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So this weekend I bought a new TV, a new surround sound system, and a PS3 Slim all connected through HDMI cables and Optical out from my TV to the receiver. My TV can stream over DLNA, but even though it has the optical out the TV downgrades to stereo sound.
So I installed PS3 Media Server on my computer so I can stream to the PS3 and get full surround sound on my videos, but came across the dreaded Cinavia DRM. Today I've been looking everywhere for more information about it. So here are my questions:
1) Some people say you can enable the optical out while still only using HDMI and that will bypass Cinavia, but in doing so you lose surround sound. Is this true?
2) Some posts say you can reconvert the videos with certain programs to get rid of the Cinavia protection. Which one(s) are best/easiest/quickest?
3) Which brings me to my third question. Is there a program that detects which files have the Cinavia DRM? I have a lot of video files and don't want to have to guess which ones are safe and which ones are "infected".
4) This should have probably been question 1, but is there actually any easier workaround, like a plugin or alternative to PS3 Media Server that will disable Cinavia on the fly while it's streaming?
Thanks in advance!
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The above mentioned page is no longer valid. I just wanted to know...
1. whether standalone players can detect Cinavia code even in files like mkv and m2ts?
2. Does extracting the audio channels to individual .wav files and remixing them using DTS encoder remove Cinavia?
I think standalone players differ too much to make generalizations about them and Cinavia detection. Some might detect Cinavia in other types of files, and some might not. Also might depend on whether you are playing from discs or from USB sticks.
Answer to your second question is no. That won't help.
Just forget the PS3 and get a decent media player for US$50 to US$100.
Last edited by jagabo; 12th Jul 2016 at 18:18.
Try CloneBD http://www.myce.com/news/slysoft-removes-cinavia-signal-from-blu-ray-movies-with-anydv...ination-75695/ Then goto https://forum.redfox.bz/forums/clonebd.89/ They will answer any questions you have
as Slysoft is out of business.
Last edited by pepegot1; 12th Jul 2016 at 18:21.
ffdshow 'crystality' to extend bandwidth - this is least possible from quality loss perspective way to remove Cinavia for today.
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Results 1 to 2 of 2
Thread: Long Transaction aborted
03-15-11, 08:06 #1Registered User
- Join Date
- Mar 2011
- Posts
- 1
Unanswered: Long Transaction aborted
Hi Friends,
Following is environment details.
Informix version = IBM Informix Dynamic Server Version 11.50.FC6
Table name = daily_records
Total Columns = 210
No of rows = 64 Millions
Size of Logical Logs = 10 GB
Transaction/minutes = 50
Existing no of indexes = 24
Reference/referenced tables = 0
OnConfig Settings related to long transaction:
we were creating online index on two columns i-e date (datetime),status(char(1)). After 14 hours we got error long transaction aborted error. Here are my two questions
1. How to calculate INDEX size in informix? (if possible share any formula)
2. What steps should we do to avoid long transaction issue? Increase logical logs or modify some parameters of onconfig file?
3. Any other things we can look?
03-15-11, 09:17 #2Registered User
- Join Date
- Sep 2010
- Location
- Germany, Brunswick
- Posts
- 55
There are some ways to avoid the long transaction:
- increase logical logs, you could create some in your datadbs
- increase LTXHWM and LTXEHWM
- set the log mode to no log, create index and set the log mode back
- create a new empty table with the index and then copy the data to the new table
- little crazy way: set LTXHWM and LTXEHWM to 100 and DYNAMIC_LOGS to 2
I think there is no easy way to calculate the index size because it depends on the data.WilhelmW

subset: commoncrawl


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Vermiculite Sand Maker Manufacturer
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BUS 505 Week 2 Discussion Questions – Strayer New
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Week 2 DQ 1
"Federal Government Source Selection" Please respond to the following:
• Assume you own a small company that makes widgets. Carefully review the federal government acquisition process and determine how you would best position yourself long before you place your first government bid. Discuss the benefits of your preparations.
• Analyze the elements of both the technical evaluation and the past performance evaluation. Next, determine which is the most difficult to evaluate from the federal government perspective and how you (as a business owner) could make the evaluation process easier. Then, directly respond to the assessment of a fellow learner and evaluate his or her post (on-ground students will discuss the positions).
Week 2 DQ 2
"Strategic Business Planning" Please respond to the following:
• Assume you own a company that manufactures a specific product of your choice. Create a one-paragraph mission statement that addresses the what, who, how, and why of your company. Then, discuss how each component is addressed in your mission statement.
• Based on the same company you described above, create a strategic business model that incorporates the four major elements of strategic business modeling discussed in Chapter 4 of the textbook.


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Photos from Faire-on-the-Square, Watertown, Sept 26, 2015.
Photos from our recent community outreach at Faire-on-the-Square, Watertown, MA on Sept 26th, 2015. What a wonderful day! Many locals and visitors to the fair came by to view our poster display, talk with members and learn various new facts about 9/11. Quite a few were already aware of some of the issues and welcomed the opportunity to learn more.
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We might turn the links into functional hyperlinks, to make it easier on visitors.


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Rainbow Smoothie Recipes for KidsWe LOVE healthy fruit and veggie smoothies in our house. When the kids hear the blender blending, they come running! So when I saw this smoothie recipe from Jodie Fitz linked up on Share It Saturday this week, I knew I had to feature it. I love the rainbow of colors in the smoothie recipe Jodi put together. Then I started thinking that we need more colors of smoothies here! I can't wait to try all of these smoothie recipes with my kids. We'll sip our way through the rainbow!
A Rainbow of Smoothie Recipes:RED SMOOTHIE: Watermelon and Lime Smoothie from Housing a Forest
ORANGE SMOOTHIE: Tropical Orange Delight smoothie from mom Endeavors
YELLOW SMOOTHIE: Banana smoothie from My Life and Kids
GREEN SMOOTHIE: Spinach smoothie from My Life and Kids
BLUE SMOOTHIE: Blueberry Kale smoothie from Coffee Cups and Crayons
PURPLE SMOOTHIE: Very Berry smoothie from Crazy Adventures in Parenting
And make a rainbow of colors with a Rainbow smoothie recipe from Jodie Fitz
What is your favorite smoothie recipe?
Check out who the other hosts are featuring today:
AND be sure to stop by our guest host for the month of February, Jaime at Frogs and Snails and Puppy Dog Tails.


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Affiliate Marketing is a great way for bloggers and writers to earn a commission from selling other people's products. I use and recommend the companies, services, and products listed under this category.
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why we run a deficit
So just venting here, but I do speak from fact. A person may need a leg up once and a while and Ontario has programs in place to provide that. They are welfare and Ontario works. If your not aware people abuse these programs, I know I know I was shocked too, but did you know that regardless of that you will continue to get the support. Let me give you an example, did you know you can be found guilty of fraud, in that you may be on Ontario works plead guilty to fraud because you received $39000 in benefits over a number of years, while you were employed and earned lets say $50000 a year. So now your sentenced to repay that amount, you make a tiny dent the day you plead, and then not again till you face new charges, why because you never paid like you were suppose to. So now let's go back your out of work and go back on benefits from Ontario works and you make a small payment why because you now have some money and you want it to look good on your trail date. So I leave you with this who is paying back Ontario works the criminal or Ontario works. Look at it this way I loan you $10 you can't pay me back I loan you another 10 you give it back and say were even. We wonder why Ontario can't turn a profit.


