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Okazaki K prostate supplements that work rogaine 5 60 ml with amex, et al: Autoimmune-related pancreatitis is associated with autoantibodies and Th1/Th2-type cellular immune response, Gastroenterology 118(3):573­581, 2000. Otsuki M, et al: Asian diagnostic criteria for autoimmune pancreatitis: consensus of the Japan-Korea Symposium on Autoimmune Pancreatitis, J Gastroenterol 43(6):403­408, 2008. Owyang C, et al: Pancreatic exocrine function in severe human chronic renal failure, Gut 23(5):357­361, 1982. Paliwal S, et al: Genetic and phenotypic heterogeneity in tropical calcific pancreatitis, World J Gastroenterol 20(46):17314­17323, 2014. Sahel J, et al: Multicenter pathological study of chronic pancreatitis: morphological regional variations and differences between chronic calcifying pancreatitis and obstructive pancreatitis, Pancreas 1(6): 471­477, 1986. Sahin-Tóth M: Human cationic trypsinogen: role of Asn-21 in zymogen activation and implications in hereditary pancreatitis, J Biol Chem 275:22750­22755, 2000. Sahin-Tóth M, Tóth M: Gain-of-function mutations associated with hereditary pancreatitis enhance autoactivation of human cationic trypsinogen, Biochem Biophys Res Commun 278(2):286­289, 2000. Sarles H: Etiopathogenesis and definition of chronic pancreatitis, Dig Dis Sci 31(9 Suppl):91S­107S, 1986. Sarles H: Definitions and classifications of pancreatitis, Pancreas 6(4): 470­474, 1991. Sarles H, et al: Pathogenesis and epidemiology of chronic pancreatitis, Annu Rev Med 40:453­468, 1989. Sarles H, et al: Renaming pancreatic stone protein as "lithostathine, Gastroenterology 99(3):900­901, 1990. Standop J, et al: ErbB2 oncogene expression supports the acute pancreatitis-chronic pancreatitis sequence, Virchows Arch 441(4):385­ 391, 2002. Stevens T, et al: Pathogenesis of chronic pancreatitis: an evidence-based review of past theories and recent developments, Am J Gastroenterol 99(11):2256­2270, 2004. Suda K, et al: Histopathologic and immunohistochemical studies on alcoholic pancreatitis and chronic obstructive pancreatitis: special emphasis on ductal obstruction and genesis of pancreatitis, Am J Gastroenterol 85(3):271­276, 1990. Talamini G, et al: Cigarette smoking: an independent risk factor in alcoholic pancreatitis, Pancreas 12(2):131­137, 1996. Teich N, et al: Clinical implications of genetic risk factors of chronic pancreatitis, Internist 46(2):123­130, 2005. Truninger K, et al: Mutations of the serine protease inhibitor, Kazal type 1 gene, in patients with idiopathic chronic pancreatitis, Am J Gastroenterol 97(5):1133­1137, 2002. Witt H, et al: Mutations in the gene encoding the serine protease inhibitor, Kazal type 1, are associated with chronic pancreatitis, Nat Genet 25(2):213­216, 2000. Current evidence suggests that a combination of predisposing factors-environmental, toxic, and genetic-is likely involved in most cases rather than a single factor (Braganza et al, 2011). Scarring of the parenchyma can be focal or patchy initially and may progress to become diffuse. The progressive loss of acinar tissue may lead to exocrine insufficiency, and ultimately, loss of islet tissue with diabetes (Conwell et al, 2014). Formation of metaplastic ductal lesions (tubular complexes and pancreatic intraepithelial neoplasia), focal necrosis and cysts (Klöppel, 2007), and neural hypertrophy with perineural inflammation can be observed (Ceyhan et al, 2009). Patients may also present with symptoms of endocrine insufficiency (diabetes mellitus) and exocrine insufficiency (diarrhea, steatorrhea, malnutrition, and weight loss), as well as with numerous acute and chronic complications. Inflammatory ductal changes and intraductal calculi (pancreatolithiasis) may result in obstruction of the pancreatic duct or of the intrapancreatic portion of the bile duct. An inflammatory mass of the pancreatic head frequently results in obstruction of the duodenum and may also affect the splenic, superior mesenteric, or portal veins with subsequent thrombosis. Development of pancreatic pseudocysts may result in obstruction, abscess formation, or in ascites or pleural effusions in case of rupture. The main goal of the therapy for pancreatic exocrine dysfunction is to avoid fat maldigestion. Reasons for earlier and more severe impairment of fat digestion compared with protein and carbohydrate digestion in patients with pancreatic insufficiency are that (1) impairment of pancreatic lipase synthesis and secretion occurs earlier; (2) more rapid and complete inactivation of lipase occurs in the acidic duodenum as a result of impaired bicarbonate output; (3) proteolytic degradation of lipase occurs earlier during aboral transit than that of amylase and proteases; (4) impairment of pancreatic bicarbonate secretion decreases duodenal pH, resulting in precipitation of glycine-conjugated bile acids and further deterioration of fat digestion; and (5) extrapancreatic sources of lipase are unable to compensate for loss of pancreatic lipase activity.

