Anesthesia and perioperative management of bariatric surgery in a patient with BMI over 70 kg/m2: a case report.

The anesthesia protocol of bariatric surgery has not been standardized in detail. This report introduced an optimized anesthesia strategy for a severely obese male patient for laparoscopic sleeve gastrectomy and a continuous follow-up for 12 months. A 34-year-old male patient was admitted for super-super-obesity with obstructive sleep apnea-hypopnea syndrome. Based on the results of the examination before laparoscopic sleeve gastrectomy, he received an efficient preoperative exercise guidance for pulmonary function promotion and diet restriction. Multiple analgesia scheme consisted of regional nerve block and analgesics cocktail. He lost 103 kg without any complications till postoperative 12 months. His mental characteristics were also improved gradually. This case presented a superior composition in perioperative anesthesia management for laparoscopic sleeve gastrectomy. To provide a reference for promoting the implementation of enhanced recovery after surgery protocols in bariatric surgery.

Changes in gut microbiota and cytokines following laparoscopic sleeve gastrectomy are associated with cognitive function improvement.

Purpose: Variations of cytokines and gut microbiota diversity with improved cognitive function in patients with obesity following bariatric surgery were poorly understood. The aim of this study was to testify the relationship among gut microbiota, cytokines and cognitive function in patients with obesity before and after laparoscopic sleeve gastrectomy (LSG). Methods: Forty patients were enrolled in this study. Demographics, and serum and stool specimens were collected from all patients before and 3 months after LSG. The Montreal Cognitive Assessment (MoCA) scale, as well as assessment of immediate and delayed memory were used to evaluate self-perceived cognitive improvement after LSG. Results: LSG resulted in significant weight loss and improvement in cognitive functions, as measured by questionnaires. Bariatric surgery tended to increase gut microbiota relative abundance and diversity. The intestinal flora increased in the proportion of Bacteroidetes and Fusobacteria phyla, and decreased in the proportion of Firmicutes, Proteobacteria, and Actinobacteria phyla after LSG. Plasma IL-1ß and TNF-α levels were significantly decreased following LSG, while IL-4 was significantly increased. MoCA test scores were significant correlated with IL-4, TNF-α and IL-1ß. In addition, Firmicutes had a positive correlation with TNF-α, while Fuscobacteria had a negative correlation with IL-1ß. Bacteroidetes was negatively correlated with IL-4. Conclusion: Changes in gut microbiota were positive relationship with cognitive function improvement following LSG. Inflammation cytokines maybe played as a mediator between gut microbiota and cognitive function through gut-microbiota-brain axis.

ST36 acupoint injection with anisodamine for postoperative nausea and vomiting in female patients after bariatric surgery: a prospective, randomized controlled trial.

BACKGROUND: The use of multimodal pharmacological prophylactic regimes has decreased postoperative nausea and vomiting (PONV) in general but it still occurs in over 60% of female patients after bariatric surgery. This study aimed to evaluate the efficacy of ST36 acupoint injection with anisodamine in prevention of PONV among female patients after bariatric surgery. METHODS: Ninety patients undergoing laparoscopic sleeve gastrectomy were randomly allocated to anisodamine or control group at the ratio of 2:1. Anisodamine or normal saline was injected into Zusanli (ST36) bilaterally after induction of general anesthesia. The incidence and severity of PONV were assessed during the first 3 postoperative days and at 3 months. The quality of early recovery of anesthesia, gastrointestinal function, sleep quality, anxiety, depression, and complications were also evaluated. RESULTS: Baseline and perioperative characteristics were comparable between two groups. In the anisodamine group, 25 patients (42.4%) experienced vomiting within postoperative 24 h compared with 21 (72.4%) in the control group (relative risk 0.59; 95% confidence interval 0.40-0.85). Time to first rescue antiemetic was 6.5 h in anisodamine group, and 1.7 h in the control group (P = 0.011). Less rescue antiemetic was required during the first 24 h in the anisodamine group (P = 0.024). There were no differences in either postoperative nausea or other recovery characteristics. CONCLUSIONS: The addition of ST36 acupoint injection with anisodamine significantly reduced postoperative vomiting without affecting nausea in female patients with obesity undergoing laparoscopic sleeve gastrectomy.

