Regulation and function of IL-22 in peritoneal adhesion formation after abdominal surgery.

Peritoneal adhesion occurs frequently after gastrointestinal/gynecological surgery. Tissue repair and regeneration are very important during this process. IL-22 is an important cytokine that is secreted from immune cells but functions on mesenchymal cells, such as mesothelial cells. The objective of this study was to investigate the roles of IL-22 and its regulators during adhesion formation. Postsurgical peritoneal drainage fluid from patients and rodent models was examined by enzyme-linked immunosorbent assay and fluorescence-activated cell sorting. It was observed that IL-22 expression in the abdominal cavity was rapidly induced 12 hours after surgery and then slowly decreased to a lower, steady level for up to 7 days after surgery. However, neutralizing IL-22 at the time point at which the highest level of expression was observed failed to reduce adhesion, but neutralizing IL-22 at a later time point, i.e., 3 days after surgery, prevented adhesion significantly. The IL-22 receptor was induced on the mesothelial membrane, and IL-22BP, an inhibitor of IL-22, was reduced 3 days after surgery. Furthermore, IFN-γ was identified to have the ability to induce IL-22R, and IL-18, which was induced by the infiltrating macrophages, was found to inhibit IL-22BP expression both in vivo and in vitro. Together, these data suggest that IL-22 may promote adhesion formation and that the regulation of IL-22, IL-22R, and IL-22BP may have therapeutic potential to prevent adhesion formation after surgery without disturbing the normal immune process.

The effects of bupropion alone and combined with naltrexone on weight loss: a systematic review and meta-regression analysis of randomized controlled trials.

BACKGROUND: The global prevalence of obesity and overweight is a significant concern in the field of public health. However, addressing and combating these conditions pose considerable challenges. Numerous interventional studies have been conducted to assess the possible impact of bupropion on weight reduction. The primary objective of this study was to conduct a comprehensive investigation into the effects of bupropiona alone and in combination with naltrexone on weight, body mass index (BMI), and waist circumferences (WC). METHODS: A systematic search was conducted in five databases using established keywords. The purpose of this search was to uncover controlled trials that examined the impact of bupropion, either as a standalone intervention or in combination with naltrexone, on weight loss outcomes. The random-effects model analysis was used to provide pooled weighted mean difference and 95% confidence intervals. RESULTS: Twenty five studies with 22,165 participants' were included in this article. The pooled findings showed that bupropion administration has an effect on lowering weight (WMD: -3.67 kg, 95% CI: -4.43 to -2.93) and WC (WMD: -2.98 cm, 95% CI -3.78 to -2.19) in compared with control groups. The analysis also showed that the effects of the present intervention on weight and WC during the intervention are > 26 weeks and ≤ 26 weeks compared to the other group, respectively. In addition, changes in weight loss and WC after receiving bupropion together with naltrexone were more compared to bupropion alone. CONCLUSIONS: In conclusion, the addition of combination therapies like bupropion and naltrexone to lifestyle modifications including diet would cause significant weight loss.

Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats.

Nesfatin-1, a novel hypothalamic peptide, inhibits nocturnal feeding behavior and gastrointestinal motility in rodents. The effects of nesfatin-1 on gastrointestinal secretory function, including gastric acid production, have not been evaluated. Nesfatin-1 was injected into the fourth intracerebral ventricle (4V) of chronically cannulated rats to identify a nesfatin dose sufficient to inhibit food intake. Nesfatin-1 (2 µg) inhibited dark-phase food intake, in a dose-dependent fashion, for >3 h. Gastric acid production was evaluated in urethane-anesthetized rats. Nesfatin-1 (2 µg) was introduced via the 4V following endocrine stimulation of gastric acid secretion by pentagastrin (2 µg·kg(-1)·h(-1) iv), vagal stimulation with 2-deoxy-D-glucose (200 mg/kg sc), or no stimulus. Gastric secretions were collected via gastric cannula and neutralized by titration to determine acid content. Nesfatin-1 did not affect basal and pentagastrin-stimulated gastric acid secretion, whereas 2-deoxy-D-glucose-stimulated gastric acid production was inhibited by nesfatin-1 in a dose-dependent manner. c-Fos immunofluorescence in brain sections was used to evaluate in vivo neuronal activation by nesfatin-1 administered via the 4V. Nesfatin-1 caused activation of efferent vagal neurons, as evidenced by a 16-fold increase in the mean number of c-Fos-positive neurons in the dorsal motor nucleus of the vagus (DMNV) in nesfatin-1-treated animals vs. controls (P < 0.01). Finally, nesfatin-induced Ca(2+) signaling was evaluated in primary cultured DMNV neurons from neonatal rats. Nesfatin-1 caused dose-dependent Ca(2+) increments in 95% of cultured DMNV neurons. These studies demonstrate that central administration of nesfatin-1, at doses sufficient to inhibit food intake, results in inhibition of vagally stimulated secretion of gastric acid. Nesfatin-1 activates DMNV efferent vagal neurons in vivo and triggers Ca(2+) signaling in cultured DMNV neurons.

