut into cubs
- 4 eggs
- 1 1/2 cups sugar
- 1/2 cup fresh squeezed lemon juice
- 1/4 cup flour
- 1/2 tsp baking powder
- Preheat oven to 350 degree. Spray a 13x9 inch pan with non-stick spray. Set aside.
- In a large bowl combine flour, powdered sugar, and butter. Using your hands, mix until it comes together as a dough. Press into the prepared baking dish.
- Bake for 20-25 minutes, until lightly golden brown. Remove from the oven.
- Meanwhile in an electric mixer bowl mix together sugar, eggs, and lemon juice. Mix on medium speed for 4-5 minutes; until light, fluffy, and the sugar is completely dissolved. Add flour and baking powder, and mix until well incorporated.
- Pour over the baked crust. Return to the oven and bake for 22-25 minutes.
- Remove from the oven, and cool completely before dusting with powdered sugar, and serving.
Adapted from [Food.com


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VANCOUVER, Nov. 16, 2012 /CNW/ - Callinan Royalties Corporation has received interim quarterly royalty payments totaling $3,359,471.50 from HudBay Minerals Inc.
The royalty payments include a payment of $ 3,238,004.00 from the 6⅔% Net Profits Interest Royalty and $121,467.50 from the production royalty of $0.25 per ton of ore for the quarter ended September 30, 2012.
The Net Profits Interest payment represents 75% of an estimate by HudBay Minerals Inc. The remaining 25% is paid annually, in mid-July, 130 business days after the financial year end of HudBay Minerals Inc.as per the agreement.
The quarterly payments are due to Callinan's royalty interests on lands that include the 777 Mine at Flin Flon, Manitoba, Canada, which is the principal mining operation of HudBay Minerals Inc.
Additionally, the Annual General Meeting of the Company will be held on Friday, November 30, 2012 at 11 a.m. (PST) at the offices of Boughton Law Corporation, 700 - 595 Burrard Street, Vancouver, British Columbia, V7X 1S8.
On Behalf of the Board of Directors,
Roland Butler
Roland Butler, CEO
About Callinan Royalties
Callinan Royalties is a Canadian company that creates and acquires mineral royalties. The company uses its royalty income to provide alternative financing options to mineral exploration and development companies with attractive projects. Callinan's strategy is to create shareholder value over the long term by generating a portfolio of profitable mineral royalties.
The Corporation currently has two producing royalties. Callinan holds a 6⅔% net profits interest royalty and a $0.25 per ton production royalty on lands that include the 777 Mine owned by HudBay Minerals Inc. located in Flin Flon, Manitoba, Canada as well as the adjacent 777 North Mine scheduled for production in 2012. Callinan also holds the 777 Deeps (War Baby) property and an associated royalty option on the property, which is located adjacent to the 777 Mine.
Callinan is a dividend paying Tier 1 company listed on the TSX Venture Exchange under the symbol CAA. The Corporation has a strong financial position with no debt, approximately $29 million in cash and approximately 48.2 million shares outstanding.
Cautionary Statement on Forward-Looking Information
Neither the TSX Venture Exchange nor its Regulation Services Provider (as that term is defined in the policies of the TSX Venture Exchange) accepts responsibility for the adequacy or accuracy of this release. Certain of the information presented in this News Release may constitute "forward-looking statements" or "forward-looking information" within the meaning of Canadian securities legislation (together referred to as "forward-looking statements"). The forward-looking statements are subject to risks, uncertainties and other factors that may cause actual results to be materially different from those expressed or implied by such forward-looking statements, including any delays in the receipt of consents or approvals. Although Callinan Royalties has attempted to identify important factors that could cause actual actions, events or results to differ materially from those described in forward-looking statements, there may be other factors that cause actions, events or results not to be as anticipated, estimated or intended. There can be no assurance that such statements will prove to be accurate as actual results and future events could differ materially from those anticipated in such statements. Accordingly, readers should not place undue reliance on forward-looking statements contained in this News Release and in any document referred to in this News Release. Forward-looking statements are made based on management's beliefs, estimates and opinions on the date the statements are made and Callinan Royalties undertakes no obligation to update forward-looking statements if these beliefs, estimates and opinions or other circumstances should change, except as required by applicable law.
