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This patient may be having an palpitations, anxious, heart rate of 90, anxiety attack. This patient has classic non-cardiac chest pain when coughing, productive cough symptoms, despite having chest pain. High risk for acute arterial left foot, a history of diabetes requiring insulin occlusion. This patient most likely has a urinary frequency and voiding in small urinary tract infection which does not amounts. High risk for ectopic pregnancy, quadrant pain abdominal, denies vaginal unless the triage nurse can confirm bleeding. Most likely this is a threatened cramping and vaginal bleeding, 14 weeks abortion which does not require pregnant, vital signs stable. High risk for neutropenia and receiving chemotherapy, and a temperature infection of 102. High risk for pleural effusion, increasing shortness of breath over the past pulmonary embolus and other few days. While may be dehydrated, this She is able to drink, has a wet diaper, and is does not appear to be a high-risk fussy and crying tears during triage. She is unable to drink, hasnt wet a diaper for several hours, is unable to hold anything down, and has very dry mucous membranes. Moderate respiratory distress wheezing that is audible during triage without indicates a possible high risk for auscultation, oxygen saturation of 97% on deterioration. Unable to injury and possible epidural remember the events, moderately severe hematoma. Is the Patient Experiencing Society Board of Directors each approved a joint New Onset Confusion, position statement which articulates 14 core Lethargy, or Disorientation While patient have new onset confusion, lethargy, or rapid treatment of pain is important, careful disorientation Not all meet level 2 criteria because the dementia is not patients with a pain score of >7 should be considered to be of new onset. Indeed, the patient may have a fracture and criteria include patients with diabetic ketoacidosis, be experiencing severe pain. Again, if elevation, and analgesics (if standing orders are in the patient has new onset confusion, lethargy, or place) to reduce the pain. It is not possible to manage pain at triage for patients with renal colic, cancer, or sickle cell crisis. These are hospital specific, to rate their pain using a scale such as the visual protocol driven responses. The triage nurse concludes that it would be Summary inappropriate for this patient to wait and would We have reviewed the key components and assign this patient to the last open bed.

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Rather, it is narrowly tailored and applies only to diagnostic use of gene patents in the context of patient care. Privately funded genetic research, which is supplemental to Government-funded genetic research, is often driven by the desire to develop a therapeutic, whether in the form of a drug or a gene-based therapeutic. Because patents on genes would remain available and enforceable for therapeutic uses with this statutory change, the prospect of a patent on a gene or on a therapeutic would still serve to stimulate private investment in basic genetic research. The narrow tailoring of the exemption also leaves undisturbed the ability to enforce patent rights to test kits, platform technologies, and methods of genetic analysis that do not rely on specific patent claims on human genes. Second Recommended Statutory Change the second principal legal change that the Committee proposes is the creation of an exemption from patent infringement liability for those who use patent-protected genes in the pursuit of research. It is not clear whether patent rights holders have consistently sought to enforce their patent rights to prevent such research, but even if patents have not been enforced against such research, an exemption from liability would provide complete assurance to scientists that such research is permissible. Since the Committees focus is strictly on addressing potential impediments to the development of and patient access to genetic tests, it did not evaluate the appropriateness of, nor recommend, a general research exemption in all areas of science. The Committees narrow focus on nucleic-acid-based genetic tests limits its recommendations in other ways as well. Specifically, the Committees recommendations do not extend to patents on proteins. These patents were excluded from the scope of the study because most genetic tests detect genetic sequences rather than proteins. However, if there are any concerns about the effects of protein patents on the development of and access to protein-based genetic tests, other groups may wish to undertake a study of this issue and may well find that analogous recommendations are appropriate. Finally, the Committee is cognizant of the fact that patent and licensing practices should not be changed lightly or without sufficient cause. Indeed, in the realm of commodities or consumer electronics it may well be that dramatic harms and a profound lack of benefit should be required to compel any recommendation for change. Thus, the current systems net negative effects on test development and patient access to these tests argue strongly for the narrowly tailored changes that are proposed. If enacted, the first recommended statutory change would allow service providers to offer gene based diagnostic testing unimpeded by fear of infringing patent claims on genes and would apply to both commercial and noncommercial laboratories. It would also allow test kit manufacturers to make, offer for sale, and sell genetic test kits without the need to obtain licenses to any patented nucleic acid molecules included in kits.