Increased plasma genistein after bariatric surgery could promote remission of NAFLD in patients with obesity.

Background: Bariatric surgery is associated with a positive effect on the progress of non-alcoholic associated fatty liver disease (NAFLD). Although weight loss is the obvious mechanism, there are also weight-independent mechanisms. Methods: We collected blood samples from 5 patients with obesity before and 3 months after surgery and performed an LC-MS-based untargeted metabolomics test to detect potential systemic changes. We also constructed sleeve gastrectomy (SG) mice models. The plasma, liver and intestine samples were collected and analyzed by qPCR, ELISA and HPLC. Cohousing experiments and feces transplantation experiments were performed on mice to study the effect of gut microbiota. Genistein administration experiments were used to study the in vivo function of the metabolites. Results: Plasma genistein (GE) was identified to be elevated after surgery. Both clinical data and rodent models suggested that plasma GE is negatively related to the degree of NAFLD. We fed diet-induced obese (DIO) mice with GE, and we found that there was significant remission of NAFLD. Both in vivo and in vitro experiments showed that GE could restrict the inflammation state in the liver and thus relieve NAFLD. Finally, we used co-housing experiments to alter the gut microbiota in mice, and it was identified that sleeve gastrectomy (SG) mice had a special gut microbiota phenotype, which could result in higher plasma GE levels. By feces transplantation experiment (FMT), we found that only feces from the SG mice (and not from other lean mice) could induce higher plasma GE levels. Conclusion: Our studies showed that SG but not calorie restriction could induce higher plasma GE levels by altering the gut microbiota. This change could promote NAFLD remission. Our study provides new insights into the systemic effects of bariatric surgery. Bariatric surgery could affect remote organs via altered metabolites from the gut microbiota. Our study also identified that additional supplement of GE after surgery could be a therapy for NAFLD.

Pancreatic fat infiltration, ß-cell function and insulin resistance: A study of the young patients with obesity.

OBJECTIVE: This study aimed to investigate the relationship between pancreatic fat infiltration (PFI) and glucose metabolism disorder, ß-cell function and insulin resistance in patients with obesity. METHODS: Pancreatic fat fraction (PFF) was quantified by MRI IDEAL-IQ technique. PFF greater than 6.2 % was defined as PFI, and 34 obese patients were divided into PFI and non-PFI groups. The 5-point plasma glucose and insulin values during oral glucose tolerance test (OGTT) were recorded. OGTT-derived indices of insulin resistance and ß-cell function were calculated. RESULTS: Glucose values levels at 0-120 min during OGTT were significantly higher and ß-cell function variables were lower in PFI group than non-PFI group. While indices of insulin resistance were not significantly different between two groups. Correlation analysis showed that PFF was positively correlated with glucose levels at 0, 30 and 60 min, negatively correlated with ß-cell function variables and not significantly correlated with indices of insulin resistance. However, these associations of PFF with ß-cell function and glucose levels were only present in type 2 diabetes mellitus (T2DM) group but not in non-T2DM group. CONCLUSION: There is an association between PFI and impaired ß-cell function, and increased pancreatic fat may be a potential risk factor for the development of T2DM.

Ankyrin repeat and SOCS box containing protein 4 (Asb-4) colocalizes with insulin receptor substrate 4 (IRS4) in the hypothalamic neurons and mediates IRS4 degradation.