SOURCE: Callinan Royalties Corporation
For further information:
please visit www.callinan.com or contact:
Roland Butler, CEO
Callinan Royalties Corporation
+1 709 535 3433
Tamara Edwards, CFO
Callinan Royalties Corporation
+1 604 605 0885
Corporate Office:
1110 - 555 West Hastings Street
Vancouver, BC
Canada, V6B 4N4
Callinan Royalties Corporation
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text: 4/05/16 5/12/14 POPSUGAR Love Nostalgia 1950s Winter Wedding Inspiration A Retro Winter Wonderland Wedding May 12, 2014 by Tara Block 183 Shares Chat with us on Facebook Messenger. Learn what's trending across POPSUGAR. View On One Page Photo 16 of 73 ADVERTISEMENT () Start Slideshow Share This Link Copy What's Your Reaction? Thanks for your reaction Don't forget to share this with your friends! ← Use Arrows Keys → 16 Photo by Kristilee Parish Photography 0 previous images 42 more images Previous Next Start Slideshow Real WeddingsNostalgiaWedding


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From: Michelle Kulp
Thank you for visiting my website! I'm so glad our paths have crossed and we have connected!
If you're like me, you've probably thought about these questions:
- How can I make money and make a difference in the world?
- How can I find more meaning and purpose in my life?
- How can I get paid to do what I love?
I think it begins with caring about those things; caring about yourself, your dreams and what you want from life! We have to make a conscious decision that we want to live that way.
I made a conscious decision in 2002 that I wanted to live life on my own terms, do what I love, make a difference and be well paid for sharing my gifts with the world! That one decision changed my whole life.
**See my personal story below of exactly how, as a struggling single mother of 3, living paycheck to paycheck, working in a job I hated as a paralegal and legal secretary…I was able to leave my soul-draining job and create a life of my dreams!
But before I tell you that story, let's talk about how you can have more FREEDOM in your life…
I believe one of the main characteristics of women who have time and money freedom is they have learned how to leverage their time . They know that trading hours for dollars doesn't work long term because there are only so many hours in the day; time is finite. Even if you have a high paying 9-5 job; typically, if you don't go to work, you don't get paid!
Wouldn't you rather have passive income streams that come in on automatic pilot? Passive income that allows you to do the work once and get paid over and over! It's truly the fastest path to becoming a 6-figure woman.
I am passionate about helping women create more TIME and MONEY FREEDOM in their lives! Think of what you could do with more TIME:
- Time to spend with your children, spouse, family and friends;
- Time to engage in hobbies that make your heart sing;
- Time to do daydream! Many successful entrepreneurs have a lot of down time which allows the creative ideas to come flowing in!
- Time to take vacations and see the world or even just see places nearby;
- Time to take care of your loved ones. A family member of mine had some serious health challenges recently, and my flexible schedule allowed me to time to spend with them.
Unfortunately, I know first hand about trading hours for dollars because I worked for 17 years in the legal field (see my story below ) and at the end I was still broke and living paycheck to paycheck! It wasn't until I began to leverage my time in 2004 that I became a 6-figure Woman.
Let me ask you a few questions:
- When you think of making money online, do you feel overwhelmed about all the options out there?
- Have you tried other programs and you still haven't made any money online?
- Do you know you have a message to share with others, but just need some help and maybe even a little hand holding?
Creating an online business can be very intimidating for most people. My gift is taking tasks which are complex and transforming them into simple, bite-size pieces which will help you move forward and achieve your goals and dreams!
I am a heart-centered web strategist who can help you clarify as well as monetize your message through an online business.
I love helping women come out of hiding and into the spotlight! I'm here to tell you that you can combine a higher calling with higher profits.
One of the great parts about having your own online business is that you have "options". Instead of relying on one source of income like many people do (and like I did for 17 years), I'll teach you how to have multiple streams of online income.
