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This substitution changed the leucine of human H3 to a glutamine residue coumadin 1 mg visa, the same residue found in the ancestral avian H3 subtype purchase coumadin 2mg visa. This substitution caused the modi- ﬁed virus to avoid α(2 purchase coumadin 1mg on line, 6) binding and interference by horse serum and allowed binding to α(2 discount coumadin 1 mg without a prescription, 3)-bearing receptors as in the ancestral avian type. They began with aduckH3isolate that had glutamine at position 226 and favored bind- ing to α(2, 3) sialic acid linkages. Binding to erythrocytes selected vari- ants that favor the α(2, 6) linkage. Viruses bound to erythrocytes were eluted and used to infect Madin-Darby canine kidney (MDCK) cells, a standard culture vehicle for human inﬂuenza isolates. This selection process caused replacement of glutamine at position 226 by leucine, which inturnfavoredbindingofα(2, 6)-overα(2, 3)-linked sialic acid. The same sort of experimental evolution on H1 isolates would be very interesting. If selection of avian H1 for a change from α(2, 3) to α(2, 6) binding causes the same substitutions as occurred in the human H1 lin- eage, then the diﬀerent genetic background of avian H1 compared with H3 would be implicated in shaping the particular amino acid substitu- tions. By contrast, if experimental evolution favors a change at posi- tion 226 as in H3, then the evolution of human H1 receptor binding may have followed a more complex pathway than simple selection for α(2, 6)-linked sialic acid. Various steps have been proposed for adaptation of aquatic bird iso- latestohumans. NA re- moves sialic acid from HA receptors, apparently facilitating release of viral progeny from the surface of host cells. If a viral lineage switches its HA speciﬁcity from the avian α(2, 3) to the human α(2, 6) form, but NA retains the avian speciﬁcity, then the lineage may have diﬃculty spread- ing in humans. Complex pathways may be required for joint adaptation of HA and NA (Matrosovich et al. These studies raise the general problem of evolutionary pathways by which pathogens change host receptors. If two or more pathogen func- tions must change simultaneously, then changes in receptor aﬃnity may be rare. The need for joint change may cause signiﬁcant constraint on amino acid substitutions in receptor binding factors. In an experimen- tal setting, one begins with a particular, deﬁned genotype as the genetic back- ground for further analysis. One then obtains single amino acid substitutions or small numbers of substitutions derived from the original background ge- notype. Substitutions may be obtained by imposing selective pressures such as antibodies in an experimental evolution regime or by imposing site-directed or random mutagenesis. Substitutions aﬀect various components of ﬁtness as described in the text. Each of these processes relates ﬁtness to diﬀerent kinetic aspects of surface binding. First, changes in cell binding and entry aﬀect the performance of in- tracellular pathogens. The relationship between binding kinetics and ﬁtness may be rather complex. In that ﬁgure, the substitutions 190 E→A, 225 G→R, and 228 S→Gallhavestronger binding aﬃnity than the common wild type. HA has a relatively low aﬃnity for its host-cell receptors (Skehel and Wiley 2000). The fact that some substitutions raise aﬃnity suggests that binding has been adjusted by selection to an intermediate rate. It may be possible to test this idea in various experimental systems by competing viruses with diﬀerent cell binding kinetics. Robertson (1993, 1999) reviews experimental evolution work on the adaptation of inﬂuenza to culture conditions in chicken eggs and Madin- Darby canine kidney (MDCK) cells. Those in vitro systems allow study of competition between diﬀerent viral genotypes (Robertson et al. EXPERIMENTAL EVOLUTION: INFLUENZA 219 Simple in vitro culture conditions may select for higher binding aﬃn- itybetween pathogen and host cells (Robertson et al. It would be interesting to compare the ﬁtnesses in vivo between wild type and mutants selected for higher binding aﬃnity in vitro.
Systematic reviews begin with careful formulation of research questions cheap coumadin 1mg line. The goal is to select questions that are important to patients and clinicians then to examine how well the scientific literature answers those questions purchase coumadin 5mg visa. Terms commonly used in systematic reviews order coumadin 5mg free shipping, such as statistical terms generic coumadin 1 mg otc, are provided in Appendix C and are defined as they apply to reports produced by the Drug Effectiveness Review Project. Systematic reviews emphasize the patient’s perspective in the choice of outcome measures used to answer research questions. Studies that measure health outcomes (events or conditions that the patient can feel, such as fractures, functional status, and quality of life) are preferred over studies of intermediate outcomes (such as change in bone density). Reviews also emphasize measures that are easily interpreted in a clinical context. Specifically, measures of absolute risk or the probability of disease are preferred to measures such as relative risk. The difference in absolute risk between interventions depends on the number of events in each group, such that the difference (absolute risk reduction) is smaller when there are fewer events. In contrast, the difference in relative risk is fairly constant between groups with different baseline risk for the event, such that the difference (relative risk reduction) is similar across these groups. Relative risk reduction is often more impressive than absolute risk reduction. Another useful measure is the number needed to treat (or harm). The number needed to treat is the number of patients who would need be treated with an intervention for 1 additional patient to benefit (experience a positive outcome or avoid a negative outcome). The absolute risk reduction is used to calculate the number needed to treat. Systematic reviews weigh the quality of the evidence, allowing a greater contribution from studies that meet high methodological standards and, thereby, reducing the likelihood of biased results. In general, for questions about the relative benefit of a drug, the results of well- executed randomized controlled trials are considered better evidence than results of cohort, case- control, and cross-sectional studies. In turn, these studies provide better evidence than uncontrolled trials and case series. For questions about tolerability and harms, observational study designs may provide important information that is not available from controlled trials. Within the hierarchy of observational studies, well-conducted cohort designs are preferred for assessing a common outcome. Case-control studies are preferred only when the outcome measure is rare and the study is well conducted. Systematic reviews pay particular attention to whether results of efficacy studies can be generalized to broader applications. Efficacy studies provide the best information about how a drug performs in a controlled setting. These studies attempt to tightly control potential confounding factors and bias; however, for this reason the results of efficacy studies may not be applicable to many, and sometimes to most, patients seen in everyday practice. Most efficacy studies use strict eligibility criteria that may exclude patients based on their age, sex, adherence to treatment, or severity of illness. For many drug classes, including the antipsychotics, unstable or severely impaired patients are often excluded from trials. In addition, efficacy studies Nonsteroidal antiinflammatory drugs (NSAIDs) 10 of 72 Final Report Update 4 Drug Effectiveness Review Project frequently exclude patients who have comorbid disease, meaning disease other than the one under study. Efficacy studies may also use dosing regimens and follow-up protocols that are impractical in typical practice settings. These studies often restrict options that are of value in actual practice, such as combination therapies and switching to other drugs. Efficacy studies also often examine the short-term effects of drugs that in practice are used for much longer periods. Finally, efficacy studies tend to assess effects by using objective measures that do not capture all of the benefits and harms of a drug or do not reflect the outcomes that are most important to patients and their families. Systematic reviews highlight studies that reflect actual clinical effectiveness in unselected patients and community practice settings. Effectiveness studies conducted in primary care or office-based settings use less stringent eligibility criteria, more often assess health outcomes, and have longer follow-up periods than most efficacy studies.