BACKGROUND: The arcuate nucleus of the hypothalamus regulates food intake. Ankyrin repeat and SOCS box containing protein 4 (Asb-4) is expressed in neuropeptide Y and proopiomelanocortin (POMC) neurons in the arcuate nucleus, target neurons in the regulation of food intake and metabolism by insulin and leptin. However, the target protein(s) of Asb-4 in these neurons remains unknown. Insulin receptor substrate 4 (IRS4) is an adaptor molecule involved in the signal transduction by both insulin and leptin. In the present study we examined the colocalization and interaction of Asb-4 with IRS4 and the involvement of Asb-4 in insulin signaling. RESULTS: In situ hybridization showed that the expression pattern of Asb-4 was consistent with that of IRS4 in the rat brain. Double in situ hybridization showed that IRS4 colocalized with Asb-4, and both Asb-4 and IRS4 mRNA were expressed in proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons within the arcuate nucleus of the hypothalamus. In HEK293 cells co-transfected with Myc-tagged Asb-4 and Flag-tagged IRS4, Asb-4 co-immunoprecipitated with IRS4; In these cells endogenous IRS4 also co-immunoprecipitated with transfected Myc-Asb-4; Furthermore, Asb-4 co-immunoprecipitated with IRS4 in rat hypothalamic extracts. In HEK293 cells over expression of Asb-4 decreased IRS4 protein levels and deletion of the SOCS box abolished this effect. Asb-4 increased the ubiquitination of IRS4; Deletion of SOCS box abolished this effect. Expression of Asb-4 decreased both basal and insulin-stimulated phosphorylation of AKT at Thr308. CONCLUSIONS: These data demonstrated that Asb-4 co-localizes and interacts with IRS4 in hypothalamic neurons. The interaction of Asb-4 with IRS4 in cell lines mediates the degradation of IRS4 and decreases insulin signaling.

Role of Indole-3-Acetic Acid in NAFLD Amelioration After Sleeve Gastrectomy.

BACKGROUND: This study aimed to investigate the weight-independent mechanism of sleeve gastrectomy on the relief of nonalcoholic fatty liver disease (NAFLD). METHODS: A total of 58 obese patients who had undergone sleeve gastrostomy (SG) were recruited. Plasma levels of indole-3-acetic acid (I3A), a metabolite from gut microbiota before and after SG were investigated. In addition, we had 78 C57BL/6J mice included in the study. High-fat diet (HFD) was used to induce obesity in mice. Sleeve gastrectomy (SG) was then performed. The liver of the mice was analyzed by HE and oil red staining to study lipid accumulation. Fluorescence-activated cell sorting (FACS) analysis was performed to study the phenotype of macrophages in the liver. The levels of I3A in serum, stool, and liver were tested by ELISA. Macrophages and hepatocytes were cultured in vitro and stimulated with I3A to study the effects on differentiation and proliferation/apoptosis. RESULTS: In human samples, I3A increased after SG and plasma I3A levels were positively correlated with liver CT values and negatively correlated with liver fat attenuation. In mice models, after surgery, the percentage of M2 macrophages significantly increased in the liver. Both oral gavage and in vitro stimulation of I3A could promote M2 differentiation and did not significantly affect the state of hepatocytes. CONCLUSIONS: This study suggested that increased I3A from the intestine after SG could reduce the M1/M2 ratio in the liver and thus promote relief of NAFLD in obese individuals. Graphical Abstract.

Peripheral-specific Y1 receptor antagonism increases thermogenesis and protects against diet-induced obesity.

Obesity is caused by an imbalance between food intake and energy expenditure (EE). Here we identify a conserved pathway that links signalling through peripheral Y1 receptors (Y1R) to the control of EE. Selective antagonism of peripheral Y1R, via the non-brain penetrable antagonist BIBO3304, leads to a significant reduction in body weight gain due to enhanced EE thereby reducing fat mass. Specifically thermogenesis in brown adipose tissue (BAT) due to elevated UCP1 is enhanced accompanied by extensive browning of white adipose tissue both in mice and humans. Importantly, selective ablation of Y1R from adipocytes protects against diet-induced obesity. Furthermore, peripheral specific Y1R antagonism also improves glucose homeostasis mainly driven by dynamic changes in Akt activity in BAT. Together, these data suggest that selective peripheral only Y1R antagonism via BIBO3304, or a functional analogue, could be developed as a safer and more effective treatment option to mitigate diet-induced obesity.