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Deem, Steven A., Michael K. Alberts, Michael J. Bishop, Akhil Bidani, and Erik R. Swenson.CO2 transport in normovolemic anemia: complete compensation and stability of blood CO2 tensions. J. Appl. Physiol. 83(1): 240–246, 1997.—Isovolemic hemodilution does not appear to impair CO2 elimination nor cause CO2 retention despite the important role of red blood cells in blood CO2 transport. We studied this phenomenon and its physiological basis in eight New Zealand White rabbits that were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Isovolemic anemia was induced by simultaneous blood withdrawal and infusion of 6% hetastarch in sequential stages; exchange transfusions ranged from 15–30 ml in volume. Variables measured after each hemodilution included hematocrit (Hct), arterial and venous blood gases, mixed expired and , and blood pressure; also, O2 consumption, CO2 production, cardiac output (Q˙), and physiological dead space were calculated. Data were analyzed by comparison of changes in variables with changes in Hct and by using the model of capillary gas exchange described by Bidani (J. Appl. Physiol. 70: 1686–1699, 1991). There was complete compensation for anemia with stability of venous and arterial between Hct values of 36 ± 3 and 12 ± 1%, which was predicted by the mathematical model. Over this range of hemodilution,Q˙ rose 50%, and the O2 extraction ratio increased 61% without a decline in CO2production or a rise in alveolar ventilation. The dominant compensations maintaining CO2transport in normovolemic anemia include an increasedQ˙ and an augmented Haldane effect arising from the accompanying greater O2extraction.
- anemia
- carbon dioxide
- hemodilution
- pulmonary gas exchange
the quantitative importance of red blood cells in blood O2 transport is a function of the direct binding of O2 to hemoglobin. The nearly equivalent role of red blood cells in blood CO2 transport is not generally appreciated, since CO2 is roughly twenty times more soluble than O2in plasma and only 5% of total blood CO2 is bound to hemoglobin. However, physically dissolved CO2accounts for only another 5% of CO2 content; the remainder of CO2 carriage in blood occurs because of the contributions of hemoglobin and two other red cell proteins, carbonic anhydrase and band 3 protein (a membrane-bound Cl−/ exchanger). Although direct CO2binding to hemoglobin as carbamate accounts for only 5% of blood CO2 content, it contributes roughly 15% to CO2 exchange because of the oxylabile characteristics of hemoglobin (Haldane effect). More importantly, 80% of CO2 is carried in blood in the form of , the formation of which is catalyzed within the red blood cell by carbonic anhydrase (7, 24,43). A high rate of formation within the red blood cell is promoted by the large oxylabile buffering capacity of hemoglobin and rapid extrusion of into plasma across the red cell membrane in exchange for Cl−(Cl− shift). These processes forestall a rate-limiting accumulation of H+ and , thereby facilitating greater formation from CO2. The net result is the transport of large amounts of CO2at the expense of only small tissue-to-blood and blood-to-alveolar differences (7, 24, 43).
The effect of a diminished red blood cell concentration on CO2 homeostasis can be predicted by mathematical modeling. With a sophisticated model of human blood-gas transport, Bidani and Crandall (6) predicted that moderate anemia [hematocrit (Hct) ∼30%] will result in a 25% reduction in CO2 elimination (V˙co 2), whereas severe anemia (Hct ∼15%) will result in a 50% reduction in the absence of any compensatory changes in metabolism, ventilation-perfusion ratio (V˙a/Q˙) relationships, ventilation, and cardiac output (Q˙). Similar results were obtained in an earlier model simulation by Hill et al. (21). In vivo, a reduction inV˙co 2 would necessarily lead to CO2 retention and ultimately bring CO2 elimination back into a steady state with its production, albeit at the expense of higher venoarterial gradients. Other evidence that anemia may affect CO2 homeostasis comes from a model of brain gas exchange (40). This model predicts that without changes in metabolism or blood flow, and assuming a constant arterial ( ), brain tissue would rise ∼6 Torr with a fall in Hct from 42 to 15%. In the absence of compensations, therefore, anemia should result in either hypercarbia or a reduction in CO2 output.
Only a few studies have directly addressed the impact of anemia on CO2 transport and, in general, although documenting remarkable stability of in the presence of anemia, these studies have been incomplete in that they have not measured or controlled for all the variables involved in CO2 transport and elimination (4,12, 31). Our study was designed to measure and quantitate the relevant physiological parameters influencing CO2 homeostasis in the rabbit during isovolemic hemodilution. A second aim was to model the gas-exchange and hemodynamic data to determine whether the measured compensations to anemia in vivo are sufficient to predict our measured venous CO2 gas tension ( ) and or whether additional mechanisms of compensation need to be invoked.
The protocol was approved by the Animal Care Committee of the Seattle Veterans Affairs Medical Center. Eight New Zealand White rabbits weighing 3–4 kg were anesthetized with 15 mg/kg iv ketamine and 0.33 mg/kg iv xylazine, and their tracheas were intubated. Mechanical ventilation with a Harvard dual-phase ventilator was initiated at a tidal volume of ∼15 ml/kg and a respiratory rate of 25–30 breaths/min to achieve a baseline of 35–40 Torr. The inspired O2 fraction was set at 0.209. Bilateral femoral arterial catheters were placed surgically for blood pressure monitoring and blood withdrawal. An internal jugular venous catheter was surgically placed and advanced into the right ventricle for withdrawal of mixed venous blood gases and pressure measurements. Anesthesia was maintained with pentobarbital sodium, ∼10 mg ⋅ kg−1 ⋅ h−1by intravenous infusion, and animals were monitored closely for sudden increases in blood pressure and/or heart rate that might indicate insufficient anesthesia. Muscle relaxation was provided by intravenous pancuronium, 0.3–0.4 mg ⋅ kg−1 ⋅ h−1after tracheal intubation.
After stabilization, baseline measurements including mean arterial pressure, right ventricular pressure, Q˙, airway pressure, temperature, and Hct were recorded. Mixed venous and arterial samples were drawn for blood-gas analysis, and expired gas was sampled from a 250-ml mixing chamber attached to the expiratory limb of the ventilator circuit.
Isovolemic anemia was then induced by simultaneous blood withdrawal (via an arterial catheter) and infusion (via the jugular vein) of an equal volume 6% hetastarch in sequential stages; exchange transfusions ranged from 15 to 30 ml in volume. Repeat measurements were made 30 min after each hemodilution or when mixed expired had stabilized. Minute ventilation (V˙e) and inspired O2 fraction were maintained constant throughout each experiment, andV˙ewas measured by a timed collection of expired gas at the conclusion of the experiment. At the conclusion of the experiment (achievement of a Hct of ∼15% or severe hemodynamic derangement), the rabbits were euthanized with an overdose of pentobarbital sodium.
Venous and arterial blood gases and mixed expired CO2 and O2 were measured by an IL 1306 blood-gas machine (Instrumentation Laboratory, Lexington, MA). Mixed expired CO2 was also continuously measured by using a 1100 medical gas analyzer mass spectrometer (Perkin-Elmer, Norwalk, CT). Venous and arterial O2 content were measured using an IL 482 CO-oximeter (Instrumentation Laboratory).
O2 consumption (V˙o 2) andV˙co 2 were calculated from the volumes and concentrations of inspired and expired gases (using appropriate temperature and humidity corrections) and corrected for body weight. Q˙ was calculated by using the Fick equation. The fraction of physiological dead space (Vds/Vt)was calculated by using the Enghoff modification of the Bohr equation, and reported as a percentage. O2extraction ratio ( ) was calculated as the ratio of arteriovenous O2content difference to arterial O2 content, and reported as a fraction.
Data Analysis and Statistics
Two methods of data analysis were used.
Method 1. The slopes of the lines generated by plotting Hct vs. individual measured variables at baseline and after each hemodilution were calculated for individual rabbits by using ordinary least squares. Student'st-test (2-tailed) was then used to determine whether the mean of individual slopes was significantly different from zero. A P value of <0.05 was accepted as statistically significant.
Method 2. The experimental data were analyzed by using a previously described model of capillary gas exchange (5). Several simplifying assumptions are incorporated in the mathematical model: alveolar gas is assumed to be well mixed and uniform throughout the lung, and alveolar gas tensions are assumed to be time invariant. Blood is considered to consist of two well-mixed compartments (plasma and red blood cell) that have the same residence time in the pulmonary capillaries. Blood flow in the capillaries is assumed to be constant and uniform, and axial and radial diffusions are considered negligible. A kinetic mathematical description of pulmonary capillary O2 and CO2 exchange is obtained by deriving mass balance equations for each of the chemical species included. These include CO2, O2, water (or volume), hemoglobin-carbamate (oxygenated and reduced), , Cl−, and H+. Because the latter three exist at different concentrations in the plasma and red cell compartments, the behavior of eleven variables must be described as a function of time (from the time blood enters the pulmonary capillaries). The mass balances describing the time rates of change of the eleven variables involve: 1) rate of consumption or production of that species by chemical reaction within its compartment, and/or2) net transport of the species into or out of its compartment.
Processes included in the quantitative analysis are1) CO2-H2CO3hydration-dehydration reactions in plasma and red blood cells;2) CO2 reactions with hemoglobin;3) O2 binding to hemoglobin and the release of Bohr protons from hemoglobin on oxygenation;4) buffering of H+ intra- and extracellularly by hemoglobin and plasma proteins, respectively;5) /Cl−exchange across the red cell membrane mediated by band 3 protein;6) transcellular movement of water in responses to changes in osmolality; and7) diffusion of O2 and CO2 between alveolar gas and pulmonary capillary blood. Bohr and Haldane effects are included. Ion and water fluxes are described assuming passive diffusion down their respective electrochemical potential and osmotic gradients. Red cell anion exchange is described in terms of a "phenomenological permeability coefficient (PHC )" (5). To account for the availability of pulmonary vascular carbonic anhydrase activity to plasma during capillary transit, an acceleration factor of 200 was used (8).
The mathematical model consists of a set of eleven simultaneous nonlinear ordinary differential equations. The only difference between capillary and postcapillary equations is that net O2 and CO2 movement can take place into or out of the blood only while blood is in the pulmonary capillaries; however, after blood enters the postcapillary vessels, it becomes a closed system, and total O2 and CO2 contents remain constant.
Numerical integration of the model differential equations was implemented by using the Gear algorithm (15), ideally suited for stiff differential systems. Input parameters for solution included kinetic parameters (Table 1; Ref. 5), estimated alveolar gas tensions, central venous blood-gas parameters, and Q˙ corresponding to each experimental condition. To provide uniform groups and to include all rabbits in this analysis, plots were constructed for each variable vs. Hct and values interpolated at percentages of baseline Hct of 100, 84, 76, 52, and 44% (some rabbits did not survive <44% of baseline Hct). Interpolated values of Hct, , venous ( ), Q˙, and venous pH were entered into the model, which subsequently generated predicted values for ,V˙co 2, andV˙o 2.
Six to seven hemodilutions were performed per rabbit, with only five rabbits surviving seven hemodilutions. Data from measurements taken at baseline and with each hemodilution are reported in Table 2. Starting Hct was 36 ± 3% and fell to 12 ± 1%, or 32% of baseline, at its lowest point. There were no significant changes in , , venoarterial difference,V˙co 2, and arterial ( ) with hemodilution, whereas Vds/Vtincreased minimally (Fig. 1 and Table 2).Q˙ and both increased significantly with hemodilution (Fig.2). Despite the rise in Q˙, both systemic and right ventricular pressures remained unchanged. ,V˙o 2, and arterial pH all fell with hemodilution.
Data from the mathematical model are presented in Table3. Because of the previously described derivation by interpolation of data used in the model, the numbers of data points after baseline differ slightly from those reported in Table2. Using our input data, the model predicts that should remain virtually unchanged with each subsequent hemodilution, whereasV˙co 2 andV˙o 2 are predicted to fall only slightly. There is close agreement (<5% difference) between measured (interpolated) values and predicted values using modeling for all variables except V˙o 2. MeasuredV˙o 2 falls more than predictedV˙o 2, particularly at the last analysis point (44% of baseline Hct) where there is a 20% difference between measured and predicted values. For this last data set, if it is assumed that hemodilution and acute anemia result in a small fall in 2,3-diphosphoglycerate, with a corresponding left shift of the oxyhemoglobin dissociation curve (change in at 50% saturation of hemoglobin, ∼5 Torr), there is closer agreement between measured and predicted V˙o 2 (3% difference in values). The difference between measured and predicted , however, becomes slightly greater when using this correction, although the difference is still only 7%.
Our main findings are that acute normovolemic hemodilution to Hct values <40% of normal in anesthetized and mechanically ventilated rabbits does not alter and mixed venous or the venoarterial difference. Stability of values occurs despite an unchanged total and slightly lower alveolar ventilation and no decline in V˙co 2. AlthoughQ˙ rises with anemia, it is not fully compensatory for O2 transport, since we found the classic progressive widening of the arteriovenous difference (i.e., greater ) with decreasing Hct. Modeling of our hemodynamic and respiratory data predicts the observed stability in values.
Critique of Methods
We studied the effects of acute anemia on CO2elimination and sought to improve on previous studies by measuring all variables influencing CO2 production, transport, and elimination, including Q˙,V˙co 2, , pH, and Vds/Vt. Use of anesthesia permitted control and stability of metabolic rate, temperature, and ventilation. Intravascular volume was maintained by performing isovolemic hemodilution with hetastarch to induce acute anemia, thus allowing the expected compensatory increase in Q˙ to occur.
Comparison with Previous Studies
Well over 100 studies of anemia have documented the critical role of increased Q˙ and O2 extraction that compensate for reduced blood O2-carrying capacity in vivo. In only about one-third were measurements of made, and the great majority either failed to measure or lacked explicit description regarding ventilation and V˙co 2, two critical determinants of blood . Those whole animal and human studies that made two or more consecutive hemodilutions to achieve >50% hemodilution found no change in blood values (10, 20, 32, 33, 35, 37,41, 45, 47-49) or a nonstatistically small 1–2 Torr fall (14,22, 27). Only three studies concurrently measured ,V˙co 2, and ventilation but lacked Q˙ measurements, since these were studies in rats. Bartlett and Tenney (4) studied unanesthetized rats hemodiluted with plasma and found that over a wide Hct range (25–45%) there were no changes in tissue (as measured in a subcutaneous gas pocket),V˙e, orV˙co 2. Djordjevich et al. (12) hemodiluted anesthetized, but spontaneously breathing, rats to Hct values of <10% using 7% albumin and found that decreased with anemia from 57.7 to 39.1 Torr and decreased from 67 to 47 Torr, but the venoarterial difference was unchanged. The reason for the marked drop in values in their study may have been a combined result of a nonstatistically significant increase in respiratory rate (80–87 breaths/min) and fall inV˙co 2 (from 18.9 to 16.4 ml ⋅ min−1 ⋅ 100 g−1). Matsuoka et al. (31) found that acute hemodilution with lactated Ringer to an Hct of 50–60% of baseline resulted in ∼20% decreases in both V˙co 2 andV˙o 2, with a concomitant 30% increase in V˙e. Despite these changes, decreased only 3 Torr, implying a possible impairment in CO2 transport, although was not measured. This protocol was complicated by use of lactated Ringer in a one-to-one exchange with blood, which may have decreased intravascular volume and limited the circulatory response, as suggested by the fall in arterial pressure. Interestingly, when studied again 3 days after hemodilution, the anemic rats had similar mean arterial pressures, heart rates, respiratory rates, V˙co 2,V˙o 2, and compared with a group of sham-hemodiluted rats.
Analysis of Factors Preventing CO2Retention with Anemia
The important factors yielding complete compensation for anemia in maintaining CO2 elimination include an increased Q˙ and obligatory greater O2 extraction engendered by anemia that generates a larger Haldane effect. Other factors that may play a role in compensation for anemia include increases in ventilation, changes in metabolism (V˙co 2), and microcirculatory changes.
Q˙. Although several compensations exist to ensure maintenance of normalV˙o 2 andV˙co 2 during acute isovolemic anemia, the most important is an increase in Q˙.Q˙ increases in anemia predominantly because of a fall in blood viscosity, which results in a reduction in peripheral vascular resistance (9). An increased Q˙ will permit greater CO2 transfer for the same CO2 driving gradients as long as capillary recruitment prevents a fall in capillary transit time, since CO2 equilibration between blood and tissue or alveolar gas requires almost the entire normal transit time of 0.5–1.0 s for completion (6, 24, 43). Q˙increased in our animals by ∼50% with a reduction in Hct of 66%, similar to the findings of other studies in this area referenced above (average Q˙ increase over the same Hct range was 40–70%). As expected, this increase was not sufficient to prevent a progressive increase in O2extraction with greater anemia and would not be sufficient to prevent CO2 retention in the absence of other compensations. When using the human gas-exchange model of Bidani (5), it would be necessary to increase Q˙ 170% for the same Hct reduction if no other compensations, including an increase in O2 extraction, are permitted (Fig.3).
O2 extraction and the Haldane effect.
The increase in Q˙ in anemia is insufficient to prevent greater O2 extraction by the tissues. This important factor largely helps to explain the lack of impairment in CO2 elimination in our model, since the Haldane effect, i.e., that amount of CO2 taken up or released by blood with a change in hemoglobin saturation at constant ,accounts for a large fraction (40–50%) of the total CO2 exchange with normal Hct and average and differences (16, 21, 25). Because greater changes in hemoglobin saturation occur during gas exchange in anemia, there will be greater linkage of CO2 transport with O2 exchange. An augmented Haldane effect in vivo counteracts the intrinsic flattening of the CO2 dissociation curve that occurs with anemia (2, 11, 18, 36, 44) and allows greater CO2 transfer across smaller gradients.
Whether anemia and greater differences in hemoglobin saturation per se increase the absolute Haldane coefficient has never been studied, although a theoretical treatment by Grønlund and Garby (17) predicts that the Haldane coefficient would be increased by 16 and 9%, respectively, over the Hct and the hemoglobin saturation changes of our study. Increased O2 extraction alone, however, is limited in preventing CO2 retention with anemia without the accompanying increase in Q˙, and even an of 100% will not prevent a small rise in the venoarterial difference (Fig.4). This limitation of O2 extraction is also suggested by the marked CO2 retention and widening of the venoarterial difference that accompanies a decrease in Q˙ despite large increases in O2 extraction (1).
V˙ co 2 and metabolism. Although our study showed no fall inV˙co 2 with progressive anemia, two previously mentioned studies did document such a fall (12, 31). In both, there was a marked reduction in O2 delivery, which likely resulted in a depression ofV˙o 2 and a linked reduction in V˙co 2. We also observed a definite fall inV˙o 2 with the last hemodilution to a Hct of 12% but no change inV˙co 2. Without blood and tissue lactate measurements or more sophisticated measurement of tissue metabolism (nuclear magnetic resonance or near-infrared spectrocopy), we can only reasonably speculate that at the lowest Hct values an obligatory anaerobic lactic acidosis developed, as suggested by the declining pH at constant (Table2). Although it is possible that anemia could be compensated in part by a reduction in metabolism andV˙co 2, either by a parallel reduction in V˙o 2 or respiratory quotient, our study and others (50) establish that this is rare and may only occur with the most severe degree of anemia. It is conceivable that anesthesia may have modified the metabolic response to anemia in our study; however, Matsuoka et al. (31) found that metabolic rate was not depressed in anemic unanesthetized rats 3 days after hemodilution, arguing against a confounding effect of anesthesia.
Ventilation. Although hyperventilation might present a potent compensation to anemia, our data and those of Bartlett and Tenney (4), and, indirectly, those of Matsuoka et al. (31), demonstrate that hyperventilation is neither necessary nor evoked if hypovolemia and hypotension are avoided. The lack of hyperventilation with anemia is likely the effect of increasedQ˙ and O2extraction, which prevent any arterial hypercapnia and tissue CO2 retention from developing and which would stimulate peripheral or central chemoreceptors. Another factor locally acting to prevent CO2 retention in the central nervous system and any subsequent ventilatory response is the proportionately greater increase with anemia in blood flow to the brain than in the rest of the body, with the exception of the heart (50). These findings help to explain the lack of hyperventilation in anemia and any effect of anemia on ventilation and the hypercapnic ventilatory response (3, 19, 38) or the ventilatory response to exercise (28, 42). Indeed, Bartlett and Tenney (3) raise the interesting point that a hyperventilatory response to anemia would be ultimately counterproductive in that any slight increase in in the normoxic range would minimally affect O2 content, but that the ensuing respiratory alkalosis would hinder O2 unloading in the tissues.
Tissue and pulmonary gas-exchange efficiency. The question of whether tissue and pulmonary gas-exchange efficiency might improve with anemia has not been investigated to any extent. Improved gas-exchange efficiency could result simply from increases in Q˙and/or reduced viscosity acting to improve the distribution of perfusion through capillary recruitment or by reducing the intraorgan perfusion distribution heterogeneity (26, 30). In the tissues, these factors would improve local perfusion metabolism matching and in the lung would improve ventilation-perfusion matching.
Although the effect of anemia onV˙a/Q˙relationships has never been studied, both lower (50–75% reductions) and greater (100–300% increases) blood flows have been shown to cause moreV˙a/Q˙heterogeneity (13, 34). Neither study examined changes in Hct, and, in the case of increased perfusion, the complicating factor of pulmonary artery hypertension may have offset any potential benefit of increased flow per se, since lobe wet-to-dry weight ratios increased as well. The increases in Q˙ with anemia in the present study were considerably smaller than those studied by Domino et al. (13), and, in contrast, right ventricular pressures (as a marker of pulmonary artery pressure) did not rise. However, using the Bohr Vds/Vtas a crude index ofV˙a/Q˙mismatch and alveolar ventilation, we could show no improvement with anemia (in fact, alveolar ventilation decreased at the most severe degree of hemodilution). Direct studies with the multiple inert-gas-elimination technique and microsphere distributions will be necessary to address this hypothesis and could be complicated by associated changes in Q˙.
Several other effects of hemodilution at the microcirculatory level, not measurable by our traditional systemic analysis, could also act to improve gas exchange and mitigate the negative consequences of a reduced O2- and CO2-carrying capacity of anemia. First, faster flows in the microcirculation with anemia reduce the degree of precapillary diffusive O2 loss (26), and, in an analogous sense, this could also reduce an equivalent precapillary diffusive CO2 retention. Second, hemodilution reduces the normal two- to threefold difference between capillary and large-vessel Hct (26, 29, 39, 50) and the heterogeneity of Hct distribution in the capillary vasculature (26, 30). In vitro, King and Mazal (23) have shown that unevenness of Hct values leads to greater arteriovenous differences for CO2 and O2 when blood undergoes gas exchange than when bloods of equal Hct are mixed.
In conclusion, we have shown that CO2 elimination is well preserved in anemia, as long as compensatory responses (mainly an increase in Q˙ and attendant O2 extraction) are mobilized. A mathematical model incorporating our experimental hemodynamic and respiratory data predicts blood CO2 values comparable to those measured. Interestingly, our experimental data and modeling do not measure and incorporate potentially important effects of anemia in the microcirculation, which could theoretically mitigate the detrimental consequences of anemia. Whether these microcirculatory changes play a role in CO2 homeostasis during anemia, particularly when other systemic compensations are limited, is uncertain. In addition, the capacity of the organism to maintain CO2 homeostasis during anemia in the presence of cardiovascular and/or respiratory disease requires further investigation.
This project was supported by grants from the American Heart Association–Washington Affiliate (95-WA-503 to S. Deem) and the National Heart, Lung, and Blood Institute (2R01-HL-45571 to E.R. Swenson).
Address for reprint requests: S. Deem, Univ. of Washington, Dept. of Anesthesiology, Box 356540, Seattle, WA 98195-6540.
- Copyright © 1997 the American Physiological Society


