Endoscopic management of bariatric surgery complications: what the gastroenterologist should know.

Obesity is a serious disorder in almost the entire world. It is an important risk factor for a series of conditions that affect and threaten health. Currently, bariatric surgery is the most effective treatment for morbid obesity, and in addition to the resulting weight loss, it reduces morbidity in this population. There has been a significant increase in the number of obese patients operated on. Despite the success of bariatric surgery, an important group of patients still present with major postoperative complications. In order for endoscopy to effectively contribute to the diagnosis and treatment of complications deriving from obesity surgery, the gastroenterologist must be aware of the particularities involved in bariatric surgery. The present article is a review of the resulting anatomic aspects of the main surgical techniques employed, the most common postoperative symptoms, the potential complications, and the possibilities that endoscopic diagnosis and treatment offer. Endoscopy is a growing and continuously evolving method in the treatment of bariatric surgery complications. The aim of this review is to contribute to the preparation of gastroenterologists so they can offer adequate endoscopic diagnosis and treatment to this high-risk population.

Aerobic training prevents dexamethasone-induced peripheral insulin resistance.

This study investigated how proteins of the insulin signaling cascade could modulate insulin resistance after dexamethasone (Dexa) treatment and aerobic training. Rats were distributed into 4 groups: sedentary control (SC), sedentary+Dexa (SD), trained control (TC), and trained+Dexa (TD), and underwent aerobic training for 70 days or remained sedentary. Dexa was administered during the last 10 days (1 mg · kg(-1) per day i. p.). After 70 days, an intraperitoneal glucose tolerance test (ipGTT) was performed. Protein levels of IRS-1, AKT, and PKC-α in the tibialis anterior (TA) muscle were identified using Western blots. Dexa treatment increased blood glucose and the area under the curve (AUC) of ipGTT. Training attenuated the hyperglycemia and the AUC induced by Dexa. Dexa reduced IRS-1 (- 16%) and AKT (- 43%) protein level with no changes in PKC-α levels. Moreover, these effects on IRS-1 and AKT protein level were prevented in trained animals. These results show for the first time that aerobic exercise prevented reductions of IRS-1 and AKT level induced by Dexa in the TA muscle, suggesting that aerobic exercise is a good strategy to prevent Dexa-induced peripheral insulin resistance.

Calcitonin receptor-like receptor and receptor activity modifying protein 1 in the rat dorsal horn: localization in glutamatergic presynaptic terminals containing opioids and adrenergic alpha2C receptors.

Calcitonin gene-related peptide (CGRP) is abundant in the central terminals of primary afferents. However, the function of CGRP receptors in the spinal cord remains unclear. CGRP receptors are heterodimers of calcitonin receptor-like receptor (CRLR) and receptor activity modifying protein 1 (RAMP1). We studied the localization of CRLR and RAMP1 in the rat dorsal horn using well-characterized antibodies against them, which labeled numerous puncta in laminae I-II. In addition, RAMP1 was found in cell bodies, forming patches at the cell surface. The CRLR- and RAMP1-immunoreactive puncta were further characterized using double and triple labeling. Colocalization was quantified in confocal stacks using Imaris software. CRLR did not colocalize with primary afferent markers, indicating that these puncta were not primary afferent terminals. CRLR- and RAMP1-immunoreactive puncta contained synaptophysin and vesicular glutamate transporter-2 (VGLUT2), showing that they were glutamatergic presynaptic terminals. Electron microscopic immunohistochemistry confirmed that CRLR immunoreactivity was present in axonal boutons that were not in synaptic glomeruli. Using tyramide signal amplification for double labeling with the CRLR and RAMP1 antibodies, we found some clear instances of colocalization of CRLR with RAMP1 in puncta, but their overall colocalization was low. In particular, CRLR was absent from RAMP1-containing cells. Many of the puncta stained for CRLR and RAMP1 were labeled by anti-opioid and anti-enkephalin antibodies. CRLR and, to a lesser extent, RAMP1 also colocalized with adrenergic alpha(2C) receptors. Triple label studies demonstrated three-way colocalization of CRLR-VGLUT2-synaptophysin, CRLR-VGLUT2-opioids, and CRLR-opioids-alpha(2C) receptors. In conclusion, CRLR is located in glutamatergic presynaptic terminals in the dorsal horn that contain alpha(2C) adrenergic receptors and opioids. Some of these terminals contain RAMP1, which may form CGRP receptors with CRLR, but in others CRLR may form other receptors, possibly by dimerizing with RAMP2 or RAMP3. These findings suggest that CGRP or adrenomedullin receptors modulate opioid release in the dorsal horn.