The Interaction Between SMAD1 and YAP1 Is Correlated with Increased Resistance of Gastric Cancer Cells to Cisplatin.

Drug resistance is a major obstacle leading to treating failure and poor outcome in gastric cancer (GC). This study explores the interaction between SMAD family member 1 (SMAD1) and Yes1-associated transcriptional regulator (YAP1) and their roles in cisplatin (DDP) resistance in GC. Transcriptome analysis predicted that SMAD1 is highly expressed in DDP-resistant cells. Elevated SMAD1 expression was detected in GC tissue and cells, especially in DDP-resistant cells (MKN-45/DDP and AGS/DDP). SMAD1 downregulation in cells decreased 50% inhibition value of DDP, reduced proliferation, migration, and invasion, and promoted cell cycle arrest and apoptosis. A protein-protein interaction network suggested a possible SMAD1 and YAP1 interaction in GC. The SMAD1 and YAP1 interaction was validated by chromatin immunoprecipitation (ChIP), co-immunoprecipitation (Co-IP), and luciferase assays. SMAD1 bound to YAP1 and activated its transcription. SMAD1 formed complexes with YAP1 in nucleus, and YAP1 upregulation enhanced SMAD1 activity as well. Upregulation of YAP1 restored the malignant behaviors of GC cells suppressed by SMAD1 silencing. In vivo, SMAD1 silencing suppressed growth and DDP resistance of xenograft tumors in nude mice, and this suppression was blocked by YAP1 overexpression again. In conclusion, this study demonstrates that SMAD1 can interact with YAP1 to enhance the DDP resistance of GC cells.

Analgesic Efficacy of Transverse Abdominis Plane Block and Quadratus Lumborum Block in Laparoscopic Sleeve Gastrectomy: A Randomized Double-Blinded Clinical Trial.

INTRODUCTION: The analgesic effect and safety of transversus abdominis plane block (TAPB) is still controversial in various abdominal procedures. Quadratus lumborum block (QLB) has been considered to provide a widespread and long-lasting analgesic effect in gynecological surgeries. However, the analgesic effects of these two techniques in patients with extreme obesity undergoing laparoscopic sleeve gastrectomy (LSG) are still unknown. METHODS: A total of 225 patients with obesity were randomly assigned to group TAPB (n = 76, 30 ml 0.33% ropivacaine with dexmedetomidine 1 µg kg-1), group QLB (n = 76, 30 ml 0.33% ropivacaine with dexmedetomidine 1 µg kg-1), or general anesthesia alone (GA, n = 73, 30 ml 0.9% saline). During the 48-h postoperative period, patients received continuous intravenous patient-controlled analgesia (PCA) containing sufentanil 2 µg kg-1, dexmedetomidine 2 µg kg-1, and granisetron 3 mg. The scores of visual analogue scale (VAS) in surgical incision and viscera, considering as the primary outcomes, were continuously recorded at postoperative 0, 0.5, 1, 2, 6, 12, 24, 48 h and discharge. RESULTS: Comparing with patients in the GA group, VAS scores of incision and viscera were consistently reduced during the initial 6-12 h after LSG in TAPB and QLB groups, and they received less propofol and remifentanil (P < 0.001) as well. In the QLB group, patients had longer duration for the first rescue analgesia, and fewer requirements of the rescue analgesia within 24 h than the GA group (P < 0.05). In addition, there were fewer PCA requirements in QLB group than GA and TAPB groups (P < 0.05). CONCLUSIONS: Ultrasound-guided transversus abdominis plane block and quadratus lumborum block could provide comparable analgesic effects for a laparoscopic sleeve gastrectomy in obese patients. TRIAL REGISTRATION: Chinese Clinical Trial Registry; ChiCTR1800019236.

Prevalence and Clinical Predictors of Hyperuricemia in Chinese Bariatric Surgery Patients.