Expression of NALP3 in the spleen of mice with portal hypertension.

This study examined the mRNA expression of NALP3 in the spleen of the mice with hypersplenism due to portal hypertension (PH). The mouse hypersplenism models were established by oral administration of tetrachloromethane (2 mL/kg/week for 12 weeks by oral gavage). All the mice were randomly divided into a control group and an experimental group. The blood routine test was conducted, spleen index was calculated and spleen was histologically examined. Portal vein sera were taken for detection of the level of uric acid. The mRNA expressions of NALP3 and IL-1beta in the spleen were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). The results showed that the platelet count was significantly lower in the experimental group [(674 + or - 102) x 10(9)/L] than in the control group [(1307 + or - 181) x 10(9)/L] (P<0.05), while the spleen index was significantly higher [(9.83 + or - 1.36) microg/g] in the experimental group than in the control group [(4.11 + or - 0.47) microg/g] (P<0.05). The histopathological changes of spleen followed the pattern of congestive splenomegaly. No significant difference was found in the uric acid level in the portal vein between the control group and the experiment group. The mRNA expressions of NALP3 and IL-1beta were up-regulated significantly in the spleen in the experimental group as compared with those in the control group (P<0.05). It was concluded that NALP3 and IL-1beta may play important roles in the pathogenesis of hypersplenism.

RYGB increases postprandial gastric nesfatin-1 and rapid relieves NAFLD via gastric nerve detachment.

BACKGROUND: Roux-en-Y gastric bypass (RYGB) could reduce nonalcoholic fatty liver disease (NAFLD) ahead of the weight-loss effects. But the detailed mechanisms remain unclear. MATERIAL AND METHODS: A high-fat diet (HFD) was fed to induce obesity. RYGB was then performed. Gastric nesfatin-1 was measured by enzyme-linked immunosorbent assay (ELISA) in portal vein and polymerase chain reaction (PCR) in gastric tissues. Modified surgeries including vagus-preserved bypass and vagectomy were performed and postprandial gastric nesfatin-1 were analyzed. The effects of nesfatin-1 on hepatocytes were studied by PCR and immunohistochemistry. Both intraperitoneal and intracerebroventricular injection (ICV) were performed to analyze the in vivo effects on liver lipid metabolism. RESULTS: Increased postprandial portal vein nesfatin-1 was observed in RYGB but not in control groups. This increase is mainly due to induction of gastric nesfatin-1. A modified RYGB in which the gastric vagus is preserved is conducted and, in this case, this nesfatin-1 induction effect is diminished. Mere vagectomy could also induce a similar nesfatin-1 increase pattern. The infusion of nesfatin-1 in the brain could inhibit the expression of gastric nesfatin-1, and the effects are diminished after gastric vagectomy. In vivo and in vitro nesfatin-1 stimulation in the liver resulted in improvements in lipid metabolism. CONCLUSIONS: Severing the gastric vagus during RYGB could cut off the negative control from the central nervous system (CNS) and result in increased postprandial gastric nesfatin-1 post surgery, which in turn, improves NAFLD.

Obesity and mortality of COVID-19. Meta-analysis.

BACKGROUND: Obesity is a global disease with at least 2.8 million people dying each year as a result of being overweight or obese according to the world health organization figures. This paper aims to explore the links between obesity and mortality in COVID-19. METHODS: Electronic search was made for the papers studying obesity as a risk factor for mortality following COVID-19 infection. Three authors independently selected the papers and agreed for final inclusion. The outcomes were the age, gender, body mass index, severe comorbidities, respiratory support and the critical illness related mortality in COVID-19. 572 publications were identified and 42 studies were selected including one unpublished study data. Only 14 studies were selected for quantitative analysis. RESULTS: All the primary points but the gender are significantly associated with COVID-19 mortality. The age >70, [odd ratio (OR): 0.17, CI; 95%, P-value: <0.00001], gender [OR: 0.89; CI: 95%, P-value: 0.32], BMI > 25 kg/m2 [OR: 3.68, CI: 95%, P-value: <0.003], severe comorbidities [OR: 1.84, CI:95%, P-value: <0.00001], advanced respiratory support [OR: 6.98, CI: 95%, P-value: <0.00001], and critical illness [OR: 2.03, CI: 95%, P-value: <0.00001]. CONCLUSIONS: Patients with obesity are at high risk of mortality from COVID-19 infection.