So whether you've had a bad experience before or you're just getting started, I can show you how to start making money online!
What's important to look for in a mentor online is transparency and longevity. I've been running an online business for 10 years and I'm committed to helping women create an online business so they can live richer…and more flexible lives!
Here's my my PERSONAL STORY of how I got started with my online business:
After graduating college in 1983, I worked as a paralegal and legal secretary for the next 17 years! I enjoyed my job for about 10 years, but then I experienced something called "career creep". Career creep is when the job you started
out in changes so much, that you wake up one day and you're in a job you don't recognize or like.
I dreaded going to work every day and literally would think of how I could "not" go to work. I didn't have many options as a single divorced mom with 3 young children living paycheck to paycheck.
As fate would have it, the law firm I was working at gave me the pink slip in 2000; they told me, "The department you work in is being re-structured and your job no longer exists." Fear came over me as I wondered how on earth I would support my family. I was happy to be out of a job I hated, but worried about the future.
Things worked out over time as I learned to trust and put my faith in God that I was being led to create a new life…one with purpose, passion, fun, and meaning!
Back in 1992 (on my birthday), I met Billy Ray Cyrus, you can read that story here .
During our time together, Billy Ray asked me what my dreams were, to which I told him, "I don't have any dreams, my life is about survival." Billy Ray encouraged me to go out and find my dreams and never, ever give up on them. He said that everyone has a dream and our purpose in life is to find out what our dream is.
So I went searching for this elusive dream that Billy Ray spoke of (which is hard to find when you're living paycheck to paycheck and worried about money, but I kept looking and trusting)…and one day I was in Borders bookstore when I came upon a book by Richard Bolles called "How to Find Your Mission in Life ". I recognized the author, Richard Bolles, because he also wrote a very large career guide called "What Color is your Parachute?"
I read that book and there was a question in it that led me directly to my dream! That question was: "What do you LOVE to do that you lose all sense of time? "
I pondered that question for a long time and then the answer came to me. I loved to write! When I sat down to write, 5 hours could go by and to me it felt like 5 minutes. (Like right now while I'm writing this story). I was so happy to finally discover my dream of writing!
I didn't know where my dream of writing was going to lead me; I just took one step and then another and then another. I used spiritual tools such as meditation, journaling, artist dates, reading inspirational books, walking in nature, yoga, and anything that connected me back to my "essential self".
Martha Beck, author of "Finding Your Own North Star" says that we have an essential self (our true self) and a social self (the part of us who is all about being accepted, finding approval and fitting in with society). Unfortunately, many of us end up abandoning our essential selves and following our social selves. I'm certain that's what happened to me.
I believed in (and trusted) my dream of writing, which led me to public speaking and teaching classes and then that led me to start an online business. By taking one step in the direction of my dreams, other doors opened up that I could have never imagined. What I love most is being able to reach women all over the world with my online courses and programs.
My advice to you is to start listening to your essential self and to your heart. It knows what you want and it led you here! I'd love to connect with you further!
Don't put off following your dreams any longer. It's time!
Here are some ways we can Connect:
- Get Started for FREE is for women on a tight budget yet who are committed to taking the necessary steps towards their goal of having an online business.
- How to Make Your First $1000 Online is my 6-week online course that will educate and empower you to starting an online business.
- Creating Online Courses for Profits is my 6-week online course that is great for coaches, consultants, speakers, entrepreneurs and anyone else who would like to turn their expertise into an online course and sell to "many" instead of just selling to 1! This course is all about leveraging your time!
- You can also start creating an online income by publishing your book on Amazon! I have a 6-week online course just for you: Become an Amazon Best Selling Autho r ! One of my students of this course, Nancy Hartwell, is making $2300 a month on Amazon from one ebook after following my program!
- My Heart-Centered Online Business Program is for women who are ready to build an online platform and need a website so they can share their message and gifts with the world!
- If you'd like to have a FREE 30-minute business strategy session with me, you can apply here .
You're Calling is Calling! Are You Listening?