BACKGROUND: Despite a known significant association between hyperuricemia and obesity, this correlation in bariatric surgery patients remains unknown. OBJECTIVES: To evaluate the prevalence and predictors of pre- and postoperative hyperuricemia in Chinese bariatric surgery patients. METHODS: A retrospective study was performed in 333 bariatric surgery patients from our hospital. The clinical data was collected before surgery and at 3, 6, and 12 months postoperatively. Univariable and multivariate analyses were used for investigating the independent predictors of hyperuricemia and serum uric acid (SUA) change. RESULTS: Altogether, 62.9% of patients fulfilled the diagnostic criteria for hyperuricemia. The prevalence of hyperuricemia among males was 81.8% and 62.3% in the women. Multiple logistic regression analyses showed that age (OR = 0.951, 95%CI:0.926-0.976, P = 0.000), high-density lipoprotein cholesterol (HDL-c) (OR = 0.217, 95%CI:0.074-0.637, P = 0.005), γ-glutamyltransferase (γ-GT) (OR = 1.016, 95%CI:1.004-1.027, P = 0.006), and creatinine (Cr) (OR = 1.042, 95%CI: 1.017-1.067, P = 0.001) were independent predictors of hyperuricemia. SUA levels significantly declined in all patients from 443.1 ± 118.2 µmol/L before surgery to 370.1 + 113.4 µmol/L at 12 months after surgery. The prevalence of hyperuricemia also declined from 69.4% before surgery to 25.5% at 12 months. Multiple linear regression analyses confirmed that changes in Cr and body mass index (BMI) were independent predictors of a decrease in SUA levels, 12 months postoperatively. CONCLUSIONS: Hyperuricemia in Chinese bariatric surgery candidates are common, especially in males. Age, HDL-c, γ-GT and Cr were determined to be independent predictors of hyperuricemia. Bariatric surgery may effectively reduce the prevalence of hyperuricemia in this population, through postoperative weight loss and changes in creatinine following the procedure.

LncRNA ADAMTS9-AS1, as prognostic marker, promotes cell proliferation and EMT in colorectal cancer.

The long non-coding RNA antisense 1 ADAMTS9-AS1 has been reported to predict the survival in several tumors, including bladder cancer and breast cancer. However, the clinical significance and biological behaviors of ADAMTS9-AS1 in colorectal cancer (CRC) have not been reported yet. In this study, the expression of ADAMTS9-AS1 was measured in CRC tissues and cell lines using quantitative real-time PCR analysis. The clinical significance of ADAMTS9-AS1 was evaluated with Chi-squared test, Kaplan-Meier method and Cox regression analysis in CRC patients. CCK8 assay, colony formation assay, flow cytometry and transwell assay were used to explore the biological function of ADAMTS9-AS1 knockdown in CRC cell lines (SW1116 and HT29). We further explore the role of ADAMTS9-AS1 in vivo though xenograft tumor assay. Our data showed that ADAMTS9-AS1 expression level was significantly up-regulated in CRC tissues and cell lines compared with corresponding controls. High ADAMTS9-AS1 level was associated with TNM stage, lymph node invasion and worse survival prognosis. Depletion of ADAMTS9-AS1 significantly suppressed cell proliferation, G1/S transition, migration and invasion, as well as suppressed CDK4/Cyclin D1 and epithelial-mesenchymal transition (EMT). To sum up, these findings illustrated that ADAMTS9-AS1 might be a promising therapeutic target and prognostic factor for CRC.

CircRNA-PTN Sponges miR-326 to Promote Proliferation in Hepatocellular Carcinoma.

BACKGROUND: Mounting evidences reveal that circular RNAs (circRNAs) are critical to regulate biological behavior and process of tumor. Our objective is to explore the role of circRNA-PTN (circPTN) and explain the exact mechanism in hepatocellular carcinoma (HCC). METHODS: Real-time polymerase chain reaction assay was used to detect the level of circPTN and miR-326. The proliferation of cell was measured by CCK-8 assay and EdU assay. Western blot assay was performed to assess ErbB/PI3K expression. Luciferase and RNA pull-down assays were carried out to confirm the interaction between circPTN and miR-326. RESULTS: Our results indicated that circPTN was upregulated in human hepatocellular carcinoma tumor tissues and cell lines, compared with paratumor tissues and immortalized normal liver cell line. circPTN could significantly promote HCC tumor growth according to gain-and loss-of-function assays. Additionally, we determined that circPTN acted as a sponge through interacting with miR-326. Overexpression of miR-326 could rescue the cell proliferation inhibition and ErbB/PI3K downregulation in HCC cells by circPTN. Besides, the effects of miR-326 on HCC were missing when circPTN binding sites were mutated. CONCLUSION: Our study indicates that circPTN acts as an oncogenic factor via sponging miR-326 in HCC.