Three tendinous intersections ﬁrmly attach the anterior sheath wall The contents of the spermatic cord include the: to the muscle itself discount coumadin 5 mg with mastercard. They are situated at the level of the xiphoid coumadin 2mg online, the • Ductus (vas) deferens (or round ligament) buy cheap coumadin 1 mg on-line. These give the abdominal ‘six- • Testicular artery: a branch of the abdominal aorta order coumadin 1 mg without a prescription. Short gastric Red labels: ventral branches Spleen Blue labels: lateral branches Green labels: branches to body wall Gastroduodenal Superior Pancreatic pancreatico- branches duodenal Left Right gastroepiploic gastro- epiploic Omental branch Inferior pancreatico- duodenal Jejunal and Superior ileal branches Superior mesenteric pancreaticoduodenal artery Inferior Fig. Superior The three primary branches are labelled in red mesenteric Middle colic Jejunal and ileal branches Right colic Ileocolic Anterior and posterior caecal branches Fig. Note the anastomosis with the inferior rectal artery (green) halfway down the anal canal The abdominal aorta (Fig. It descends in the of the oesophagus to the second part of the duodenum. The vertebral part of the duodenum to the distal transverse colon. The main relation to the right of the abdominal transverse colon to the upper half of the anal canal. These include the: • Ileocolic artery: passes in the root of the mesentery over the right • Left gastric artery: passes upwards to supply the lower oesophagus ureter and gonadal vessels to reach the caecum where it divides into ter- by branches which ascend through the oesophageal hiatus in the minal caecal and appendicular branches (Fig. The left gastric then descends in the lesser omentum along • Jejunal and ileal branches: a total of 12–15 branches arise from the the lesser curve of the stomach which it supplies. These branches divide and reunite within the • Splenic artery: passes along the superior border of the pancreas small bowel mesentery to form a series of arcades which then give rise in the posterior wall of the lesser sac to reach the upper pole of the left to small straight terminal branches which supply the gut wall. From here it passes to the hilum of the spleen in the lienorenal • Right colic artery: passes horizontally in the posterior abdominal ligament. The splenic artery also gives rise to short gastric branches, wall to supply the ascending colon. It then passes between These arise from the abdominal aorta at the level of L2. Before reaching the porta hepatis it divides into right and left on the posterior abdominal wall to reach the ovary in the female, or pass hepatic arteries and from the right branch the cystic artery is usually through the inguinal canal in the male to reach the testis. Prior to its ascent towards the porta hepatis the hepatic artery gives rise to gastroduodenal and right gastric branches. The former The inferior mesenteric artery arises from the abdominal aorta at the passes behind the ﬁrst part of the duodenum and then branches further level of L3. It passes downwards and to the left and crosses the left into superior pancreaticoduodenal and right gastroepiploic branches. Its branches include: curvature to supply the stomach. From above downwards, it passes over the left renal vein • The superior rectal artery: passes into the pelvis behind the rectum behind the neck of the pancreas, over the uncinate process and anterior to form an anastomosis with the middle and inferior rectal arteries. It then passes obliquely downwards supplies the rectum and upper half of the anal canal. This establishes a strong branches of the superior mesenteric artery include the: collateral circulation throughout the colon. The arteries of the abdomen 33 13 The veins and lymphatics of the abdomen Inferior phrenic Suprarenal Ureteric branch Renal Lumbar Gonadal Common iliac Median sacral Fig. Note the anastomoses with the systemic system (orange) in the oesophagus and the anal canal 34 Abdomen and pelvis The portal vein (Fig. It serves to transfer blood level of the umbilicus drains to the anterior axillary lymph nodes. Effer- to the liver where the products of digestion can be metabolized and ent lymph from the skin below the umbilicus drains to the superﬁcial stored. Blood from the liver ultimately gains access to the inferior vena inguinal nodes. The portal vein is formed behind the neck of the pancreas by the union of the superior mesenteric and splenic The lymph nodes and trunks veins. It passes behind the ﬁrst part of the duodenum in front of the in- The two main lymph node groups of the abdomen are closely related to ferior vena cava and enters the free border of the lesser omentum.
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