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The mortality is about 10% in recent reports (Farges et al androgen vs hormone purchase rogaine 5 on line amex, 2013; Kenjo et al, 2014), which is much higher than hepatectomy alone for liver tumors. First, the procedure for perihilar tumor accompanies extrahepatic procedures of bile duct resection and lymphadenectomy. Second, the liver is impaired by cholestasis or cholangitis even after biliary drainage; assessment of functional reserve has not been standardized. Thus hepatectomy for perihilar tumors requires specific management to maximize patient safety after surgery. In addition, an imaging analysis using plug-in simulation software in the processing workstation enables a virtual hepatectomy (Radtke et al, 2010; Takamoto et al, 2013). Therefore, the extent of lateral extension could be assessed in only those 40 patients (55%) with a hyperattenuated tumor. The diagnostic accuracy of the extent of ductal cancer infiltration was 76% and 82% in the proximal and the distal direction, respectively. The extent of cancer was underestimated by 24% and 15% at the proximal and the distal borders, respectively, because of superficial spread, minimal invasive cancer extension, or both. Meanwhile, 3D portography clearly shows the portal branch anatomy and site/length of portal vein invasion. Three-dimensional portography facilitates the design of the resection and reconstruction procedure (wedge vs. Diagnosis based on the presence or absence of the low-density plane showed an accuracy of 85% with a sensitivity of 100% and specificity of 77%, which was superior to that of the contact length and contact angle. Cholangiography Cholangiograms precisely delineate the segmental anatomy of the intrahepatic bile duct (Ohkubo et al, 2004), the tumor configuration, and the extent of the tumor border (see Chapters C. Most perihilar cholangiocarcinomas are infiltrating tumors, in which cancer cells are likely to extend in the subepithelial layer rather than in the epithelial layer. Histologically, direct and lymphatic invasion are common routes for invasion to the ductal wall, evoking reactive fibrosis (Sakamoto et al, 1998). These changes cause rigidity, narrowing, tapering, and obstruction of the duct on the cholangiogram. The border of these findings on cholangiograms correspond to the leading edge of cancer infiltration (Sakamoto et al, 1998), although the cholangiographic findings are modified by the extent of opacification of the contrast media. Consequently, Western surgeons have used biliary drainage in select patients with malnutrition, hypoalbuminemia, prolonged cholestasis, or cholangitis. However, these studies were conducted 30 years ago and involved patients undergoing bypass surgeries or palliative resections. The incidence of bacterobilia and fungobilia was 85% and 40%, respectively (Jethwa et al, 2007), leading to infectious complications after hepatectomy (Hochwald et al, 1999; Jethwa et al, 2007; Nomura et al, 1999; Shigeta et al, 2002;). These observations might partially support the limited indications for biliary drainage. Recently, some have questioned whether overall analysis misleads conclusions about the impact of biliary drainage on mortality (Farges et al, 2013; Kennedy et al, 2009). When stratifying by the extent of hepatectomy, the mortality was more than 10% after extended hepatectomy in patients with jaundice, mainly because of hepatic failure. Perihilar cholangiocarcinomas frequently separate the intrahepatic biliary tree into several units. Under such challenging conditions, the optimal method of biliary drainage remains controversial (endoscopic vs. Early complications, such as acute cholangitis, dislodgement, and hemobilia, occurred 14. Furthermore, there is no risk of portal bleeding after removing the catheter sheath because the punctured portal branch is embolized. Portograms are obtained at two or three of the following different projections to confirm the individual anatomy of the portal system: supine position, right anterior oblique projection, and right anterior oblique projection with caudally tilting 20 degrees (Nishio et al, 2003). Selective catheterization of the right portal branches is also important for complete occlusion without migration of the embolic material. Notably, left trisectionectomy is a technically demanding and challenging procedure associated with a higher morbidity than other anatomic hepatectomies (Taguchi et al, 2014). This technique is simple and useful in patients with locally advanced perihilar cholangiocarcinoma that requires combined hepatic artery and portal vein resection, in whom hilar dissection cannot be completed before liver resection. Absolute ethanol injection followed by the placement of a steel coil is routinely used in our clinic (Ebata et al, 2012b). Because absolute ethanol has no radiopacity, permeates into the peripheral portal system, and induces endothelial injury/ thrombosis, it must be carefully and slowly administered in 0.

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Rare macrocystic (oligocystic) mens health weight loss cheap rogaine 5 60 ml buy on line, unicystic and solid examples occur, and recent studies have shown that these do not significantly differ from the more common microcystic variant, perhaps with the exception of their higher propensity to be mimic (and be misdiagnosed as) other macrocystic tumors or neuroendocrine neoplasms (Reid et al, 2015). Serous cystic tumors are one of the few ductal neoplasms of the pancreas that do not produce mucin, possibly reflecting a recapitulation of the centroacinar cells that are nonmucinous. Along the same lines, the cyst contents are devoid of the mucin-related glycoproteins and oncoproteins that typically are found in mucinous pancreatic tumors, a feature that may help in the preoperative diagnosis (Brugge et al, 2004). Serous cystadenomas often are reported to coexist or "collide" with other pancreatic neoplasms and with congenital pathologic conditions (Reid et al, 2015; Yip-Schneider et al, 2014). Convincing examples of malignant serous tumors (serous cystadenocarcinomas or carcinomas ex microcystic adenoma) are exceedingly rare (Zhu et al, 2012). The uniform cells are arranged in nests, with trabecula, and are separated by a richly vascularstroma. Rarely, cystic degeneration may be seen (Adsay & Klimstra, 2000; Deshpande & Lauwers, 2007; Singhi et al, 2012), with a central unilocular cyst lined by a cuff of viable tumor. The correlation of serum hormone levels and immunoexpression of the corresponding hormone in the tumor itself is often imperfect. Most insulinomas follow a benign clinical course, likely because insulinomas typically are highly symptomatic, even when they are small, which leads to their early detection. Thus, other than Ki-67 (see later), prognostic biomarkers are not in general clinical use. It further predicted "benign behavior" or "uncertain behavior" in the former group based on size less than 2 cm, mitotic rate less than 2 per 10 high-power fields (hpfs), Ki-67 labeling index less than 2%, and absence of vascular or perineural invasion. However, studies demonstrated that most patients who fall in the uncertain behavior group still experience recurrence and metastasis (Ferrone et al, 2007; Hochwald et al, 2002; Schmitt et al, 2007); therefore, it is clear that even this group should be considered malignant. This system has an advantage in that it does not combine grading and staging parameters (which each independently predict outcome) and thus allows prognostication in the face of metastatic disease. In all these studies, the two groups exhibited a highly significant difference in prognosis, although no subset was regarded to be benign. Recently, a multidisciplinary group of international experts proposed a set of parameters to be included in pathology reports on neuroendocrine neoplasms (Klimstra et al, 2010). Acinar Neoplasms Although acinar tissue constitutes most of the pancreas, acinar neoplasms are rare. Acinar