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Photos: Eddie Mathews' 1958 Topps baseball card, front and back, from my collection
Okay, so we'll start off the revamped site with one of my favorite HOF players nobody remembers. I'll start off with him because I've always tried to Remember James (he was Jesus's brother), which is what I call an attempt to purposely remember someone or something who everyone else has forgotten. (It's the title of one of my WIPs, too.) I'm also starting off with this exact card because it was one of the three awesome ones my better half gave me for Christmas. (She also gave me Sox/Rangers tix, too!) I thought it'd be nice to start it off with one of the three she gave me, rather than the one of the several thousands I owned beforehand.
The Card
The card is in very good shape. Well, it's PSA-graded very good to excellent, but you know what I mean. The corners are sharp; the front and back are clean. The picture is still a little glossy. The only blemish, really, is the truly bad cut of the card: it's very off-center. Since this card is not for sale, that doesn't matter as much to me. (My better half bought it for me because she liked the blue backdrop and white stars.) It's got a great aesthetics look, and it looks great in the case--and it has nice sentimental value. The back has a grid layout with his 1957 stats for the season, and against each team in his division. It doesn't have his career totals. (This is odd for any Topps card.) The grid on the back was a Topps staple, in one form or another, throughout the 50s and up until 1960. Topps cards throughout the 50s looked great. The card number is in the upper left in a star, and the blurb is written by the editors of Sport Magazine--as it says. The copywriter pre-dated Bill James by a few years when he made it a point to notice that Mathews hit many more homers on the road than he did at home. His 30 road homers (out of 47) was a Major League record. I'll bet that his home ballpark cost him quite a few homers in his career--and he still managed to hit 512!
Nobody remembers Eddie Mathews today because he played on the same team, for a great many years, as Hank Aaron. Though Aaron was clearly the better player, it wasn't always very clear that he would be. A quick glance at the opening day lineup in 1957, when the Braves won the World Series, showed that Aaron batted second (?!) and Mathews third. Joe Adcock, a power-hitting first basemen, hit cleanup, if you're wondering. You should be, because though Adcock was a good player, he wasn't Mathews or Aaron, and the fifth-place hitter was Bobby Thomson, whose name you should know. He hit the Homer Heard 'Round the World, which was a big deal because he normally did not hit homers or drive in runs--which Mathews and Aaron did, prodigiously. For those who don't know, the 1st and 2nd place hitters in a lineup are supposed to get on base so that the 3rd, 4th and 5th hitters can drive them in. Hank Aaron should not hit second--ever. That's a waste of his resources--which were among the best ever, as were Mathews, on a lesser level. Mathews was Aaron lite, you might say. You want a line-drive, walking, taking pitches guy hitting second, not Hank Aaron. Though Dustin Pedroia can drive in runs hitting 4th, it is very rare to have a contact hitter who is valuable hitting 2nd and 4th--and I'll bet Pedroia has more value for his team overall hitting 2nd. Aaron wouldn't.
Why all this? Because if you look at Mathews stats, for 1957 and for his career (which you should here, his stats page at baseball-reference.com--my source for all stats unless stated otherwise in the text), you'll see that he didn't drive in as many runs as he should've. You would think that on Opening Day of a World Series winning year, the manager would put his best hitting lineup out there, barring injury. The manager thought, for some reason, that Aaron should hit second, and Mathews third. (I'd put Aaron third, Mathews fourth and Adcock, or whoever, fifth. Aaron hits third because his average is a lot better than Mathews', with equal or far greater power production, so you'd want him to bat more often, on average.) If the lineup was jockeyed like this, this would be one reason why Mathews didn't drive in as many runs as he should have--even with Aaron still hitting in front of him. (Aaron hitting 2nd makes even less sense when you consider that the pitcher hits, so Aaron has the 9th and 1st place batters hitting in front of him, which drastically reduces his chances to drive in runs.) Mathews did have some monster years--135 RBIs one year, 114 another--but he drove in over 100 just five times, which is a low number considering that he batted on the same team as Hank Aaron for a long time. They had good supplementary hitters, too, like Bobby Thomson, Joe Adcock and Wes Covington, and so on. The point is, someone hitting with these guys is expected to drive in a lot of runs. Mathews did--1,453 of them--but with 512 homers, and hitting with those guys just mentioned, that isn't a ton. He had a lot of years with 80-95 RBIs, hitting with Aaron and Thompson, and I'd need more time to research why. He'd hit over .300 one year, then .260 the next, with medium to high walk totals and low strikeout totals (for a homerun hitter). Oddly, he scored over 100 runs frequently, but with totals between 100 and 109. You'd expect someone hitting with these guys, who walks a lot (and consistently among the league-leaders in on-base percentage), to score more runs than that. He hit .265, .263 and .233 for three straight years, with decent power and OBP numbers, then had a very good year for power (32/95) but with a bad batting average and OBP. Then his skills eroded.
He still had enough in the tank to win a World Series with the Tigers in 1968 (if you knew that, go to the head of the class), after appearances with the Braves, against the Yanks, in 1957 and 1958. He was considered the National League's best third baseman before Mike Schmidt came along, and he was elected to the Hall on his fifth try in the late 70s. (You wonder why the best power-hitting third baseman in baseball history before Schmidt would need multiple tries to get into the Hall.) He died of a pnuemonia-related illness in 2001.
In short, as great as he was, Mathews wasn't able to put it all together and have many consecutive monster years, and he fell off the grid after 1966. He played 17 total seasons, but only about five great ones, and maybe six or seven good or above-average ones. Hitting on a good hitting team with great pitching (Warren Spahn won the opening game of '57), he could've, and should've, done better. The lineups didn't help; the home ballparks hurt him; and I suspect a lingering injury or succession of injuries that he just played through.
P.S.--He was thought a very handsome guy. He was sort of quiet, but a fiery and intense competitor when the time called (not all the time, like Brett), and, despite some heavy drinking, was well-liked and well-respected.