It takes determination, courage, and a strong desire to live life on your own terms. Most people are living a default life and are very unhappy with what they do for a living.
I'm challenging you to step out in faith, believe in yourself and your abilities, and to work with me! Because at the end of the day, your success is my success!
All you need to do is take one small step in the direction of your dreams…
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i am running both 2.12 and latest v3 on my blogs,i just recently was accepted in ebay affiliates.
When I click on "bid now" link in the post it redirecting me back to my site.
What could it be?How can I fix that?
P.S. checked on on posts made with 2.12


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Bonding through books
"My business has grown up with my children. When I started Kids Gallery, my daughters were four and two, and now they are 19 and 16. They are my focus group," says Hotung.
She is now the managing director of the KG Group, the parent of Kids' Gallery, which has grown to include the Star English language centres and Face Productions, a production company that puts on shows for and by kids.
Hotung decided to go into an education-related business when her daughters were in kindergarten. She says she felt the need to teach children the ability to think for themselves rather than telling them what to think.
She now has a total of 70 staff at Kids Gallery. With an MBA degree and a background in management consultancy - she was a management trainee at Marks & Spencer and a management consultant at Coopers & Lybrand (which merged with another firm to form PricewaterhouseCoopers) - Hotung has made Kids Gallery a very structured and systematic place to work in. "We are quite informal with our policies and we do a lot of training and peer reviews," she says.
"Because I was in consultancy, I was able to work on projects with senior people from other companies and I got to see how other companies worked. It was a huge learning experience," she explains. "And then I had my first MBA. In fact, my final dissertation for my MBA was my business plan for Kids Gallery."
Hotung was trained to look at companies and identify their strengths and weaknesses, something she does with her own business. "I am always reviewing, thinking if I can be more efficient, more organised and provide better services," she says.
Working with children can be demanding and management intensive, she notes. As her business grows, she has had to work six days a week.
As an ongoing issue for all service industries, finding and retaining the right staff are the two greatest challenges for Hotung and she constantly looks for "people who want to be there".
In September, Kids Gallery will celebrate its 15th anniversary and two of her staff will be honoured for their 15 years of service.
Hotung is also very involved in charity work for children. In addition to being the founding president of the Hong Kong Juvenile Diabetes Association and a committee member of the Playright Children's Play Association, she is also the board governor of Bring Me a Book Hong Kong - a non-profit organisation which serves children who do not have access to quality books and who are not read aloud to on a regular basis.
"I love books and I always read a lot. My parents filled our house with books," she says. "I really believe that books, apart from educating, can bring joy to children. I think it's a shame when children don't read."
Hotung made sure she read to her daughters every night when they were growing up, maybe just a few lines if she was tired. Apart from the reading, it is the sharing and togetherness that count.
"You may not see your children all day, and when you get home from work, you are tired. But if you could spend a few minutes just reading to them at the end of the day, it is really important for the family to get close," she says.


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My Dearest Friend
By Tess Irons, 29th Feb 2012 | Follow this author
| RSS Feed | Short URL http://nut.bz/2dfr-yfk/
Posted in WikinutWritingPoetry
This poem is for a special friend who is many miles away from me. This is my way of expressing how I cherish our friendship.
I Miss You
I think of you each day and night
I wonder how your day went by
It's been a while since I saw your smile
I wish you well and hope you're alright
No matter how far you are from me
Thousand miles apart from me
Rest assured that you'll always be
A very special friend to me
You're In My Heart
I cherish our friendship
You're someone I'll keep
Like precious gem
So genuine and rare
Stay that way, I hope you will
Sweet and gentle, you've always been
Those traits of you that I have seen
Make you closer to me than you've ever been
You'll always be a part of me
You're so far, yet close to me
And in my heart, there will always be
A place for you reserved dearly
I love you, my friend!