Naringenin ameliorates insulin resistance by modulating endoplasmic reticulum stress in hepatitis C virus-infected liver.

Hepatitis C virus (HCV) infection may lead to hepatic insulin resistance (IR), and endoplasmic reticulum (ER) stress has been found to induce IR. In our previous study, naringenin (NGEN) had an insulin sensitization effect on the HCV core protein (HCVCP) infected mouse livers. In the present study, we examined the effects of NGEN on HCVCP infection-induced ER stress and investigated the insulin sensitization mechanism involved. We found that XBP1s was up-regulated in the livers of HCV-infected patients, in hepatocytes with HCV infection, and in HCVCP-infected mice. HCVCP induces ER stress in the mouse liver and hepatocytes by increasing XBP1s and downstream gene expression. Pre-treatment with NGEN inhibited the ER stress and downstream gene expression both in vivo and in vitro. Similar to the HCVCP infection results, NGEN also inhibited the ER stress in tunicamycin-treated Huh-7.5.1 cells. In addition, the role of IRE1α in HCVCP-induced IR was detected, and knockdown of IRE1α abolished HCVCP-stimulated IR. Overexpression induced IR but could be abolished by NGEN. NGEN also blocked the HCVCP-induced IRE1α expression levels that were up-regulated in vivo. Our data reveal that ER stress may be associated with HCV-induced IR, and NGEN treatment inhibited ER stress activity and increased insulin sensitivity by decreasing the expression of IRE1α.

Silencing of SAA1 inhibits palmitate- or high-fat diet induced insulin resistance through suppression of the NF-κB pathway.

BACKGROUND: Obesity is one of the leading causes of insulin resistance. Accumulating reports have highlighted that serum amyloid A-1 (SAA1) is a potential candidate that is capable of attenuating insulin resistance. Hence, we conducted the current study with aims of investigating our proposed hypothesis that silencing SAA1 could inhibit the progression of obesity-induced insulin resistance through the NF-κB pathway. METHODS: Gene expression microarray analysis was initially performed to screen differentially expressed genes (DEGs) associated with obesity. Palmitate (PA)-induced insulin resistance Huh7 cell models and high-fat diet (HFD)-induced mouse models were established to elucidate the effect of SAA1/Saa1 on insulin resistance. The NF-κB pathway-related expression was subsequently determined through the application of reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. RESULTS: Saa1 was identified as an obesity-related gene based on the microarray data of GSE39549. Saa1 was determined to be highly expressed in HFD-induced insulin resistance mouse models. PA-induced Huh7 cells, treated with silenced SAA1 or NF-κB pathway inhibition using BAY 11-7082, displayed a marked decrease in both Saa1 and SOCS3 as well as an elevation in 2DG, IRS1 and the extent of IRS1 phosphorylation. HFD mice treated with silenced Saa1 or inhibited NF-κB pathway exhibited improved fasting blood glucose (FBG) levels as well as fasting plasma insulin (FPI) levels, glucose tolerance and systemic insulin sensitivity. Saa1/SAA1 was determined to show a stimulatory effect on the transport of the NF-κBp65 protein from the cytoplasm to the nucleus both in vivo and in vitro, suggesting that Saa1/SAA1 could activate the NF-κB pathway. CONCLUSION: Taken together, our key findings highlight a novel mechanism by which silencing of SAA1 hinders PA or HFD-induced insulin resistance through inhibition of the NF-κB pathway.

Short-term outcome and early effect on blood pressure of laparoscopic sleeve gastrectomy in morbidly obese patients.