Upregulation of Intestinal NLRP6 Inflammasomes After Roux-en-Y Gastric Bypass Promotes Gut Immune Homeostasis.

OBJECTIVE: Roux-en-Y gastric bypass (RYGB) could affect immunological activity after surgery. We examined the role of RYGB on the NOD-like receptor pyrin domain containing-6 (NLRP6) in the intestine after surgery in rat models. METHODS: Expression of intestinal NLRP6 in the lean, obesity, RYGB, and sham-pair fed (PF) groups was analyzed by quantitative RT-PCR, Western blotting, and immunohistochemistry. Gut microbiota abundance was determined by 16S rRNA sequencing. Cohousing experiments were conducted to analyze the effects of gut microbiota. Inflammatory cell infiltration and gut permeability were further validated. RESULTS: Obese rats had decreased intestinal NLRP6 levels, which could be restored by RYGB but not by calorie restriction. This regulation was dependent on the gut microbiota-related metabolites, taurine, and histamine. After RYGB, there were increased levels of taurine, which could positively affect NLRP6 expression. The pair-fed groups showed increased histamine, which had the opposite effects on NLRP6. Obese rats had greater intestinal permeability along with increased CD8+ T cell infiltration. However, RYGB but not calorie restriction could restore these changes in a manner, dependent on gut NLRP6 expression. CONCLUSIONS: In rat models, RYGB could efficiently restore abnormal gut permeability and reduce inflammation in the intestine, depending on reactivation of NLRP6.

Global obesity research trends during 1999 to 2017: A bibliometric analysis.

BACKGROUND: The interest in obesity has considerably increased in the scientific community in the last 2 decades. We present a bibliometric analysis to find out the future research hotspot and trends of obesity. METHODS: Data were based on the Science Citation Index Expanded (SCI-E), from the Institute of Scientific Information Web of Science database and the 5-year impact factor of a journal were issued from the Journal Citation Reports (JCR) in 2017. Articles referring to obesity during 1999 to 2017 were concentrated on the analysis by scientific output characters and the frequency of author keywords used. RESULTS: Globally, 50,246 articles meet the inclusion criteria during 1999 to 2017. The cumulative number of publication about obesity followed exponential distribution (R = 0.9974) from 2008. USA was the most productive countries in both independent and international collaborative papers, the countries/regions with the highest average Times Cited scores for independent articles was France and The United Kingdom scored the highest in average Times Cited for international collaborative papers. Collaboration among countries, playing an ever-growing role in contemporary scientific research. The 2 most prolific journals are Obesity Surgery and International Journal of Obesity, responsible for 3.95% of the publication. CONCLUSION: Obesity has been a field of intense research in the last 19 years. By reasonably analyzing the author keywords and the distribution of journals, "bariatric surgery" (especially "sleeve gastrectomy") and "obese complications" (especially "diabetes mellitus," "metabolic syndrome," "depression," and "polycystic ovary syndrome") will undoubtedly maintain the hotspots of obesity research in the next few decades.

Optimization of a Technique to Standardize the Rodent Roux-En-Y Gastric Bypass Model and Troubleshooting of Postoperative Failures.

BACKGROUND: Rodent models are required in studies on the mechanism of Roux-en-Y gastric bypass (RYGB). However, the construction of the model is hard, and there are various causes of death after surgery in rats. METHODS: RYGB models with procedures containing a series of anatomic landmark were established in rats. Optimized procedures during surgery, possible complications after surgery, and corresponding solutions were studied. RESULTS: With the introduction of perioperative nursing and optimized surgery procedures, less time-consuming surgeries were performed and higher survival rates were achieved. Trouble-shooting data based on death time points are listed and discussed for various causes of failure. CONCLUSIONS: This study provides practical suggestions for investigators to perform RYGB surgery on rats. The troubleshooting suggestions will help operators to efficiently identify problems in their procedures.