Image Credits:


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In full J.O. Food Revolution mood, I made the tikka masala paste from scratch or you can purchase the already made sauce at the store. I do not like using pre-made sauces because there is too much sodium and additional preservatives that I rather not think about. Besides when you make your own sauce from scratch, you learn more about the food. The tikka masala paste was similar to making a pesto. It was very easy to prepare, but only if you have the proper tools. My beautiful marble mortar and pestle came in handy for the paste, and my mini food processor, too. This was such a great dish and we really enjoyed the classic tikka flavours with the creamy, slightly sweet sauce. The chicken was light and the fluffy basmati rice was not too heavy, and it all paired well with a simple green salad.
Adapted from Jaime's Food Revolution: Rediscover how to cook simple, delicious, affordable meals
4 skinless chicken breasts, cut into 2-inch strips
2 medium onions
1 fresh red chile
1 tablespoon ginger, thinly sliced or grated
1 small handful of fresh cilantro - separated - cilantro stalks, chopped fine, and cilantro leaves
Peanut oil
1/2 cup tikka masala paste or tikka masala (Recipe below)
Salt & pepper
a pat of butter
1 x 14 ounce can of coconut milk
8 ounces of low-sodium chicken broth
1 x 14 ounce can of diced tomatoes
1 cup natural yogurt
small handful of sliced almonds
1 lemon
Tikka Masala Paste - 2 cloves garlic (minced), thumb-size piece ginger, 1 teaspoon cayenne pepper, 1 tablespoon smoked paprika, 2 teaspoons garam masala, 1/2 teaspoon salt, 2 tablespoons of peanut oil, 2 tablespoons tomato paste, 2 fresh red chiles, small bunch of cilantro, 1 tablespoon unsweetened shredded coconut, 2 tablespoons almond flour (I had used sliced almonds), 1 teaspoon cumin seeds, 1 teaspoon coriander seeds
- Toast the spices for a couple of minutes, and add toasted spices to mortar and pestle and grind until fine. Add all the ingredients into a food processor until you have a smooth paste. This makes 1 full cup.
1. Put a large dutch oven (or wok) on medium to high heat and add 2 tablespoons of oil and butter. Add the onions, chile, ginger, and cilantro stalks and cook for 10 minutes until transculent.
2. Add the curry paste and mix, and let it cook together for at least 1 minute. Add the chicken chunks and mix well. Season with salt and pepper.
3. Add the canned tomatoes and coconut milk. Fill 1/2 of the empty cans with low-sodium chicken broth, pour into pan and stir again.
4. Bring mixture to a boil, and then turn the heat down and simmer for 20 minutes with the lid on.
5. When the meat is tender and cooked, taste and season with salt and pepper.
Serve with basmati rice and almonds and garnish with cilantro leaves. Pair it with a little lemon-dressed green salad.


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ANAHEIM – A man suspected by police of holding up a bank died Friday when he crashed a car into a light pole while leading officers on a high-speed chase, police said.
A second man, who was in the car's passenger seat, was in critical condition. Police said they believe he was also involved in the bank robbery Friday afternoon at a Bank of the West branch in the 4500 block of East La Palma Avenue.
Two men entered the bank shortly before 2 p.m. to carry out a robbery, Anaheim police Lt. Tim Schmidt said. They reportedly handed a teller a note claiming to be armed, although no weapon was seen, and also robbed a customer on the way out the bank.
Witnesses saw the men leaving and called police with a description of the Honda Civic they got into. Some witnesses followed the men until police picked up the chase, Schmidt said.
The men led police on a 10-minute chase on La Palma Avenue and through an industrial park, Schmidt said. At times, the men drove on the wrong side of the roadway and through several red lights.
The Civic crashed into a light pole in front of a Kaiser Permanente building on East La Palma Avenue. Both men were taken to hospitals, where the driver was pronounced dead.
Authorities found money in the vehicle that they believe may have been taken during the robbery.
Police were not releasing the men's identities. Homicide detectives were investigating. East La Palma Avenue was closed from North Tustin Avenue to North Kraemer Boulevard.
The FBI is assisting with the investigation. Authorities have not determined whether the men are tied to other robberies.
Register staff writers Doug Irving and Sean Emery contributed to this report.
Contact the writer: 714-704-3764 or email@example.com