Bariatric surgery has been used to reduce weight and shown to be beneficial for hypertension control. However, little is known about the changes in blood pressure in early stage after laparoscopic sleeve gastrectomy (LSG). We conducted a prospective study of 60 LSG patients with one year-follow-up. The blood pressure of the patients was measured preoperatively and from day 1 to 12 months postoperatively. The use of antihypertensives, body weight, ghrelin and leptin levels were also recorded. Following LSG, excess weight loss (EWL) was 72.6 ± 22.3% and 83.1 ± 19.3% 6 and 12 months after operation, respectively. At 12 months after operation, the average body mass index and body weight decreased by 14.1 kg/m2 and 39 kg, respectively. Dyslipidemia was resolved in 86% (15/18) of the patients within 12 months. Diabetes was resolved in 90% (16/18) patients within 6 months and joint pain was resolved in 78% patients and 86% of the patients no longer had sleep apnea syndrome within 12 months. The blood pressure of some hypertensive patients returned to normal on the first day after operation. Significant reduction in blood pressure was observed within 10 days after operation. Both Ghrelin and Leptin levels lowered after LSG, particularly within 10 day after operation. 12 months after the operation, hypertension was resolved in 87% and lowered in 100% of the patients. Our work demonstrates that LSG reduces blood pressure before significant weight loss occurs, suggesting that there might be neural and hormonal mechanisms involved in the blood pressure reduction.

Naringenin improve hepatitis C virus infection induced insulin resistance by increase PTEN expression via p53-dependent manner.

Hepatitis C virus (HCV) infection may finally lead to hepatocellular carcinoma (HCC), and also associated with insulin resistance (IR). Naringenin (NGEN), a flavonoid found in grapefruit, has anti-virus, anti-inflammation and insulin sensitization effects. In the present study we examined the effects of NGEN on HCV core protein (HCVCP) infection induced IR and investigated the mechanism involved. We found that NGEN ameliorated IR and glucose tolerance in HCVCP infected mice by increase the phosphorylation of Akt at both Ser473 and Thr308 site, and also inhibited the inflammation cytokine production and T-cell immune response. Similar to the in vivo results, NGEN also improved the insulin response and showed anti-inflammation effect in HCVCP infected Huh-7.5.1 cells. In addition, NGEN up-regulated the phosphatase and tensin homolog deleted on chromosome ten (PTEN) both in protein and mRNA levels. Furthermore, overexpress of PTEN abolished the HCVCP-stimulated IR and decreased the inflammation cytokine release. NGEN also blocked the interaction between HCVCP and p53, upregulated the endogenous p21/waf1 expression which indiacting the activation of p53. The p53 wild type could upregulate NGEN-stimulated PTEN expression while R273H mut-p53 showed no similar function. Our data reveals that NGEN increases insulin sensitivity in HCVCP infected liver by up-regulating PTEN in p53-dependent manner.

Expression of MicroRNA-448 and SIRT1 and Prognosis of Obese Type 2 Diabetic Mellitus Patients After Laparoscopic Bariatric Surgery.

BACKGROUND/AIMS: This study sought to investigate the expression and prognostic value of peripheral blood microRNA-448 (miR-448) and its target gene SIRT1 after laparoscopic bariatric surgery in obese type 2 diabetic mellitus (T2DM) patients. METHODS: Obese T2DM patients were selected and treated with laparoscopic bariatric surgery. Enzyme-linked immunosorbent assay (ELISA) was used to measure SIRT1 protein expression. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was employed to determine the mRNA expression of the related gene. Endothelial progenitor cells (EPCs) were grouped into blank, negative control (NC), miR-448 mimic, miR-448 inhibitor, siRNA-SIRT1 and miR-448 inhibitor + siRNA-SIRT1 groups. Transwell assays and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays were applied to determine cell invasion and cell viability. A tube formation assay and an adherence test were utilized to assess the angiogenic and adhesive capacities of the cells. RESULTS: In peripheral blood, the expression of miR-448 was reduced, whereas the mRNA and protein expression of SIRT1 was increased after surgery compared to before surgery. miR-448 expression was lower and mRNA and protein expression of SIRT1 was higher in the effective group than in the ineffective group after surgery. SIRT1 is a target gene of miR-448. miR-448 can suppress viability and invasion, and it reflects the angiogenic and adhesive capacity of EPCs and the protein expression of relative genes in EPCs through targeting SIRT1. CONCLUSION: The results demonstrated that miR-448 and its target gene SIRT1 can serve as prognostic indicators for obese T2DM patients after laparoscopic bariatric surgery.

MicroRNA-429 sensitizes pancreatic cancer cells to gemcitabine through regulation of PDCD4.