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Pune, India (PressExposure) May 30, 2014 -- A remarkable marvel in the historical backdrop of Bharat in the twentieth century is the conception and endless development of Rashtriy Swayansevak Sangh (RSS). The Sangh's effective reach has been spreading far and wide like the brilliance of a numerous splendored precious stone. Sangh enlivened establishments and developments today structure a solid vicinity in every field of patriot attempt. To know more about RSS, the largest and the most influential organization in India tune into Reportaaz "Sangh Parivar"a special show on RSS only on IBN-Lokmat at 11:30 am on Sunday 1st May, 2014.
Rashtriya Swayamsevak Sangh (RSS) likewise called Rashtriya Seva Sangh association established in 1925 by Keshav Baliram Hedgewar, as a feature of the development against British guideline and as a reaction to revolting between Hindus and Muslim. Hedgewar formed the RSS as a disciplined cadre consisting mostly of upper-caste Brahmins who were dedicated to independence and the protection of Hindu political, cultural, and religious interests. The RSS presents itself as a cultural, not a political, organization that nevertheless advocates a Hindu nationalistic agenda under the banner of hindutva, or "Hindu-ness." The group is structured hierarchically under the guidance of a national leader, while regional leaders are charged with overseeing the local branches. Paramilitary training and daily exercise and drills are part of this discipline. RSS has political wing known as Bhartiya Janata Party, other wings are - Vanvasi Kalyan Ashram, Vishv Hindu Parishad, AkhilBhartiy Vidyarthi Parishad, Rashtrsevikasamiti, Majdursangh, sansakrbharti and many more. Our newly elected Prime Minister Narendra Modi was a tower of strength and a very influential Sangh Pracharak of RSS in the 90s.
Communicated in the most straightforward terms, the target of the Sangh is to convey the country to the zenith of grandness, through arranging the whole public opinion and guaranteeing security of Hindu Dharma. Having recognized this objective, the Sangh made a strategy for work in consonance with that ideal. Decades of working has affirmed that this is the best method for sorting out the society.The RSS has historically played a major role in the Hindu nationalist movement. Some of the major political leaders of India's Bharatiya JanatÄ Party were or still are members of the RSS.
Tune into Reportaaz "Sangh Parivar" a special show on RSS which will capture the significance of national volunteer organization RSS only on IBN-Lokmat at 11:30 am on Sunday 1st May, 2014.


