ABSTRACT
We evaluated the bone regeneration and healing effect of Medicarpin (med) in cortical bone defect model that heals by intramembranous ossification. For the study, female Sprague-Dawley rats were ovariectomized and rendered osteopenic. A drill hole injury was generated in mid femoral bones of all the animals. Med treatment was commenced the day after and continued for 15 days. PTH was taken as a reference standard. Fifteen days post-treatment, animals were sacrificed. Bones were collected for histomorphometry studies at the injury site by micro-computed tomography (µCT) and confocal microscopy. RNA and protein was harvested from newly generated bone. For immunohistochemistry, 5µm sections of decalcified femur bone adjoining the drill hole site were cut. By µCT analysis and calcein labeling of newly generated bone it was found that med promotes bone healing and new bone formation at the injury site and was comparable to PTH in many aspects. Med treatment led to increase in the Runx-2 and osteocalcin signals indicating expansion of osteoprogenitors at the injury site as evaluated by qPCR and immunohistochemical localization. It was observed that med promoted bone regeneration by activating canonical Wnt and notch signaling pathway. This was evident by increased transcript and protein levels of Wnt and notch signaling components in the defect region. Finally, we confirmed that med treatment leads to elevated bone healing in pre-osteoblasts by co localization of beta catenin with osteoblast marker alkaline phosphatase. In conclusion, med treatment promotes new bone regeneration and healing at the injury site by activating Wnt/canonical and notch signaling pathways. This study also forms a strong case for evaluation of med in delayed union and non-union fracture cases.
Subject(s)
Bone and Bones/pathology , Pterocarpans/pharmacology , Receptors, Notch/metabolism , Wnt Signaling Pathway/drug effects , Wound Healing/drug effects , Animals , Biomarkers/metabolism , Bone Density/drug effects , Bone Diseases, Metabolic/drug therapy , Bone Diseases, Metabolic/physiopathology , Bone Regeneration/drug effects , Bone Regeneration/genetics , Bone and Bones/drug effects , Bone and Bones/physiopathology , Cell Differentiation/drug effects , Female , Gene Expression Regulation/drug effects , Ovariectomy , Rats, Sprague-Dawley , Staining and Labeling , Stem Cells/cytology , Stem Cells/drug effects , Stem Cells/metabolismABSTRACT
BACKGROUND: The reported incidence of postoperative liver failure in cirrhotic patients is highly varied with diverse risk factors identified to predict risk, mainly drawn from organ or disease-specific studies. We aimed to assess risk factors for the development of postoperative liver failure in a specific cohort of patients with cirrhosis undergoing abdominal cancer resection. METHODS: From November 2007 to October 2012, 30 cirrhotic patients who underwent curative resection for abdominal cancer were analyzed. The postoperative trends in liver function were followed and the incidence of postoperative liver failure was demonstrated. RESULTS: Among the 30 patients, the tumors were located in the stomach (n = 5), pancreas (n = 5), colon/rectum (6), liver (n = 11), gallbladder (n = 1), and retroperitoneum (n = 2). Eighteen (60 %) patients experienced postoperative liver failure of which 7 (23 %) patients required deviation from the clinical course or management. There was one mortality due to grade C liver failure and hepatorenal syndrome. On multivariate analysis, only age (>55 years) was found to be statistically significant to predict postoperative liver failure (p = 0.024). CONCLUSION: Liver dysfunction remains a major problem during the postoperative phase of major gastrointestinal cancer resections. However, less than one fourth of well-selected patients will develop significant postoperative liver failure. This incidence may be further reduced if the selection is restricted to younger patients.
Subject(s)
Abdominal Neoplasms/complications , Abdominal Neoplasms/surgery , Liver Cirrhosis/complications , Liver Failure/etiology , Postoperative Complications/etiology , Adult , Age Factors , Aged , Cohort Studies , Female , Forecasting , Humans , Incidence , India/epidemiology , Liver Cirrhosis/etiology , Liver Failure/epidemiology , Male , Middle Aged , Multivariate Analysis , Patient Selection , Postoperative Complications/epidemiology , Prospective Studies , Risk FactorsABSTRACT
INTRODUCTION: Gallbladder torsion is a rare entity, which is often difficult to diagnose preoperatively. Since its first description in 1898 by Wendel, there have been over 500 documented cases in the literature. It is defined as rotation of the gallbladder on its mesentery along the axis of the cystic duct and cystic artery. Gallbladder torsion is more frequently encountered in the elderly with peak incidence in the 65-75 year old group, and a 3:1 female predominance. Gallbladder torsion typically presents as an acute abdomen requiring emergency surgery, and most cases are found as a surprise at surgery since preoperative diagnosis of gallbladder torsion is difficult. We report a case of acute gallbladder torsion in an elderly male and review the clinical aspect of gallbladder torsion. CASE REPORT: A 54-year old male presented to our department with a 5-day history of sudden onset colicky abdominal pain associated with vomiting, progressive abdominal distension and fever. Laparotomy through a chevron incision was performed and findings at operation included a gallbladder, which was necrotic and gangrenous, not attached to the liver by any mesentery. It was hanging by the attachments of cystic duct and cystic artery only, with a 360-degree clockwise torsion. CONCLUSION: Gallbladder torsion is rare surgical emergency which requires a high index of suspicion for early preoperative diagnosis and prompt intervention. Treatment consists of cholecystectomy with a prior detorsion to avoid injury to the common duct.