neoplasms are characterized by the production of pancreatic enzymes, such as trypsin, chymotrypsin, and lipase. Although there is a benign cystic variant, acinar cell cystadenoma, no benign solid acinar cell neoplasm has been defined. Acinar cell carcinomas form relatively large tumors (mean, 10 cm), usually in older men (mean age, 63 years) (Kitagami et al, 2007; Klimstra, 2007; La Rosa et al, 2012; Wisnoski et al, 2008), although some occur in children (Shorter et al, 2002). In a small percentage of cases (10%), patients experience a "lipase hypersecretion syndrome" (Klimstra & Adsay, 2001) characterized by subcutaneous fat necrosis, polyarthralgia, and peripheral eosinophilia, usually in the presence of hepatic metastases. Half of acinar cell carcinomas have metastases at diagnosis, usually in the liver and/or regional lymph nodes (Holen et al, 2002). Once believed to be almost as aggressive clinically as ductal adenocarcinomas, with a 5-year survival of 10% (Holen et al, 2002; Klimstra et al, 1992), more recent studies place acinar cell carcinomas in a somewhat more indolent category (Holen et al, 2002; La Rosa et al, 2015b; Wood & Klimstra, 2014), with some studies reporting a 5-year survival of 30% to 40% (Kitagami et al, 2007; La Rosa et al, 2012; Wisnoski et al, 2008). In contrast to ductal adenocarcinomas, acinar cell carcinomas are stromapoor cellular tumors composed of solid nests of cells and small glands (acini). A subset of acinar cell carcinomas is characterized by prominent intraductal growth (Ban et al, 2010; Basturk et al, 2007). Immunohistochemistry discloses scattered neuroendocrine cells in 30% to 40% of acinar cell carcinomas. Some cases have a significant neuroendocrine component that may or may not be evident microscopically (Klimstra et al, 1992). Similarly, acinar cell carcinomas with more than 25% ductal differentiation are classified as mixed acinarductal carcinoma (Stelow et al, 2010). Rarely, acinar cell carcinomas may show a grossly cystic pattern and are designated acinar cell cystadenocarcinoma (Cantrell et al, 1981; Stamm et al, 1987). Pancreatoblastoma Pancreatoblastoma is an extremely rare childhood tumor of the pancreas (mean age, 4 years), which can also occasionally arise in adults (Dhebri et al, 2004; Klimstra et al, 1995; Shorter et al, 2002) (see Chapters 61 and 62). Pancreatoblastomas are malignant tumors with a 5-year survival of about 25%, although children diagnosed before the development of metastases have had more favorable outcomes.

Syndromes

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  • Skin that is turning blue
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  • Laxative
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  • Hypothyroidism (underactive thyroid)
  • Two boys without the disease
  • 1 - 3 years: 20 mcg/day

The main reason for long-term failure was the occurrence of gastric varices prostate 101 cheap rogaine 5 express, but clearly this does not occur in all cases, and some studies suggest that the occurrence of spontaneous shunts after successful sclerotherapy negates the need for shunt surgery altogether (Goenka et al, 1993) (see Chapters 82 and 83). Surgery may be required for patients with extrahepatic portal hypertension with preserved liver function for recurrent bleeding or, rarely, for massive hypersplenism. Although earlier outcomes of portosystemic shunts were disappointing, some recent reports of have shown recurrence of bleeding in only 2. Nonselective mesocaval shunts and the more selective distal splenorenal shunt have been the procedures of choice in the past, although a central splenorenal shunt with splenectomy is sometimes advocated if massive hypersplenism and pain from splenic infarcts are present. However, these shunts may not be technically possible because of thrombotic involvement of splenic or mesenteric veins, and in some cases, particularly where varices are derived from the cavernoma, certain shunts may not alter variceal pressures to the coronary esophageal