Intestinal Glucose Absorption Was Reduced by Vertical Sleeve Gastrectomy via Decreased Gastric Leptin Secretion.

BACKGROUND: The unique effects of gastric resection after vertical sleeve gastrectomy (VSG) on type 2 diabetes mellitus remain unclear. This work aimed to investigate the effects of VSG on gastric leptin expression and intestinal glucose absorption in high-fat diet-induced obesity. METHODS: Male C57BL/6J mice were fed a high-fat diet (HFD) to induce obesity. HFD mice were randomized into VSG and sham-operation groups, and the relevant parameters were measured at 8 weeks postoperation. RESULTS: Higher gastric leptin expression and increased intestinal glucose transport were observed in the HFD mice. Furthermore, VSG reduced gastric leptin expression and the intestinal absorption of alimentary glucose. Both exogenous leptin replenishment during the oral glucose tolerance test (OGTT) and the addition of leptin into the everted isolated jejunum loops in vitro restored the glucose transport capacity in VSG-operated mice, and this effect was abolished when the glucose transporter GLUT2 was blocked with phloretin. Moreover, phloretin almost completely suppressed glucose transport in the HFD mice. Intestinal immunohistochemistry in the obese mice showed increased GLUT2 and diminished sodium glucose co-transporter 1 (SGLT-1) in the apical membrane of enterocytes. Decreased GLUT2 and enhanced SGLT1 were observed following VSG. VSG also reduced the phosphorylation status of protein kinase C isoenzyme ß II (PKCß II) in the jejunum, which was stimulated by the combination of leptin and glucose. CONCLUSION: Our data demonstrated that the decreased secretion of gastric leptin in VSG results in a decrease in intestinal glucose absorption via modulation of GLUT2 translocation.

Synthesis of Hierarchically Structured Hybrid Materials by Controlled Self-Assembly of Metal-Organic Framework with Mesoporous Silica for CO2 Adsorption.

The HKUST-1@SBA-15 composites with hierarchical pore structure were constructed by in situ self-assembly of metal-organic framework (MOF) with mesoporous silica. The structure directing role of SBA-15 had an obvious impact on the growth of MOF crystals, which in turn affected the morphologies and structural properties of the composites. The pristine HKUST-1 and the composites with different content of SBA-15 were characterized by XRD, N2 adsorption-desorption, SEM, TEM, FT-IR, TG, XPS, and CO2-TPD techniques. It was found that the composites were assembled by oriented growth of MOF nanocrystals on the surfaces of SBA-15 matrix. The interactions between surface silanol groups and metal centers induced structural changes and resulted in the increases in surface areas as well as micropore volumes of hybrid materials. Besides, the additional constraints from SBA-15 also restrained the expansion of HKUST-1, contributing to their smaller crystal sizes in the composites. The adsorption isotherms of CO2 on the materials were measured and applied to calculate the isosteric heats of adsorption. The HS-1 composite exhibited an increase of 15.9% in CO2 uptake capacity compared with that of HKUST-1. Moreover, its higher isosteric heats of CO2 adsorption indicated the stronger interactions between the surfaces and CO2 molecules. The adsorption rate of the composite was also improved due to the introduction of mesopores. Ten cycles of CO2 adsorption-desorption experiments implied that the HS-1 had excellent reversibility of CO2 adsorption. This study was intended to provide the possibility of assembling new composites with tailored properties based on MOF and mesoporous silica to satisfy the requirements of various applications.

Gastric cancer in a situs inversus totalis patient with multiple intestinal and vessel variations related to gastrectomy surgery: A case report and literature review.

