Extensive small intestinal wall thickening in a cat

Experimental Study on Acute Ischemic Small Bowel Changes Induced by Superselective Embolization of Superior Mesenteric Artery Branches with N-Butyl Cyanoacrylate

Hereditary angioedema (HAE) is a hereditary disorder (deficiency of C1 esterase inhibitor) with spontaneous cutaneous and subcutaneous edemas, which involve the gastrointestinal tract in 50 - 75 %. Recurrent abdominal pain attacks in younger patients with an ultrasonographic evidence of aszites (up to 1 - 2 litres are frequent), should always let think of a HAE. Additionally in one female patient we found pleural effusion repeatedly during the episodes. HAE typically shows segments of GI-tract with a marked wall thickening. In our patients stomach (2 x), small bowel (2 x) and colon (1 x) were involved. Obstruction of the lumen by the edema may cause vomiting or ileus. By means of high-resolution sonography we could show for the first time that only mucosal and submucosal layer were affected, the L. muscularis propria was preserved. Characteristic was a hypoechoic thickening of the interior layers of the wall: In one patient we found anechoic lacunae within the mucosal layer, probably corresponding to a bullous edema. An accurate ultrasonic examination enables a reliable judgement of the severity level of HAE. It can contribute in this way to the decision whether the application of C1-INH-concentrate is necessary or not.

The Great Imitator

We here describe a case of apathetic thyrotoxicosis in a 16-year-old female subject who presented with a range of non-specific symptoms. Apart from a history of significant weight loss, there were no other signs or symptoms indicative of hyperthyroidism. The diagnosis was made incidentally upon thyroid function testing, and there was a prompt clinical response to anti-thyroid therapy. The diagnostic pitfalls of this unusual presentation in the young are highlighted. A history of weight loss and a clinical index of suspicion will lead to the diagnosis, which is readily confirmed biochemically.

Sleep is hypothesized to interact with weight gain and loss; however, modelling this relationship remains elusive. Poor sleep perpetuates a cascade of cardiovascular and metabolic consequences that may not only increase risk of adiposity, but also confound weight loss efforts. We conducted a scoping review to assess the research on sleep and weight loss interventions. We searched six databases for studies of behavioural weight loss interventions that included assessments of sleep in the general, non-clinical adult human population. Our synthesis focused on dimensions of Population, Intervention, Control, and Outcomes (PICO) to identify research and knowledge gaps. We identified 35 studies that fell into one of four categories: (a) sleep at baseline as a predictor of subsequent weight loss during an intervention, (b) sleep assessments after a history of successful weight loss, (c) concomitant changes in sleep associated with weight loss and (d) experimental manipulation of sleep and resulting weight loss. There was some evidence of improvements in sleep in response to weight-loss interventions; however, randomized controlled trials of weight loss interventions tended not to report improvements in sleep when compared to controls. We conclude that baseline sleep characteristics may predict weight loss in studies of dietary interventions and that sleep does not improve because of weight loss alone. Future studies should enrol large and diverse, normal, overweight and obese short sleepers in trials to assess the efficacy of sleep as a behavioural weight loss treatment.

This is a case report of a 57-year old farmer who presented with a 4 months history of dysphagia and weight loss. Upper gastrointestinal endoscopy revealed submucosal swellings with overlying ulcers at mid to lower part of esophagus. Repeated histopathological evaluation of endoscopic esophageal tissue biopsies showed nonspecific findings. Endoscopic ultrasound showed a hypoechoic mass at submucosal layer with periesophageal lymphadenopathy. Endosonogram guided FNA materials depicted caseating granulomas. Patient was managed with anti-tuberculosis therapy. Follow up endosonography after therapy revealed resolution of the growth and the mediastinal lymph node enlargement and patient was symptomatically improved.
 J Bangladesh Coll Phys Surg 2020; 38(3): 150-154

Although both overweight and body weight fluctuation are related to chronic disease risk, little is known about the history of and reasons for body weight change in the general population. This paper reports the incidence of intentional and unintentional weight loss episodes during adulthood in a population-based sample of 26,261 women aged 55 to 69 years. Intentional weight loss episodes of each of four amounts (5-9, 10-19, 20-49, 50+ lbs.) and unintentional weight loss episodes of 20 or more lbs. were recalled for each of three age periods (18-39, 40-54, 55+ years). At least one intentional weight loss episode of 5 or more lbs. was reported by 69% of women, 46% reported at least one intentional weight loss episode of 10 or more lbs, and 25% reported at least one intentional weight loss episode 20 or more lbs. At least one unintentional weight loss episode of 20 or more lbs. was reported by 29% of the women. Reasons for weight losses of 20 or more lbs. were also recalled. Women who had intentionally lost 20 or more lbs. were more likely to report weight losses due to low-calorie diets, exercise and weight loss groups, while women who had unintentionally lost 20 or more lbs. were more likely to report weight losses due to depression or stress. These findings question the common assumption that weight losses in adult women are primarily intentional and emphasize the need to distinguish the reasons for weight loss in studies examining the relationship between body weight changes and health outcomes.