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Dr. Dan Livingstone has had a not so secret crush on Yorkshire lass Caryn Fielding since she started working at the shelter. Taking his courage in both hands, he asks her out on a date. To his delight, she agrees.
As a retired midwife, Caryn has had to deal with heartbreak on a grand scale. Shutting herself off from the rest of the world brought her to volunteer at the shelter; Caryn finds a measure of comfort as she cares for the cats and kittens there. Could dating Dan lead to disaster?
As their relationship deepens, Caryn's secrets and anxieties are revealed. Falling in love is never without its ups and downs; but together love really can conquer all, no matter how old you are.
©2015 Books To Go Now (P)2015 Books To Go Now
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"Hey, like, Liet, wake up," Poland said as he set the breakfast tray on the nightstand next to Lithuania's bed.
"Rats," Lithuania mumbled, turning over in his sleep.
"Seriously, Liet, you don't even look cute when you're freaking asleep. You got your mouth, like, open and you're, like, drooling and stuff. It's totally disgusting. Get up!" Poland demanded as he sat down on the bed Lithuania was sleeping on.
"I…never…wanted…to…go," Lithuania mumbled, turning over in his sleep again.
"Liet! Get the crap up! You're, like, getting drool everywhere," Poland demanded, putting his hands on Lithuania's shoulders.
"Rats…are…everywhere," Lithuania mumbled in his sleep as Poland began shaking him by the shoulders.
"Why are you, like, so unresponsive? Get up! Sleep time is, like, over," Poland said as he continued shaking Lithuania by the shoulders.
"Rodents…health violation," Lithuania mumbled, still in deep sleep, as Poland continued shaking him.
"OMG! How are you, like, still asleep? Get the crap up already," Poland said, letting go of Lithuania's shoulders.
"I…never…wanted... rodents," Lithuania said in his sleep.
"You're really not cute when you're sleeping," Poland said, standing up from the bed.
"Darkness…rodents…rats…locked doors," Lithuania said, turning in his sleep.
"Maybe I should, like, get like a bucket of water," Poland said as he put his hands on his hips. "Water is, like, cold and stuff so that might, like, be able to, like, wake you."
"Locked…doors…locked…windows…rodents," Lithuania mumbled, too deep in sleep to hear Poland's threats of dumping cold water on him.
"Well, I'm going to, like, get some, like, really cold water and stuff," Poland said as he began walking towards the door. "If you, like, get up, like, now I won't have to, like, dump water on you."
"Poland…don't…ever…take…me," Lithuania mumbled, still too deep in sleep hear the threat of cold water.
"Are you, like, dreaming about me?" Poland asked, suddenly interesting about what Lithuania was mumbling about. "That's, like, so romantic and stuff!"
"I…really…don't…like…rats…Poland," Lithuania mumbled as Poland sat back down on the bed.
"This is so cute, totally! Maybe you are kinda adorable in your sleep," Poland cheered, obviously not listening to everything Lithuania was saying in his sleep.
"This is so, like, totally adorable! You're, like, dreaming of me! I love it!"
"Adorable! So freaking cute! Now you, like, want me to, like, save you. You're, like, so freaking cute in your sleep, Liet."
"Poland…rodents…I…don't like…it," Lithuania mumbled, turning over in his sleep again.
"OMG! You, like, said my name again! This is, like, so totally cute and stuff," Poland cheered while Lithuania continued stirring around in his sleep.
"Flat tire…keys…locked…in…car…rodents…everywhere."
"What you're, like, mumbling now is, like, so totally boring. Say, like, my name again," Poland said, beginning to lose some interest in Lithuania's sleep talk.
"Flat tire…health violation…rats…giant rats."
"Okay, this is, like, getting boring. Say my name again, or, like, wake up," Poland said, not really realizing that Lithuania can't hear the choice in his sleep.
"Rodents are…my…least…favorite…vegetable," Lithuania said in his sleep as Poland stood up from sitting on the bed.
"You are, like, so not cute in your sleep anymore. Either be adorable and say, like, my name in your sleep again or wake up," Poland said, putting his hands on his hips again.
"Poland…rats…are…everywhere," Lithuania mumbled bringing back Poland's interest.
"Like, yay! You said my name! Do it again!" Poland cheered, clapping his hands while jumping up and down.
"Poland…I…want…Belarus…save me…Belarus."
"Did you just, like, say that fugly slut's name?" Poland asked as he stopped jumping up and down and clapping in response to suddenly losing interest.
"Belarus…thanks," Lithuania said in his sleep not tossing and turning this time. Perhaps his dream stopped being a nightmare.
"Like, what the freaking hell, Liet! You are so, like, totally not cute in, like, your sleep!" Poland screamed, spinning around to leave the bedroom. "Like, I'm so going to dump water on, like, your face. And it's going to, like, be freezing cold water!"
"I…love…you…Belarus," Lithuania mumbled in sleep as Poland slammed the bedroom door open.
"It's going to be, like, freezing cold water!" Poland yelled leaving the bedroom.
"Sure…I'll…love…to shop…at Target…with you…Belarus," Lithuania said in his deep sleep. What the hell is Lithuania dreaming about anyway?
After a few more minutes of Lithuania mumbling stupid things about Belarus and kittens in his sleep, Poland finally came back with a bucket of cold water.
"Okay, Liet, I really don't want to, like, do this. So, I'm going to give you, like, one more chance to wake up on, like, your own," Poland said holding the bucket of cold water over Lithuania's head.
"Belarus…you…are…so beautiful."
"OMG! Belarus is, like, not hot!" Poland cried as he dumped the bucket of cold water on Lithuania.
"What happened? Why am I wet? I was having such a good dream. What happened?" Lithuania asked sitting up now awake.
"I, like, totally saved you from a nightmare about a fugly slut," Poland said, setting the bucket down on the ground.
"What?" Lithuania asked pushing the wet blankets off his body.
"You, like, really shouldn't, like, talk in your sleep," Poland stated.
"Oh," Lithuania said embarrassed.
"Like, yeah. Promise me that I, like, won't have to ever, like, dump water on you when you're, like, sleeping again."
"Huh?" Lithuania asked, standing up from the wet bed.
"Like, totally promise me that you won't have dreams about that fugly slut again," Poland demanded, picking up the breakfast tray he put on the nightstand earlier.
"Okay, I promise you that I wouldn't have dreams about 'that fugly slut' again," Lithuania promised, hoping that Belarus wasn't what Poland was calling a "fugly slut".
"Great!" Poland cheered pleased. "I, like, made you like breakfast, but I think it might be, like, cold now, cause it, like, took me a long time to, like, wake you up."
"Well, I guess that you can't, like, have it, like, in bed since the bed is all, like, wet now. So, I guess that you'll have to, like, eat it in the kitchen or, like, living room or something," Poland said turning around to leave the bedroom.
"Oh, Poland, before you go, can you promise me something?" Lithuania asked stopping Poland from leaving the room.
"Depends on what it, like, is."
"Promise me that you won't ever lock your keys in your vehicle," Lithuania said, remembering his horrible nightmare before it turned into a good dream.
"Like, why would I, like, do something stupid like that?" Poland asked, opening the door to leave the bedroom.
"I don't know. Just promise me that you won't ever lock your keys in the car."
"If I promise you that, will you, like, come eat this, like, totally fabulous breakfast I made you?'
"Then I, like, totally promise you that I, like, wouldn't ever, like, lock my keys in, like, my car," Poland promised.
The End! So, I'm not sure why it took me so long to write the ending. But hey I finished. The ending could have been better, but whatever.
Anyway, special thanks to my beyond fabulous beta reader, Oxenstierna D. Yuki-Rin. Seriously, people I never meant, go read her epic stories. I recommend her Gatsby Parody. I like it more then I care to admit.
Remember, kids, don't lock your keys in your car, or we WILL find you. JK