Immunological strategies to fight skin cancer.

Skin cancer is the most common human cancer, and is currently considered a global epidemic. Recently, there has been a growing interest in immunomodulators, or up-regulators of the immune response, for the treatment and cure of various forms of skin cancer, including melanoma and nonmelanoma skin cancers, cutaneous T-cell lymphoma, Kaposi's sarcoma, cutaneous extramammary Paget's disease, and vulvar intraepithelial carcinoma neoplasia. Strategies to augment the host's immune response against cancer cells and/or cancer cell antigenicity have been investigated, including recombinant cytokines, immunomodulators, dendritic cell immunization, tumor antigen vaccination, T-cell-based immunotherapy, and gene therapy. Although the current standard of care for most of these cancers includes Mohs micrographic surgery, curettage, and cryo-, laser-, or radiotherapy, immunomodulators are becoming essential in the treatment of patients who are poor surgical candidates and/or require noninvasive therapy.

[Effects of Bothrops alternatus venom of Argentina on muscle and different organs in mices]. / Efectos del Veneno de Bothrops alternatus de Argentina Sobre Músculo y Distintos Organos de Ratones.

Bothrops alternatus venom was inoculated in gastrocnemius muscle of mice between 18 and 20g. The dose was 50 micrograms in 0.1 ml in ClNa 0.85% solution. Groups of 5 animals were sacrified between 3, 6 and 12 hours after inoculation. Hystopathology was performed with muscle and different organs fixed with Bouin. The venom reproduced a local inflammatory reaction. Histopathology observations of muscle revealed myolytic and coagulative necrosis. There and six hours after inoculation, hepatocellular degeneration and tumefaction in area of central veins was observed. In kidneys there were cortical congestion and hydropic tumefaction of proximal and distal tubules. There were no anormality in heart, lung and brain.

Carbon tetrachloride-induced liver cell injury in the Mongolian gerbil (Meriones unguiculatus).

1. Male Mongolian gerbils (Meriones unguiculatus) liver activates CCl4 to free radicals that bind covalently to cellular components (CB) and stimulate a lipid peroxidation (LP) process to a larger extent than the rat liver. 2. CCl4 administration results in a less intense necrogenic effect in gerbils than in rats and does not cause fatty liver. 3. CCl4 causes less intense effects on liver ultrastructure or calcium metabolism but more marked depression of glucose 6 phosphatase activity (G6P-ase) in gerbils than in rats. 4. Results suggest that a better ability of gerbil liver to keep calcium homeostasis than rat liver might be the cause of their relative resistance to necrosis. Higher intensity of CB and LP in gerbils than in rats might explain more intense effects on G6P-ase.

Bothrops alternatus envenoming in young dogs

Bothrops alternatus venom was intramuscularly inoculated (3mg/kg) into 12 dogs, 30 to 65 days old. Spontaneou bleeding commenced twenty minutes later. Blood samples obtained 3 and 20 minutes after venom inoculation presented spontaneuous clotting formation. Plasmatic fibrinogen decreased within 3 minutes. Partial thromboplastin time (PTT) and one-stage prothrombin time (PT) were found. Plasma did not coagulate 40 minutes after inoculation. Platelet counts did not vary but their function was altered. Histopathology pointed out severe muscular necrosis and massive hemorrhage in the inoculation area. Regional ganglia showed intense hemorrhage. The 45 and 65-day-old animals showed alveolar thickening of the septum and generalized congestion, but the 30-day-old animals showed thrombosis of small arteries and arterioles. Renal lesions were different with the age. Cortical tubular necrosis was present in puppies, and intense cortical tubular hydropic degeneration was present in adult dogs. Thymus hemorrhage and necrosis were present.