Peripheral vascular injuries: diagnosis, management, out come, and review of risk Factors

The aim of this study is to retrospectively analyse our data regarding patients with vascular injuries admitted to Al-Noor hospital, reviewing the diagnosis, management, outcomes and identifying the risk factors associated with limb loss. Between November 2003 and January 2006, prospectively collected data for 152 patients with vascular injuries were reviewed and analysed retrospectively. The data were obtained from data base of all the hospital admissions. 88 [57.9%] patients were due to blunt trauma. In 52 [34.2%] patients the injury was due to penetrating wounds and 12 [7.3%] patients sustained firearm injuries. The upper limb was affected in 68 [44.7%] patients, lower limb in 65 [42.8%] patients, neck in 12 [7.9%] patients and pelvis in 7 [4.6%] patients. 151 arterial injuries and 28 venous injuries. Brachial artery was the most common type of injury, 36 [20.1%] of the injuries, 29 [16.2%] popliteal artery injuries, superficial femoral artery injuries were 14 [7.8%'], and 14 [7.8%] were ulnar artery injuries. 80 patients had associated fractures and dislocations. Supracondylar fracture of the numerous was the commonest [28]. Extensive soft tissue injury and open fracture were present in 30 patients, 65 of the arterial injuries were managed by vein graft repair. 62 fasciotomies were done, 50 for lower limb and 12 for upper limb injuries. 5 of our patients with combined musculoskeletal and vascular injuries of the lower limb underwent primary vascular shunt insertion, 5 arteries and 2 veins. We had 12 patients underwent amputation and 3 patients died during their hospitalisation. Blunt trauma is more serious than penetrating injuries. The most significant risk factor for limb loss was failure of revascularization

Upper limb arterial injury: Management and Outcome

In this study we are aiming to document and analyse the roles of arterial damage and associated injuries on long-term functional outcomes after upper extremity arterial trauma. In this retrospective study we reviewed patients who presented with an arterial injury to the upper limb during the period between [2003 to 2006]. The location and management of the arterial injuries, the nature and severity of concomitant nerve injuries and the overall degree of disability in the survivors were determined. 68 patients were included in this study. 34 patients [50%] sustained blunt injuries, 33 [48.5%] were presented with penetrating injuries, and one patient sustained firearm injury. The most common site of arterial injury was the brachial artery 36 patients [52.9%]. The most common method of surgical management was an autogenous vein interposition graft, placed in 24 patients [35.3%]. 28 patients were suffered serious upper limb fractures such as supracondylar fracture humerous. There were 19 nerve injuries. Residual disability was present in 13 patients [19%]. Only 2 patients had complete recovery of the injured nerves. Associated injuries, rather than the vascular injury, are the cause of long-term disability in the multisystem trauma victim who has upper extremity arterial injury

Proliferation of liver cells chronic liver disease: a study of liver in biopsies using immunohistochemical localization of prolifrating cell nuclear antigen