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Today, Congressman Kevin Cramer released the statement following his vote in support for H.R. 444, the Require a Plan Act. H.R. 444 requires the President to submit a supplemental budget by April 1, 2013 in the event that the President's initial 2014 budget submission does not achieve balance within a fiscal year covered by the initial budget.
"Every American family knows first-hand what it is like to live on a budget. Times may be tough, but we work hard, we save, we make sacrifices and we live within our means. The Senate has not passed a budget in four years and yesterday marked the fourth time in five years the President failed to deliver a budget to Congress. President Obama and his administration must lead by example in efforts to restore economic prosperity back into American households. House Republicans are committed to getting Washington spending under control, which is why I voted for the "Require a PLAN Act," to require the president explain to the American people how he intends to balance the budget. A balanced budget matters to senior citizens who rely on the benefits they earn, the middle-class Americans struggling to make ends meet and to our children whose future is in jeopardy from the out of control spending in Washington."
Source: http://cramer.house.gov/media-center/press-releases/congressman-kevin-cramer-r-nd-statement-on-his-vote-for-hr-444-the


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When: Fri., May 3, 8 p.m. 2013
For over 30 years, the OCC has heralded the return of spring with performances that combine music, spoken word… and the occasional tap-dancing dog or fish-puppet extravaganza. The OCC's 2013 spring concert series, "Heaven and Earth," continues that tradition with new and OCC-original music, both earthy and celestial. "Heaven and Earth" marks the end of an era, as Sarah Saulsbury, director for the past four years and OCC member since 1979, will be stepping down at the end of this season.
Price: $15 general; $12 seniors; kids 12 and under free


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A number of experienced insurers might well take this stance: "Why do I need a mediator to tell me how to settle my case?"
So, the simple answer is most personal injury cases do not need a mediator, as most settle without the need for a neutral's assistance. Experienced lawyers and claims handlers on both sides of the fence know their cases, and generally speaking get on with negotiating settlement when that is needed. Joint Settlement Meetings tend to work pretty well in the larger cases
That still leaves a small number of "hard nut" cases, where you would rather not go to court if you can avoid doing so, and you just cannot find a route to settlement. It may be that the other side are simply intransigent. It could well be that the Claimant doesn't listen to the advice being given, or that the lawyer isn't on top of the case. It could be that the nature of the claim means that one party finds it difficult to be objective: for example, fatalities, psychiatric injuries, chronic pain. A mediator can certainly help in some of those cases.
It is also worth considering whether there might be other reasons why mediation will prove useful. If nothing else, legal representatives need to understand the defensive reasons for considering mediation. Your client could be penalised in costs for not engaging in mediation, and Judges are beginning to flex their judicial muscles and do just that. The last year has seen a number of cases where the courts have demonstrated a willingness to penalise a party who unreasonably refuses mediation, and that includes ignoring an offer of mediation.
The Background on Refusal to Mediate and Costs Penalties
The authorities go as far back as Hurst v Leeming in 2001, but it's useful to start with the Court of Appeal guidance given in Halsey v Milton Keynes NHS Trust and the associated case of Steel v Joy & another in 2004. The guidance can be summed up as follows:
- Most cases are suitable for mediation;
- Parties may need encouragement to use mediation;
- If a party unreasonably refuses mediation, it can be penalised in costs;
- BUT the burden of showing unreasonableness lies with the party offering mediation.
- The court gave some reasons for refusal to mediate. This included reasonably believing you have a very strong case, mediation costs being disproportionate, and whether mediation has a reasonable prospect of success.
For some time, it was perceived that it was difficult to persuade a Judge that a party refusing mediation was acting unreasonably. A number of factors however demonstrate that courts are increasingly willing to make an adverse costs order against a party who refuses mediation. Firstly, Lord Justice Jackson, in his Review of Civil Litigation Costs, re- emphasised the underutilisation of ADR. He recommended that there be a central text on ADR, and we now have the "Jackson ADR Handbook", which is finding its way into an increasing number of judgments.
Last year's Cases
A number of cases decided in the last year or so demonstrate that there is now a real risk of a court imposing significant costs penalties on parties who refuse (or ignore) mediation.
- PGF II SA v OMFS Co. 1 Ltd: not a personal injury case, but it needs to be heeded by all involved in litigation. The Claimant accepted a Part 36 offer nearly a year after it was made, a day before trial. In that time, the parties had amassed £250,000 of costs between them. Despite the Part 36 rules which gave the Defendant an apparent entitlement to costs after 21 days from the Part 36 offer, the court decided to make no order for costs for that period. This was because the Defendant totally ignored the Claimant's offer to mediate. The court found that ignorance amounted to refusal and was unreasonable. The Court of Appeal upheld the decision, quoting the Jackson ADR Handbook.
- Mark Lynn v Borneos LLP T/A Borneo Linnels: this is an unreported High Court decision in a professional indemnity case. The Defendant succeeded, but the Claimant successfully argued that the Defendant had unreasonably refused to mediate. The Judge referred to "bland refusal…" to mediate. The Defendant was awarded only 60% of its costs.
- Garritt–Critchley & Others v Ronnan Solarpower PV Ltd: the Defendant accepted the Claimant's Part 36 offer after trial but before judgment had been delivered. The judge awarded indemnity costs against the Defendant, who tried to rely upon a number of the reasons set out in the Halsey decision to justify refusal of mediation. The Judge was unimpressed.
- Northrop Grumman Mission Systems Europe Ltd v BAE Systems: the Defendant won on liability issues (the dispute being entitlement to terminate a licensing agreement), and the court accepted that the Defendant reasonably considered that it had a strong case. Unlike the court in Halsey, the Judge however found that it was unreasonable to refuse mediation. In the end, the Defendant was not penalised in costs because the court took account of refusal by the Claimant of a without prejudice save as to costs offer, but a resounding warning comes out of the judgment. Even when you think you have a strong case, it may be unreasonable to refuse to mediate.
How does that affect Personal injury Claims?
The writing is firmly "on the wall". Halsey set the scene: the decision involved a personal injury claim and a clinical negligence claim. The principles in the recent cases quite clearly apply to personal injury cases.
If a party reasonably thinks it has a very strong case, what merit you might ask is there in sitting down with your opponent? It might sound fanciful, but sometimes people can be persuaded to withdraw a case. I have seen this happen in 2 cases, the first involving a litigant in person suing a police force for malicious prosecution, assault (and much more: he started by demanding £500,000 and by the end of the mediation discontinued his claim). The other involved a suspect looking RTA claim, with some suspicion of fraud.
The Claimant dropped hands at the end of a 4 hour mediation. Impossible is nothing, as Adidas once said (after Greece won the European football championships for those with no footballing experience!).
Litigants and their advisors need to have a strategy to deal with offers of mediation. Refusal creates a real risk of a costs penalty.
What about Cost-Benefit?
In the last month, the government has announced proposals to massively increase court fees. For disputes over £10,000 a 5% court fee is proposed, so a £50,000 claim could in the future face a court fee – payable up front – of £2,500. Claimant lawyers will be seriously thinking about cash flow for these claims. Defendants' insurers and Defendants footing the bill themselves may wonder if this means that less claims will be issued, but if they are and they succeed, Defendants and insurers foot the bill, so it will have to impact on thinking on the Defence side of the fence also.
How much does a mediation cost then?
A 4 hour mediation will cost about £1,650 between the parties. It used to be thought that tricky cases needed much longer than 4 hours, but recent experience shows that all except the most difficult cases can be mediated within that timeframe.
VAT is payable in addition usually, but the proposed hike in court fees makes the cost of a mediation look more attractive. It may be that we see an increase in pre litigation mediation in due course. Are there any other benefits to mediation? Obviously, in some cases an apology is a very powerful tool, and that can be done in an effective way across the mediation table. Sometimes ingenious solutions can be thought through, although it is fair to say that most personal injury claims centre around how much money is going to change hands.
Seeing your opponent in the flesh can be useful in deciding whether you really want to put the case before a Judge. It may be that the Claimant comes across in a far more sympathetic manner than you expected, and you need to review your risk assessment and perhaps offer more than you thought would be needed to settle. It may be that you learn something about the other side's case that either strengthens or weakens your own position: without that exchange, you might not have found it out until much later when significantly more legal costs had been incurred.
Whether you remain sceptical of the benefits of mediation in personal injury cases, the stark reality is that the courts are beginning to demonstrate that if parties do not engage in mediation, they will be punished with costs sanctions. Soaring court fees and delays in the court system – which seem to get worse not better – also cry out for alternatives to putting a case before a Judge except in a very small number of cases. The message is clear: ignore mediation at your peril, and if nothing else, consider your strategic position when an opponent makes a reasoned offer of mediation. How do you avoid being hit in the pocket on costs?