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In 334 these cases, the reticulum, the dorsal blind sac of the rumen, and sometimes the cranial part of 335 the ventral sac of the rumen are displaced dorsally by the effusion. Generalized peritonitis 336 may be accompanied by massive fluid accumulation, which surrounds the organs and 337 displaces them dorsally. Depending on the cell count and amount of fibrin, the fluid may 11 338 appear anechoic (Fig. Often the 341 fluid appears chambered in a sponge-like fashion by strands of fibrin (Fig. A layer of 342 sediment composed of echoic cells and fibrin and an anechoic supernatant may be seen when 343 there are many cells and a large amount of fibrin (Fig. When gastrointestinal contents escape into the peritoneal cavity, for instance after 346 abomasal or intestinal rupture, echoic ingesta may be seen coating some of the organs. The 347 intestinal walls often are thickened and echoic fibrin and inflammatory fluid are seen between 348 loops of intestines in cattle with generalized peritonitis. Intestinal motility usually is severely 349 reduced or absent because of adhesions, and diarrhea is common. However, based on 350 ultrasonographic appearance alone, it is often not possible to differentiate a transudate, a 351 modified transudate of non-inflammatory ascites, and an exudate, and the analysis of fluid 352 collected by abdominocentesis is required for a diagnosis. Peritonitis is limited to the bursa and 357 demarcated from the remaining abdominal cavity by a capsule of varying thickness. Reticular 358 foreign bodies, ruminal perforation or ulcers, abomasal ulcers, and laparotomies are the most 359 common causes. Extreme cases involve the entire ruminal width and length, 362 extending from the naval to the udder, and measure more than 10 cm vertically. The 363 ultrasonographic appearance of the fluid and the fibrin deposits vary, and the echoic leaves of 364 the bursa sometimes can be seen. A characteristic difference between omental bursitis and 365 generalized peritonitis is that the former is restricted to the region ventral and lateral to the 366 rumen on the left side, whereas the latter also involves the right side of the abdomen. A review of the causes, 372 diagnosis, and treatment of uroperitoneum in cattle was recently published. The site of bladder 382 rupture can sometimes be detected during transrectal sonographic examination. The ruptured 383 bladder may be collapsed and flaccid and contain little or no urine or contain moderate 384 amounts of urine when the defect is sealed by fibrin. Comparison of urea and 390 creatinine concentrations of the aspirated fluid and blood reliably differentiates urine and a 391 transudate. With uroperitoneum, both variables are much higher in the aspirated fluid than in 392 blood; a peritoneal fluid-to-serum creatinine concentration ratio of 2 or greater is diagnostic of 393 uroperitoneum. It is rare in cattle and always results from 401 hemorrhage from a ruptured blood vessel or spleen or is related to a clotting disorder. A symptomatic diagnosis is made when abdominocentesis produces a 13 404 hemorrhagic aspirate but the measurement of clotting factors or a laparotomy may be required 405 for an etiological diagnosis.

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This dissenting statement is organized as follows: Part I summarizes the main points of the dissent. For many years, Fannie Mae treated as subprime loans only those that it purchased from subprime originators. Tat is the standard, for example, used by the Ofce of the Comptroller of the Currency. It may have an adjustable rate, lack documentation about the borrower, require payment of interest only, or be made to an investor in rental housing, not a prospective homeowner. Government Policies Resulted in an Unprecedented Number of Risky Mortgages Tree specifc government programs were primarily responsible for the growth of subprime and Alt-A mortgages in the U. Wallison 453 moderate income7 borrowers better access to mortgage credit through Fannie Mae and Freddie Mac. This efort, probably stimulated by a desire to increase home ownership, ultimately became a set of regulations that required Fannie and Freddie to reduce the mortgage underwriting standards they used when acquiring loans from originators. Fannie Mae was established as a government agency in the New Deal era to buy mortgages from banks and other loan originators, providing them with new funds with which to make additional mortgages. The new regulations, made efective in 1995, for the frst time required insured banks and S&Ls to demonstrate that they were actually making loans in low-income communities and to low-income borrowers. With all these entities seeking the same loans, it was not likely that all of them would fnd enough borrowers who could meet the traditional mortgage lending standards that Fannie and Freddie had established. The obvious way to meet this obligation was simply to reduce the underwriting standards that impeded compliance with the governments requirements. Shiller, shows the dramatic growth of the 1997-2007 housing bubble in the United States. The Bubble According to Shiller Tat the 1997-2007 bubble lasted about twice as long as the prior housing bubbles is signifcant in itself. Mortgage quality declines as a housing bubble grows and originators try to structure mortgages that will allow buyers to meet monthly payments for more expensive homes; the fact that the most recent bubble was so long-lived was an important element in its ultimate destructiveness when it defated. Eventually, the bubble tops out, those who are still in the game run for the doors, and a defation in prices sets in. The reason for this longevity is that one 458 Dissenting Statement major participant in the market was not in it for proft and was not worried about the risks to itself or to those it was controlling. Economists have been vigorously debating whether the Feds monetary policy in the early 2000s caused the bubble by keeping interest rates too low for too long. Raghuram Rajan, a professor at the Chicago Booth School of Business, argues that the Feds low interest rates caused the bubble, but that the Fed actually followed this policy in order to combat unemployment rather than defation. Taylor, Getting Of Track, Hoover Institution Press, 2009; and Raghuram Rajan, Fault Lines: How Hidden Fractures Still Treaten the World Economy, Princeton University Press, 2010, pp.