One of the features for pancreatic cancer is that it is often resistant to chemotherapy treatment, which is one of the major hindrances in the treatment of this malignancy. Previous studies indicated that the microRNAs (miRNAs) could mediate resistance of tumor cells to chemotherapy drug in the cancer progression. In the present study, we are aimed to examine whether microRNA-429 was involved in mediating the chemo-resistance of pancreatic cancer cells to gemcitabine. Firstly, a gemcitabine-resistant pancreatic cancer cell line (SW1990/GZ) derived from cell line (SW1990) was constructed and found to possess a decreased expression of miR-429 when it is compared to the original cell line. Ectopic expression of miR-429 in SW1990/GZ increased the cellular sensibility to the treatment of gemcitabine, which is coincided with increased expression of PDCD4. As a tumor suppressor, we found that PDCD4 knockdown in SW1990/GZ cells increased its own chemo-resistance to GZ, which indicates PDCD4 also play a regulative role on the GZ-resistance in the pancreatic cancer. To further confirm the function of miR-429 and PDCD4 in gemcitabine-resistant pancreatic cancer, a xenograft nude mouse model was utilized to examine whether miR-429 can restore treatment response of gemcitabine in gemcitabine-resistant xenografts, while protein levels of PDCD4 were up-regulated. Together with those results, these findings collectively provided that miR-429 could enhancer GZ sensitivity via regulation of PDCD4 expression in pancreatic cancer cells, which may offer a novel therapeutic target for the chemotherapy resistance in pancreatic cancer.

miR-133b acts as a tumor suppressor and negatively regulates ATP citrate lyase via PPARγ in gastric cancer.

MicroRNAs (miRNAs/miRs) are a class of small noncoding RNAs that negatively regulate protein expression by binding to protein-coding mRNAs and suppressing translation. Accumulating evidence suggests that miRNAs are involved in the development and progression of cancer by regulating cancer metabolism. Meanwhile, the cytosolic enzyme ATP citrate lyase (ACLY) is a promising target in the prevention and treatment of cancer. In the present study we revealed by western blot analysis and reverse transcription­quantitative PCR that miR-133b was downregulated in human gastric cancer (GC) tissues and cell lines, while ACLY was upregulated. The overexpression of miR-133b could decrease the proliferation and invasion of MKN-74 cells by inhibiting the expression and activation of ACLY. Furthermore, the nuclear distribution of peroxisome proliferator-activated receptor-γ (PPARγ) in GC tissues and cell lines was markedly decreased, and overexpression of miR-133b could increase the levels of nuclear PPARγ in MKN-74 cells. Additionally, miR-133b decreased the transcriptional activity of ACLY in a PPARγ-dependent manner, as determined by a dual-luciferase reporter assay. These results indicate that miR-133b targets ACLY and inhibits GC cell proliferation by regulating the expression of PPARγ, suggesting that miR-133b may serve as a tumor-suppressive target in GC therapy.

Serum vaspin level as a predictive indicator in the amelioration of fatty liver and metabolic disturbance in patients with severe obesity after laparoscopic vertical banded gastroplasty.

BACKGROUND: This study is all about predicting the value of serum vaspin level in the amelioration of fatty liver and metabolic disturbance in patients with severe obesity after laparoscopic vertical banded gastroplasty (LVBG). METHODS: A total of 164 patients (from January 2012 to May 2015) with severe obesity were chosen and performed LVBG. Enzyme-linked immunosorbent assay was performed to detect the serum vaspin level. The patients were given a biochemical automatic analyzer to measure the biochemical indicators. Homeostasis model assessment (HOMA) helps in the calculation of fasting insulin level (FINS) and insulin resistance (IR). The changes in fatty liver were examined by computed tomography (CT). Receiver operating characteristic curve is used to increase the predictive value of serum vaspin level in the amelioration of liver function and disturbances in the metabolism. RESULTS: Weight, BMI, waist circumference, serum vaspin level, and triglyceride (TG) decreased, but CT value of liver increased at 4th, 7th, and 12th month after surgery. After the 7th and 12th month period of surgery, the alanine aminotransferase, aspartate aminotransferase, FINS, and HOMA-IR reduced in the patients (P <.005). The area under ROC curve (AUC) is about 0.871 ±â€Š0.031 with 95%CI of 0.810-0.931 (P <.001). The sensitivity, specificity, and accuracy of serum vaspin level ≤0.9 were 87.80%, 78.05%, and 83.28%, respectively. BMI, FINS, and serum vaspin level ≤0.9 were the influencing factors of the amelioration of fatty liver and metabolic disturbance. CONCLUSION: This study proves that the serum vaspin level serves as a predictive indicator in the amelioration of fatty liver and metabolic disturbance in patients with severe obesity after LVBG.