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MOVIE SYNOPSIS [ General Audiences ] With an impeccable performance of Brian Blackwell, this film directed by Darla Rae was premiered in cinema in 2008. The film "Dandy Kids Documentary" had an original production of USA. You can watch Dandy Kids Documentary online on TV cable or theaters with original audio in English at different dates. This film premiered in theaters in 2008.
Rating: 5 by 49 users./
Runtime: 85 minutes
Brian Blackwell, Benjamin Carson Sr., Eric Cole, Bill Dobyns, Kathy Millens, Darla Rae, Hunter Schultz, Chris Van Hollen and Heather Wilson.
85-minute film (full movie) directed by Darla Rae.
The original audio of Dandy Kids Documentary has dialogues in Dolby Digital, it was produced in USA.
It premiered in cinemas or television in 2008.
Screenplay written by Darla Rae and Karen Hemmerle.
Darla Rae and Zeke Hanson.
Zeke Hanson, Darla Rae, MaryLee Herrmann, Karen Hemmerle and Kathy Shipp.
This film was produced and / or financed by Film It Productions.
Composed by Laura Dodd.
Film It Productions.
Without commercial breaks, the full movie Dandy Kids Documentary has a duration of 85 minutes; the official trailer can be watched in streaming on the Internet. You can watch this full movie free in EnglishDolby Digital in movie TV channels, renting the DVD or with VoD services (Video On Demand player, Hulu) and PPV (Pay Per View, Netflix).
See the page of this full movie, Dandy Kids Documentary in FULLTV Movies.


text:
|Publication number
|Publication type
|Application number
|Publication date
|Apr 14, 2009
|Filing date
|Sep 14, 2007
|Priority date
|Apr 23, 2002
|Fee status
|Also published as
|Publication number
|Mary M. Morris, Duane G. Frion, Jeff Novotny, Douglas Hankner, Stuart Lahtinen
|Original Assignee
|Medtronic, Inc.
|Export Citation
|BiBTeX, EndNote, RefMan
|Patent Citations (60), Referenced by (5), Classifications (19), Legal Events (2)
|External Links: USPTO, USPTO Assignment, Espacenet
This application is a division of U.S. patent application Ser. No. 11/017,336, filed Dec. 20, 2004 (currently allowed), which is a continuation of U.S. patent application Ser. No. 10/128,708, filed Apr. 23, 2002, now U.S. Pat. No. 7,090,661, issued Aug. 15, 2006, the entire contents of both are hereby incorporated herein by reference. Priority is claimed to both referenced applications.
This application relates generally to implantable catheters, and more particularly to an anchor and method of use for mounting a catheter within a patient, for example, to the skull.
Sometimes therapeutic substances, such as drugs, biologics, etc., are infused intraparenchymally or intracerebroventricularly to treat brain disorders, such as malignancies or neurodegenerative diseases. Co-assigned U.S. patent application Ser. No. 09/540,444, filed Mar. 31, 2000 (now U.S. Pat. No. 6,551,290), and U.S. patent application Ser. No. 09/625,751, filed Jul. 26, 2000, now U.S. Pat. No. 6,945,969, issued Sep. 20, 2005 (both incorporated herein by reference) disclose catheters that are particularly well suited for intraparenchymal or intraventricular convection-enhanced infusion of therapeutic substances. As used herein, "IPA" means intraparenchymal, "ICV" means intracerebroventricular, and "intraventricular" and "ventricles" refer to cerebroventricles.
Previously, intracranial catheters have been anchored to the periosteum, which is a fibrous membrane covering the surface of bone. The periosteum has not provided as much stability as desired, and movement of the catheter anchor may result in changes in the location of the catheter tip.
Embodiments of this invention include a catheter system for intracranial delivery, such as intraparenchymal or ventricular delivery, of therapeutic substances to a patient. Embodiments of this system are adapted to anchor a flexible catheter in position relative to the skull for infusion of therapeutic substances, while allowing the anchor to be soft and pliable and thereby less likely to cause skin erosion. These embodiments are further adapted to be anchored to the skull bone rather than fragile periostium.
In a first embodiment, the catheter system generally comprises an elongate catheter (e.g., formed of silicone or polyurethane) having a lumen and at least one drug delivery orifice in fluid communication with the lumen, and an anchor formed of generally flexible, elastomeric material for mounting the catheter to the outer surface of the skull of the patient. The anchor has a through hole for receiving the catheter, and a channel extending substantially from the through hole. A portion of the catheter may be inserted into the channel to retain the portion substantially parallel to the surface of the skull. At least one flange is provided for engaging the outer surface of the skull. At least one substantially rigid standoff is mounted in the flange, with the standoff having an opening for receiving a fastener to fasten the anchor to the skull.
Most preferably, the anchor is adapted to flex and comply with adjacent tissue. For example, the generally flexible, elastomeric material of the anchor may comprise silicone.
Preferably, two flanges are provided on the anchor, with at least one standoff mounted in each flange. For example, the standoffs may be insert molded in the flanges of the anchor. The standoffs may be formed of titanium or titanium alloy. The standoffs are preferably substantially annular and have an undercut or circumferential channel helping to retain the standoff in the flange.
Also, preferably, the anchor has a body in which the through hole and channel are formed, with the body being generally elongate and coaxial with the channel. The body extends in a direction generally perpendicular to the through hole and openings of the standoffs, and the flanges extending substantially in opposite directions substantially perpendicular to the body. The channel is substantially perpendicular to the through hole.
In certain embodiments of the invention, an anchor clip is also provided, which is adapted to be fastened to the outer surface of the skull to stabilize the catheter relative to the skull. The anchor clip engages the body of the anchor adjacent the through hole. For example, the anchor clip may be generally V-shaped having two legs each having a free end and a joined end joined with the other leg. The free end of each leg has an opening for receiving a fastener to mount the anchor clip to the skull. The anchor clip also having a slot adjacent the joined ends of the legs for engagement with the anchor to stabilize the anchor.
The catheter system is preferably used in combination with an implantable therapeutic substance infusion device, such as an implantable drug pump. The catheter may be directly or indirectly connected with the implantable therapeutic substance infusion device for infusion of therapeutic substance from the implantable therapeutic substance infusion device through the lumen and orifice(s) of the catheter. Indirect connection includes without limitation intermediate connectors or tubing sections.
In another aspect of the invention, a method of implanting the catheter system comprises: (a) inserting the catheter into the parenchyma or a ventricle; (b) mounting the anchor on the catheter and the skull of a patient to retain the catheter in position; and (c) infusing a therapeutic agent into the parenchyma or a ventricle for treatment of brain tissue.
Preferably, the anchor is mounted on the catheter and the skull of a patient to retain the catheter in position by: (a) inserting the catheter into the through hole of the anchor; (b) sliding the anchor along the catheter into engagement with the skull; (c) inserting a fastener through each opening of the standoff to fasten the anchor to the skull; and (d) placing the anchor in the channel. The catheter may also be sutured in the channel.
A catheter system 30 of the invention is shown in
A preferred catheter 34 for use in the catheter system is the catheter disclosed in U.S. patent application Ser. No. 09/625,751, filed Jul. 26, 2000, now U.S. Pat. No. 6,945,969, issued Sep. 20, 2005, which is incorporated herein by reference.
As illustrated in
A through hole 48 is provided adjacent the proximal end of the body 40 of the anchor 34. The catheter 32 may be inserted into, and the anchor 34 slide along the catheter 32, to position the anchor 34 against the skull. Alternatively, the anchor 34 may be positioned adjacent the burr hole and the catheter 32 slide through the through hole 48 of the anchor 34 into position. In yet another alternative, the anchor 34 may be designed, for example, by the addition of a slit (not shown) to allow the anchor 34 to be attached to the catheter 32 in the lateral or radial direction rather than, or in addition to, being slide longitudinally relative to the catheter 32.
The through hole 48 and channel 42 are substantially oriented at right angles to one another. The longitudinal channel 42 and through hole 48 are connected so that the catheter 32 can be bent at about a right angle to be held in the channel 42 in an orientation generally parallel or tangent to the surface of the skull.
At least one flange or tab, but preferably two flanges 50 extend in generally opposite directions from the body 40. The flanges 50 are integrally molded as one continuous piece with the body 40. The flanges 50 are set back from the proximal end of the body 40 (i.e. the end with the through hole 48) so that the flanges 50 may rest on bone adjacent a burr hole (see, e.g.,
At least one generally rigid standoff 52 is provided on each flange 50 as illustrated in
The through hole 48 constitutes one preferred embodiment of an orienting means for slidably receiving the catheter and orienting the catheter relative to the parenchyma. The longitudinally-extending, catheter-receiving channel 42 constitutes one preferred embodiment of a means, generally adjacent the orienting means, for laterally receiving the catheter to retain a portion of the catheter substantially parallel to the surface of the skull.
The flanges 50 constitute a preferred embodiment of a generally flexible skull-engaging means for engaging the outer surface of the skull. The standoffs 52 constitute a preferred embodiment of a substantially rigid means in the skull engaging means for receiving a fastener to fasten the anchor to the skull.
An optional anchor clip 54 (see, e.g.,
A catheter anchor 34 is then placed on the catheter 32 and slide down the catheter 32 into position against the skull as illustrated in
An optional anchor clip 54 is attached to the anchor 34 and skull as illustrated in
The catheter 32 is then laid down through the top slot of the anchor 34 into the catheter-receiving channel 42, and sutures may be employed to retain the catheter 32 in the channel 42 as illustrated in
Thus, embodiments of the catheter anchor system and method are disclosed. One skilled in the art will appreciate that the present invention can be practiced with embodiments other than those disclosed. The disclosed embodiments are presented for purposes of illustration and not limitation, and the present invention is limited only by the claims that follow.
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|Title not available
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|U.S. Classification
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|International Classification
|Cooperative Classification
|European Classification
|Oct 15, 2012
|Fee payment
Year of fee payment: 4
|Oct 14, 2016
|Fee payment
Year of fee payment: 8