A significant proportion of chronic liver disease [CLD], consisting of chronic hepatitis and liver cirrhosis, results from chronic subclinical infection by hepatitis B and C viruses, HBV and HCV[1]. This chronic hepatitis [CH] is a forerunner of liver cirrhosis [LC] and may further progress to hepatocellular carcinoma[2-3]. The association of cirrhosis with hepatocellular carcinoma [HCC] is also well documented[4]. The exact mechanism of viral hepatocarcinogenesis is yet to be clearly defined[5]. Possibly the persistent liver cell necrosis and the resultant irregular regeneration[6]. The proliferative rate of regenerating hepatocytes may be an important pathogenetic and prognostic factor in chronic liver disease[7]. A number of markers have been used in the assessment of the proliferative status of cells, like bromodeoxyuridine[8], Ki-67[9] and DNA polymerase alpha[10]. Techniques utilizing these markers are complex, however, and require fresh or snap frozen tissue, except for Ki-67, which can be used on paraffin sections. Proliferating cell nuclear antigen [PCNA], an accessory protein of DNA polymerase delta, is one of the best markers for evaluating cell proliferation in studies on retrospective material, since the antigen can be localized in routine formalin-fixed paraffin-embedded tissue[7, 11-14]. Limited reports are available on the proliferation kinetics of normal human livers, though in recent years several studies reported on hepatocytic proliferation rates in acute and chronic liver diseases. Normal hepatocytes are generally quiescent and divide very slowly[15-17] High proliferative rates have been reported in hepatocellular carcinoma, cirrhosis and acute hepatic failure[11, 18-22]. Nakamura et al., [7] have shown that there is no significant difference in PCNA-labeling indices between chronic viral hepatitis types B and C. With increasing knowledge of the biology of hepatitis C virus infection, information on hepatocytic proliferation kinetics is emerging now. In a recent study on the prevalence of HBV- and HCV-associated chronic liver diseases in liver biopsy material over the last decade, we observed a steady rise of HCV-associated diseases and a decline in HBV-associated ones[23]. Chronicity of HCV infection leads to CH and LC much more frequently than chronic infection by other hepatitis viruses[24], and the former infection shows a higher degree of association with hepatocellular carcinoma in several parts of the world[25]. Therefore, we considered it worthwhile to examine for hepatocytic proliferation using PCNA-labeling in our material of chronic liver diseases and to note any differences between hepatitis B- and C-associated diseases

Cytokines' profile in fulminant hepatic failure: effect of hepatocyte transplantation

We used a previously described animal model of fulminant hepatic failure [FHF] to study the effect of hepatocyte transplantation [HcTx] on the cytokine profile. Three groups of Sprague Dawley rats were used. Group I [n=30] received intrasplenic HcTx. Group II [n=12] received intrasplenic injection of saline. Two days later, both groups underwent surgically induced FHF. Group III [n=30] underwent sham operation. Six animals of each group were euthanized preoperatively and on postoperative days 1, 7, 14 and 28 to study plasma cytokines; hepatocyte growth factor [HGF] and transforming growth factor beta one [TGF-beta 1]. Preoperatively, and after hepatocyte transplantation, Group I had a higher level of hepatocyte growth factor [HGF] than Groups II and III. On postoperative day 1, Group I had low levels of HGF and TGF-beta 1 and Group lI had the highest levels among the three groups. No animals in Group II survived beyond day 3 postoperatively. On day 14, HGF showed a rise in Group I as compared with Group III. HcTx has modified the level of cytokines in favor of liver regeneration in FHF rats

Up-regulation of the tumor suppressor gene P53 and WAF1 gene by IP6 in HPG2 human hepatocellular carcinoma cell line

Inositol hexaphosphate [InsP6 or IP6] is a naturally occurring polyphosphorylated carbohydrate that is present in substantial amounts in almost all plant and mammalian cells. It was recently recognized to possess multiple biological functions. IP6 exerts its effects on the body by controlling cell division. It reduces the rate of cellular proliferation, both in vivo and in vitro, and has exhibited an ability to reduce DNA synthesis and also causes differentiation of various cell lines, including HT-29 human colon carcinoma cell. We hypothesize that the tumor suppressor genes such as p53 and WAF1 may be involved in mediating the antineoplastic action of IP6. p53 acts as a molecular policeman preventing propagation of genetically damaged cells; it causes the cells to arrest in the G1 phase of cell cycle, and regulates the level of p21 wafl which acts as a growth inhibitor. We therefore investigated the effects of IP6 on the expression of p53 and WAF1/p21 in HP-G2 human hepatocellular carcinoma by immunocytochemistry. Our immunocytochemical studies with anti p53 antibodies [wild type-PAb246 and Pab 1620] and anti p21 wafl [EA10] antibodies demonstrated an increased level of p53 and p21 wafl after 3 and 6 days of treatment with 3.3 and 5 mM and 8 mM IP6. This increase was dose-dependent and a definite time-dependent increase was not observed. These data demonstrate that IP6 up-regulates the expression of the tumor suppressor gene p53 and p21waf1 gene and their modulation may be one of the mechanisms of the antineoplastic action of IP6 since loss of p53 function enhances cancer cells resistance to chemotherapeutic agents, the stimulating function of IP6 on p53 makes it an attractive adjuvant chemotherapeutic agent as well