veins. The Rex shunt, usually an internal jugular vein graft and mesenteric to left portal vein bypass, has the major theoretical advantage of restoring portal flow to the liver and reducing risk of encephalopathy, and it obviates the technical problems associated with splenic vein thrombosis (Bambini et al, 2000; de Ville de Goyet, 1999). First introduced for portal vein thrombosis after liver transplantation, this procedure may become the surgical procedure of choice for all cases of extrahepatic portal vein obstruction. Thrombosis and stenosis rates appear to be similar to those of portosystemic shunts. Patency of the intrahepatic portal system can be difficult to prove before the procedure. The use of a preprocedural portal venogram to ensure patency antegrade to the liver is important when performing any type of shunt surgery for extrahepatic venous obstruction, particularly where a cavernoma is present; selective division of the portal system. Thorough assessment of the causes, effects, venous anatomy, and consequent selective application of some or all of these options can improve quality of life, reduce the complications of portal hypertension, and decrease mortality rate. Where there is preserved liver function, children with variceal bleeding as a result of extrahepatic portal hypertension can usually be effectively and safely managed with initial direct variceal ablation by sclerotherapy or banding, which in many cases can alter the natural history of the disease and reduce the risk of rebleeding. The development of portal hypertensive gastropathy and/or rebleeding after these palliative procedures can be definitively managed by shunt surgery, preferably with the more physiologic Rex shunt. Those who are not candidates for transplantation and those who have not responded to nonsurgical treatments can have good outcomes with selective portosystemic shunts. Well-planned, definitive surgical treatments will continue to be important components in the treatment of children with portal hypertensive complications or progressive liver disease. Hepatic Cirrhosis, Portal Hypertension, and Hepatic Failure Chapter 78 Portal hypertension in children1174. Moitinho E, et al: Multicenter randomized controlled trial comparing different schedules of somatostatin in the treatment of acute variceal bleeding, J Hepatol 35(6):712­718, 2001. Shasidhar H, et al: Propranolol in prevention of portal hypertensive hemorrhage in children: a pilot study, J Pediatr Gastroenterol Nutr 29:12­17, 1999. Valayer J, et al: Shunt surgery for treatment of portal hypertension in children, World J Surg 9(2):258­268, 1985. Debray D, et al: Outcome of cystic fibrosis-associated liver cirrhosis: management of portal hypertension, J Hepatol 31(1):77­83, 1999. Garcia-Tsao G, et al: Practice Guidelines Committee of the American Association for the Study of Liver Diseases; Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis, Hepatology 46(3):922­938, 2007. Kato T, et al: Portosystemic shunting in children during the era of endoscopic therapy improved postoperative growth parameters, J Pediatr Gastroenterol Nutr 30(4):419­425, 2000. Lagier E, et al: Treatment of bleeding stomal varices using transjugular intrahepatic portosystemic shunt, J Pediatr Gastroenterol Nutr 18: 501­503, 1994. Lykaverios P, et al: Risk of gastrointestinal bleeding during adolescence and early adulthood in children with portal vein obstruction, J Pediatr 136(6):805­808, 2000. The incidence of acute liver failure following hepatitis B was 1% to 4% of hospitalized patients. In early studies, hepatitis D coinfection or superinfection was thought to increase the risk, because it was found in 34% to 43% of patients with acute liver failure due to hepatitis B, compared with 4% to 19% of less severe cases. Vaccination and antiviral therapy have altered the observed pattern of hepatitis B­related acute liver failure. The risk of acute liver failure after exposure to hepatitis C appears to be very low but has been described.

Usage: ut dict.

