Опухоль брюшной стенки - грыжа спигелевой линии, содержащая метастатическую карциному с невыявленным первичным очагом

АДЕНОКАРЦИНОМАБРЮШНАЯ СТЕНКАГРЫЖИКАРЦИНОМАКОЛОРЕКТАЛЬНЫЕ НОВООБРАЗОВАНИЯНОВООБРАЗОВАНИЯТОЛСТАЯ КИШК

Seronegative Herpes simplex Associated Esophagogastric Ulcer after Liver Transplantation

Herpes simplex infection is characterized by acute or subacute infection, often followed by a chronic carrier state. Consecutive recurrences may flare up if immunocompromise occurs. Herpes simplex associated esophagitis or duodenal ulcer have been reported in immunocompromised patients due to neoplasm, HIV/AIDS or therapeutically induced immune deficiency. Here we report the case of an HSV-DNA seronegative patient who developed grade III dysphagia 13 days after allogeneic liver transplantation. Endoscopy revealed an esophageal-gastric ulcer, and biopsy histopathology showed a distinct fibroplastic and capillary ulcer pattern highly suspicious for viral infection. Immunohistochemistry staining revealed a distinct nuclear positive anti-HSV reaction. Antiviral therapy with acyclovir and high-dose PPI led to a complete revision of clinical symptoms within 48 h. Repeat control endoscopy after 7 days showed complete healing of the former ulcer site at the gastroesophageal junction. Although the incidence of post-transplantation Herpes simplex induced gastroesophageal disease is low, the viral HSV ulcer may be included into a differential diagnosis if dysphagia occurs after transplantation even if HSV-DNA PCR is negative

beta3-Adrenergic receptor stimulation induces E-selectin-mediated adipose tissue inflammation

Inflammation induced by wound healing or infection activates local vascular endothelial cells to mediate leukocyte rolling, adhesion, and extravasation by up-regulation of leukocyte adhesion molecules such as E-selectin and P-selectin. Obesity-associated adipose tissue inflammation has been suggested to cause insulin resistance, but weight loss and lipolysis also promote adipose tissue immune responses. While leukocyte-endothelial interactions are required for obesity-induced inflammation of adipose tissue, it is not known whether lipolysis-induced inflammation requires activation of endothelial cells. Here, we show that beta(3)-adrenergic receptor stimulation by CL 316,243 promotes adipose tissue neutrophil infiltration in wild type and P-selectin-null mice but not in E-selectin-null mice. Increased expression of adipose tissue cytokines IL-1beta, CCL2, and TNF-alpha in response to CL 316,243 administration is also dependent upon E-selectin but not P-selectin. In contrast, fasting increases adipose-resident macrophages but not neutrophils, and does not activate adipose-resident endothelium. Thus, two models of lipolysis-induced inflammation induce distinct immune cell populations within adipose tissue and exhibit distinct dependences on endothelial activation. Importantly, our results indicate that beta(3)-adrenergic stimulation acts through up-regulation of E-selectin in adipose tissue endothelial cells to induce neutrophil infiltration

IL-1 signaling in obesity-induced hepatic lipogenesis and steatosis.

Non-alcoholic fatty liver disease is prevalent in human obesity and type 2 diabetes, and is characterized by increases in both hepatic triglyceride accumulation (denoted as steatosis) and expression of pro-inflammatory cytokines such as IL-1β. We report here that the development of hepatic steatosis requires IL-1 signaling, which upregulates Fatty acid synthase to promote hepatic lipogenesis. Using clodronate liposomes to selectively deplete liver Kupffer cells in ob/ob mice, we observed remarkable amelioration of obesity-induced hepatic steatosis and reductions in liver weight, triglyceride content and lipogenic enzyme expressions. Similar results were obtained with diet-induced obese mice, although visceral adipose tissue macrophage depletion also occurred in response to clodronate liposomes in this model. There were no differences in the food intake, whole body metabolic parameters, serum β-hydroxybutyrate levels or lipid profiles due to clodronate-treatment, but hepatic cytokine gene expressions including IL-1β were decreased. Conversely, treatment of primary mouse hepatocytes with IL-1β significantly increased triglyceride accumulation and Fatty acid synthase expression. Furthermore, the administration of IL-1 receptor antagonist to obese mice markedly reduced obesity-induced steatosis and hepatic lipogenic gene expression. Collectively, our findings suggest that IL-1β signaling upregulates hepatic lipogenesis in obesity, and is essential for the induction of pathogenic hepatic steatosis in obese mice

A model of ischemic isolated acute liver failure in pigs: standardizing monitoring and treatment

Acute liver failure (ALF) models in pigs have been widely used for evaluating newly developed liver support systems. But hardly any guidelines are available for the surgical methods and the clinical management

Physiological concentrations of IL-1β elicit a biological response in primary mouse hepatocytes to increase TG accumulation and lipogenic gene expression.

<p>Primary hepatocytes from wild type mice were isolated via perfusion, stimulated with the indicated doses of recombinant mouse IL-1β and evaluated after 24-hours. <i>A</i>.) Cells were fixed in 10% formalin and stained with Oil-Red-O to assess TG accumulation. <i>B</i>.) Fas expression was analyzed in primary hepatocyte cell lysates after a 24-hour stimulation with the indicated doses of recombinant IL-1β and normalized to β-actin. <i>C</i>). Relative densitometry from B. <i>D</i>.) TGs were extracted and measured after a 24-hour stimulation with recombinant IL-1β (10 ng/mL) and normalized to the amount of total protein. The data are representative of 4 experiments. All stimulations were performed in duplicate. Values represent the mean ± SEM. A paired student’s t<i>-</i>test was used for comparisons between groups <i>*</i>P≤0.05, ***P≤0.001.</p

Pharmacological intervention via inhibition of IL-1 signaling improves the glucose tolerance in DIO mice.

<p>Wild type mice were fed a HFD for 13 weeks. At 32 days prior to sacrifice, mice were started on daily injections of IL-1Ra (Anakinra; 32 mg/kg) or saline by i.p. administration. Data are representative of 10 mice per group. At the end of 13 weeks, Anakinra-treated mice displayed no changes in <i>A.</i>) total animal body weight and were more glucose tolerant as demonstrated by a reduction in <i>B</i>.) area under the curve (AUC) for the intraperitoneal GTT and <i>C</i>.) fasting insulin levels. Values represent the mean ± SEM. An unpaired student’s t<i>-</i>test was used for comparisons between groups. <i>*</i>P≤0.05, **P≤0.01.</p