text:
The American Society for Testing and Materials (ASTM) issues standards on material properties and testing. The American Society of Mechanical Engineers (ASME), meanwhile, specifies standards for materials to be used in construction and infrastructure. The correct standard to use is based on the specific contract or on local laws. The difference between the two sets of standards is less concrete -- even for concrete.
In his book "Biomaterials Science: An Introduction to Materials in Medicine," Buddy Ratner states that ASTM material standards can include the chemical, mechanical, physical and electrical properties of the material. These standards include both a description of test methods to be performed on building materials, and the size and shape that these materials are to take. Building materials like concrete can be required by local law in the USA to meet ASTM standards before being used in construction.
According to the "Companion Guide to the ASME Boiler & Pressure Vessel Code" by K.R. Rao, ASME material specifications are based on those published by the ASTM, AWS and other recognised national and international standards. ASME standards are legally required when building infrastructure in the USA like bridges, power plant piping and boilers.
Example of joint standards
The ASME Boiler & Pressure Vessel Code was first published in 1914. The original material specifications were developed in a joint effort of the ASME and ASTM for ferrous and nonferrous materials. However, this joint standard did not include filler materials.
- "Companion Guide to the ASME Boiler & Pressure Vessel Code"; K.R. Rao; 2001
- "Handbook of Advanced Materials: Enabling New Designs"; James Wessel; 2004
- "Biomaterials Science: An Introduction to Materials in Medicine"; Buddy D. Ratner; 2004
- "Masonry Skills"; R.T. Kreh; 2002
- "The Use of Glass in Buildings"; Valerie L. Block; 2002


text:
Herkel's New Party Will Pass Parliamentary Threshold, Says Former Politician ({{commentsTotal}})
Businessman and co-founder of Res Publica, Olari Taal, has said that he has no doubt that Andres Herkel's as-yet-unnamed new political party will pass the minimum voter threshold at the parliamentary elections next year.
He told Postimees on Monday that Estonia's political landscape has room for more than one new party, as nearly half of voters recognize the need for extensive state reform.
Ex-IRL MP Herkel announced on Sunday his intention to move ahead with plans to build a political party from the election coalition Free Patriotic Citizen and the NGO A Better Estonia.
Taal said that the two groups bring together both the support, in the case of Free Patriotic Citizen, and the administrative and organizational skills, in the case of A Better Estonia, that are needed to create a successful political force. He said that if the two work well together, it will spell rainy days for IRL and the Reform Party.


text:
Dota 2 Free PC Game Free Download Full version for windows.
Dota 2 is an online free pc game dota 2 is an online battle arena game dota 2 defence of ancients.In Dota 2 two team's with each other to win the battle the game is totally free to play online multiplayer.The game fully and officially released on July 9,2013 for the public.The game was developed by Valve Corporation a game developing company Dota 2 dota_2 is free to download.The game is available for multiple platforms from Linux,windows the game was released for Linux on July 18,Dota 2 is full version game.The game starts with two teams ready for battle both teams are held at the end of the map the both teams have to build their own Ancient both teams have to defend their own Ancient Buildings from the enemy team.
Dota 2 free pc game development began in 2009 they first hired "Icefrog" the maste head behind the development of Dota 2 PC game.The game is available for free download on Steam and the game is free to play multiplayer no fees or charges required,The game became so famous around the world that tournaments started within the dota 2 teams Big price bounties where given to those who win the matches and were awarded several trophies and medals.The game has various types of game mods its has a total of 107 game modes and Heroes in "Dota 2".Dota 2 has now become the most popular and good game on steam and has more then 700,000 online peak players every day.Players are given 6 inventory slots in which you can enter your own items and things you buy in the game.
Other Free PC Games.
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VGA:512 Mb nividia,ATI
OS:Win XP,Win 7,Win 8,Win Vista.


text:
Published: Tuesday 31st March 2015 by The News Editor
Strong winds and even a risk of snow are set to bring the first quarter of the year to a blustery end.
Motorists are being warned of "difficult" conditions as a yellow be aware warning for wind remains in place for much of the day.
Parts of north Wales, the Bristol Channel and East Anglia saw winds of up to 70mph overnight and the gales will continue for some parts.
"While the winds should gradually ease, it's going to stay a pretty windy day," said Met Office forecaster Kirk Waite.
"There could potentially be some quite difficult conditions throughout the course of the morning for those getting up and heading out to work.
"The north west of the country is going to see some quite blustery showers moving in – it's probably going to see the strongest winds today."
While there may be a slight let-up, Mr Waite said the best we can expect are "some sunny spells".
Northern parts of Scotland are subject to an ice warning until mid-morning, bringing with it a risk of snow on higher ground and, Mr Waite said, some "potentially treacherous conditions on northern routes".
While strong winds have died down after a blustery night for Northern Ireland the day ahead is set to be a wet one with scattered showers for much of the day.
Looking forward to Easter, Mr Waite said the weekend will be breezy to begin with but things should "gradually quieten down".
On Sunday gusts hit the famous Father Time weather vane at Lord's cricket ground, knocking it parallel to the ground at the St John's Wood venue in London.
The Dartford Crossing has been closed to all vehicles due to strong winds, the Highways Agency said.
Cheshire Police tweeted overnight that high winds and rain had been "creating chaos on the roads".
Chiltern Railways said services between Aylesbury and London Marylebone are suspended because of a tree on the line between Moor Park and Amersham.
Published: Tuesday 31st March 2015 by The News Editor