Hytiroglou P prostate cancer kidney failure prognosis purchase 60 ml rogaine 5 visa, et al: Hepatic precancerous lesions and small hepatocellular carcinoma, Gastroenterol Clin North Am 36:867­887, 2007. International Consensus Group for Hepatocellular Neoplasia: Pathologic diagnosis of early hepatocellular carcinoma: a report of the International Consensus Group for Hepatocellular Neoplasia, Hepatology 49(2):658­664, 2009. International Working Party: Terminology of nodular hepatocellular lesions, Hepatology 22(3):983­993, 1995. Iwai M, et al: Cholestatic liver disease in a 20-yr-old woman with histiocytosis X, Am J Gastroenterol 83(2):164­168, 1988. Jia D, et al: Exome sequencing of hepatoblastoma reveals novel mutations and cancer genes in the Wnt pathway and ubiquitin ligase complex, Hepatology 60(5):1686­1696, 2014. Clinicopathologic and immunohistochemical studies of 14 autopsy cases, Cancer 59(2):310­316, 1987. Report of a giant tumor studied by light and electron microscopy, Cancer 52(9):1662­1665, 1983. A clinical and pathologic analysis of 57 hepatectomy cases, Cancer 51:542­548, 1983. Klastkin G: Adenocarcinomas of the hepatic duct at its bifurcation within the porta hepatitis. An unusual tumor with distinctive clinical and pathological features, Am J Med 38:241­256, 1965. Kloppel G, et al: Precancerous lesions of the biliary tree, Best Pract Res Clin Gastroenterol 27(2):285­297, 2013. Kobayashi M, et al: Dysplastic nodules frequently develop into hepatocellular carcinoma in patients with chronic viral hepatitis and cirrhosis, Cancer 106:636­647, 2006. Kobayashi M, et al: Incidence of primary cholangiocellular carcinoma of the liver in japanese patients with hepatitis C virus-related cirrhosis, Cancer 88(11):2471­2477, 2000. Kojiro M: Focus on dysplastic nodules and early hepatocellular carcinoma: an Eastern point of view, Liver Transpl 10:3­8, 2004. Pathomorphologic study of 29 autopsy cases, Arch Pathol Lab Med 109(9):853­857, 1985. Kojiro M, Roskams T: Early hepatocellular carcinoma and dysplastic nodules, Semin Liver Dis 25:133­142, 2005. Kojiro M, et al: Hepatocellular carcinoma with sarcomatous change: a special reference to the relationship with anticancer therapy, Cancer Chemother Pharmacol 23(Suppl):4­8, 1989. Komori K, et al: Mesothelial cyst of the liver in a neonate, Pediatr Surg Int 24(4):463­465, 2008. Komuta M, et al: Clinicopathological study on cholangiolocellular carcinoma suggesting hepatic progenitor cell origin, Hepatology 47(5):1544­1556, 2008. Kondo F: Benign nodular hepatocellular lesions caused by abnormal hepatic circulation: etiological analysis and introduction of a new concept, J Gastroenterol Hepatol 16:1319­1328, 2001. Kondo F, et al: Histological features and clinical course of large regenerative nodules: evaluation of their precancerous potentiality, Hepatology 12(1698171):592­598, 1990. Kondo F, et al: Nodular lesions associated with abnormal liver circulation, Intervirology 47:277­287, 2004. Kottke-Marchant K, et al: Localized fibrous tumor (localized fibrous mesothelioma) of the liver, Cancer 64(5):1096­1102, 1989. Kuma S, et al: Leiomyosarcoma originating from the superior mesenteric vein: a case report and review of the literature, Ann Vasc Surg 22(3):453­455, 2008. Kuwano H, et al: Hepatocellular carcinoma with osteoclast-like giant cells, Cancer 54(6331629):837­842, 1984. Clinical and pathologic study of 16 cases with emphasis on immunohistochemical features, Am J Surg Pathol 15(1):1­16, 1991. Lee J-S, et al: Classification and prediction of survival in hepatocellular carcinoma by gene expression profiling, Hepatology 40:667­676, 2004. Lepreux S, et al: Expression of fibrillin-1 in focal nodular hyperplasia of the liver: a role in microcirculation adaptability, Comp Hepatol 3(Suppl 1):S57, 2004. Leung C, et al: Characteristics of hepatocellular carcinoma in cirrhotic and non-cirrhotic non-alcoholic fatty liver disease, World J Gastroenterol 21(4):1189­1196, 2015. Libbrecht L, et al: Preneoplastic lesions in human hepatocarcinogenesis, Liver Int 25:16­27, 2005. Spectrum of morphologic changes and clinical findings, Mayo Clin Proc 50(5):255­ 263, 1975. Maeda T, et al: Combined hepatocellular and cholangiocarcinoma: proposed criteria according to cytokeratin expression and analysis of clinicopathologic features, Hum Pathol 26(9):956­964, 1995.

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