RATIONALE: Situs inversus totalis (SIT) is a rare congenital anomaly characterized by complete inversion of the abdominal and thoracic organs, and often involves multiple genetic mutations. The most suitable surgical technique for patients with multiple vessel and organ variations as well as SIT remains unclear. Furthermore, there has been insufficient clinical evidence that demonstrates which surgical techniques achieve the best outcomes. Finally, the standard of care has not yet been determined. We present the case of a 60-year-old man with SIT, who was diagnosed with moderately and poorly differentiated adenocarcinoma at the gastroesophageal junction. We further describe the advantage of using robotic-assisted laparoscopic surgery in patients with this anomaly. PATIENT CONCERNS: A 60-year-old man complained of pain in his upper abdomen for 3 months. Physical examination revealed an apex beat in the right fifth intercostal space, and vascular anomalies were noted on abdominal angiographic computed tomography. DIAGNOSES: Moderately and poorly differentiated adenocarcinoma at the gastroesophageal junction with SIT. INTERVENTIONS: Robot-assisted total gastrectomy with D2 lymph node dissection and hand-sewn Roux-en-Y anastomosis was performed. OUTCOMES: The postoperative course was uneventful, and the patient was discharged on the seventh postoperative day. LESSONS: Robotic surgery for gastric cancer is a safe and feasible alternative to laparoscopic surgery and it can be successfully used to treat gastric cancer in patients with SIT with multiple anatomic variations. As exemplified by our case, SIT might be accompanied by multiple anatomic variations. Detailed preoperative detailed imaging of the blood vessels and gastrointestinal tract is useful in these patients.

IFN-γ secretion in gut of Ob/Ob mice after vertical sleeve gastrectomy and its function in weight loss mechanism.

Vertical sleeve gastrectomy (VSG) is becoming more and more popular among the world. Despite its dramatic efficacy, however, the mechanism of VSG remains largely undetermined. This study aimed to test interferon (IFN)-γ secretion n of mesenteric lymph nodes in obese mice (ob/ob mice), a model of VSG, and its relationship with farnesoid X receptor (FXR) expression in the liver and small intestine, and to investigate the weight loss mechanism of VSG. The wild type (WT) mice and ob/ob mice were divided into four groups: A (WT+Sham), B (WT+VSG), C (ob/ob+Sham), and D (ob/ob+VSG). Body weight values were monitored. The IFN-γ expression in mesenteric lymph nodes of ob/ob mice pre- and post-operation was detected by flow cytometry (FCM). The FXR expression in the liver and small intestine was detected by Western blotting. The mouse AML-12 liver cells were stimulated with IFN-γ at different concentrations in vitro. The changes of FXR expression were also examined. The results showed that the body weight of ob/ob mice was significantly declined from (40.6±2.7) g to (27.5±3.8) g on the 30th day after VSG (P<0.05). At the same time, VSG induced a higher level secretion of IFN-γ in mesenteric lymph nodes of ob/ob mice than that pre-operation (P<0.05). The FXR expression levels in the liver and small intestine after VSG were respectively 0.97±0.07 and 0.84±0.07 fold of GAPDH, which were significantly higher than pre-operative levels of 0.50±0.06 and 0.48±0.06 respectively (P<0.05). After the stimulation of AML-12 liver cells in vitro by different concentrations of IFN-γ (0, 10, 25, 50, 100, and 200 ng/mL), the relative FXR expression levels were 0.22±0.04, 0.31±0.04, 0.39±0.05, 0.38±0.05, 0.56±0.06, and 0.35±0.05, respectively, suggesting IFN-γ could distinctly promote the FXR expression in a dose-dependent manner in comparison to those cells without IFN-γ stimulation (P<0.05). It was concluded that VSG induces a weight loss in ob/ob mice by increasing IFN-γ secretion of mesenteric lymph nodes, which then increases the FXR expression of the liver and small intestine.

Preparation and acute toxicology of nano-magnetic ferrofluid.

The nano-magnetic ferrofluid was prepared by chemical coprecipitation and its acute toxicology was investigated. The effective diameter (Eff. Diam. ) of the magnetic particles was about 19.9 nm, and the concentration of the ferrofluid was 17. 54 mg/ml. The acute toxic reaction and the main viscera pathological morphology of mice were evaluated after oral, intravenous and intraperitoneal administration of the nano-magnetic ferrofluid of different doses respectively. Half lethal dose (LD50) > 2104. 8 mg/kg,maximum non-effect dose (ED0) = 320. 10mg/kg with oral; LDs,> 438. 50 mg/kg, EDo = 160. 05 mg/kg with intravenous route; and LDso >1578. 6 mg/kg, ED0 = 320. 10 mg/kg with intraperitoneal administration. Degeneration and necrosis of viscera were not found. So the nano-magnetic ferrofluid, of which toxicity is very low, may be used as a drug carrier.