Background: The success of adipose stromal/stem cell (ASC)-based therapies may depend on donor characteristics such as body mass index (BMI). A high BMI may negatively impact the therapeutic potential of ASCs, but the effects of weight loss on ASC-mediated immunoregulation have not been extensively studied. Methods: ASCs were obtained from donors with obesity (obASCs) undergoing bariatric surgery and from the same donors after weight loss (wlASCs). Plasma samples, adipose tissue histology, and ASC characteristics, such as mitochondrial respiration and inflammatory factors, were studied before and after weight loss. The immunomodulatory capacity of ob/wlASCs was evaluated in cocultures with prepolarized and preactivated proinflammatory (M1) and anti-inflammatory (M2) macrophages by determining macrophage surface markers, gene expression, and cytokine secretion. Results: Weight loss significantly decreased plasma leptin levels and increased adiponectin levels. After weight loss, crown-like structures (CLSs) were undetectable, and the adipocyte size decreased. Weight loss significantly improved mitochondrial respiration in ASCs and resulted in a notable increase in their proliferative capacity. The proinflammatory marker genes tumor necrosis factor alpha (TNF-α), chemokine ligand 5 (CCL5), and cyclooxygenase-2 (COX2), as well as the proinflammatory cytokine interleukin 12p70 (IL-12p70), were significantly downregulated, while the anti-inflammatory gene tumor necrosis factor-inducible gene 6 (TSG6) was also significantly downregulated in ASC monocultures after weight loss. Following weight loss, ASCs exhibited increased proinflammatory properties when cocultured with macrophages, characterized by the downregulation of anti-inflammatory factors, along with the upregulation of several proinflammatory factors, compared with the effects of macrophage monocultures. Conversely, wlASCs demonstrated improved immunosuppressive functions in coculture with macrophages, as indicated by the upregulation of TSG6 gene expression and interleukin 4 (IL-4) secretion. Conclusions: Weight loss improved donors' metabolic health and partially recovered ASCs' anti-inflammatory gene expression and cytokine secretion profiles in monocultures. However, it was inadequate to fully restore the immunosuppressive functions of ASCs in cocultures with macrophages. Therefore, not only donor BMI but also weight loss history, among other donor characteristics, might be considered for optimal ASC-based therapy.

Potato fiber protects the small intestinal wall against the toxic influence of acrylamide

Neoechinorhynchus buttnerae (Acanthocephala) infection in farmed Colossoma macropomum: A pathological approach

The histopathology induced by Camallanus oxycephalus and Spinitectus carolini in the intestine of green sunfish Lepomis cyanellus was examined. At what is assumed to be more recent attachment sites, penetration of C. oxycephalus was restricted to the mucosal layer, causing complete destruction of the columnar epithelium. At what appeared to be older attachment sites, the parasite penetrated deep into the intestinal wall, even to the circular muscle layer. At these sites of attachment, there were flask-shaped ulcers in the mucosal and submucosal layers. Surrounding the ulcers, there was granulomatous tissue, with extensive fibrosis at the surface; the fibrosis probably reduced the loss of body fluids and blood cells from the intestinal wall. The number of goblet cells in the posterior end of the intestine increased significantly, from 92.6 cells/mm in uninfected fish to 168.4 cells/mm in fish infected with more than 5 C. oxycephalus. Adult S. carolini also causes severe damage to the intestinal wall of green sunfish. Parasite penetration was not limited to the mucosal layer. Mature worms were observed invading both the muscular and serosal layers. Penetration by the parasite was usually associated with the local loss of columnar epithelium and infiltration by lymphocytes and granulocytic leukocytes. Fibrosis in the mucosal layer was commonly observed. There was goblet cell hyperplasia in the anterior portion of the intestine, with numbers of goblet cells increasing from 64.4 cells/mm in uninfected fish to 95.0 cells/mm in heavily infected fish.

Evaluation of an Endorectal Electrode for Performing Focused Irreversible Electroporation Ablations in the Swine Rectum

Background:The purpose of this research was to determine the index that contributes the most to assessing the effectiveness of weight loss 1 year following bariatric surgery and to implement it as the clinical outcome to develop and confirm a nomogram to predict whether bariatric surgery would be effective.Methods:Patient information was extracted from the Chinese Obesity and Metabolic Surgery Database for this retrospective study. The most contributing weight loss effectiveness evaluation index was created using canonical correlation analysis (CCA), and the predictors were screened using logistic regression analysis. A nomogram for estimating the likelihood of effectiveness of weight loss was constructed, and its performance was further verified.Results:Information was obtained for 540 patients, including 30 variables. According to the CCA, ≥25 percentage total weight loss was found to be the most correlated with patient information and contribute the most as a weight loss effectiveness evaluation index. Logistic regression analysis and nomogram scores identified age, surgical strategy, abdominal circumference, weight loss history, and hyperlipidemia as predictors of effectiveness in weight loss. The prediction model’s discrimination, accuracy, and clinical benefit were demonstrated by the consistency index, calibration curve, and decision curve analysis.Conclusions:The authors determined a 25 percentage total weight loss as an index for weight loss effectiveness assessment by CCA and next established and validated a nomogram, which demonstrated promising performance in predicting the probability of effectiveness of weight loss in bariatric surgery. The nomogram might be a valuable tool in clinical practice.

The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-beta) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-beta and its downstream target CTGF in patients with cholecystolithiasis. Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-beta1 and CTGF in the gallbladder tissue samples. By northern blot analysis there was an enhanced TGF-beta1 mRNA expression (eightfold increase; P < 0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P < 0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-beta1 and CTGF was observed. In addition, TGF-beta1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-beta1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P < 0.04, r = 0.5). Our data indicate that TGF-beta and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the "TGF-beta pathway," predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder.

Changes of the extracellular matrix as a risk factor for anastomotic leakage after large bowel surgery