Expression of PER, CRY, and TIM genes for the pathological features of colorectal cancer patients.

As typical clock gene machinery, period (PER1, PER2, and PER3), cryptochrome (CRY1 and CRY2), and timeless (TIM), could control proliferation, cellular metabolism, and many key functions, such as recognition and repair of DNA damage, dysfunction of the circadian clock could result in tumorigenesis of colorectal cancer (CRC). In this study, the expression levels of PER1, PER2, and PER3, as well as CRY1, CRY2, and TIM in the tumor tissue and apparently healthy mucosa from CRC patients were examined and compared via quantitative real-time polymerase chain reaction. Compared with the healthy mucosa from CRC patients, expression levels of PER1, PER2, PER3, and CRY2 in their tumor tissue are much lower, while TIM level was much enhanced. There was no significant difference in the CRY1 expression level. High levels of TIM mRNA were much prevalent in the tumor mucosa with proximal lymph nodes. CRC patients with lower expression of PER1 and PER3 in the tumor tissue showed significantly poorer survival rates. The abnormal expression levels of PER and TIM genes in CRC tissue could be related to the genesis process of the tumor, influencing host-tumor interactions.

Cecropin-P17, an analog of Cecropin B, inhibits human hepatocellular carcinoma cell HepG-2 proliferation via regulation of ROS, Caspase, Bax, and Bcl-2.

Cecropin-P17 is a peptide derived from Cecropin B. In this study, we investigated the effects and relative mechanisms of Cecropin-P17 in a human liver cancer cell line (HepG-2) in vitro and in vivo. A cell viability assay, Annexin V/propidium iodide assay, western blot, flow cytometry, quantitative real-time polymerase chain reaction, and a tumor-xenograft model were applied to elucidate the mechanism exerted by Cecropin-P17 on HepG-2 cells. Cecropin-P17 significantly inhibited the proliferation of HepG-2 cells and demonstrated low cytotoxicity to normal liver cells in vitro. The apoptotic rate of HepG-2 cells was increased after Cecropin-P17 treatment together with increased production of reactive oxygen species. Moreover, Cecropin-P17 stimulated caspase-3, caspase-9, and Bax and inhibited Bcl-2 on both the transcriptional and translational levels. Finally, Cecropin-P17 significantly suppressed tumor growth in a HepG-2-bearing nude mouse model. All of these results indicated that Cecropin-P17 could be a potential agent for the treatment of liver cancer.

Resveratrol induces gastric cancer cell apoptosis via reactive oxygen species, but independent of sirtuin1.

The currently available chemotherapeutic regimens against gastric cancer are not very effective, leading to high recurrence and poor survival. Resveratrol is a naturally occurring polyphenol with potent apoptosis-inducing activity. However, the mechanism underlying its actions remains unknown. In the present study, human gastric adenocarcinoma SGC7901 cells were treated with resveratrol (0, 25, 50, 100 and 200 µmol/L) for 48 h, and cellular apoptosis DNA damage were determined. In certain experiments, cells were incubated with superoxide dismutase (100 U/mL), catalase (300 U/mL) or sirtinol (10 µmol/L) to determine the role of reactive oxygen species (ROS) and sirtuin1 in resveratrol-induced cellular apoptosis. Treatment with resveratrol (50-200 µmol/L) for 48 h significantly induced apoptosis and DNA damage in human gastric cancer SGC7901 cells. This was due to the increased generation of ROS following resveratrol treatment because incubation of cells with superoxide dismutase (100 U/mL) or catalase (300 U/mL) attenuated resveratrol-induced cellular apoptosis. Interestingly, treatment with resveratrol (25-200 µmol/L) did not affect the level and activity of sirtuin1, whereas the sirtuin1 inhibitor sirtinol (10 µmol/L) significantly reduced sirtuin1 activity. Furthermore, treatment with sirtinol (10 µmol/L) did not have any effect on apoptosis induced by resveratrol. These data provide evidence that resveratrol induces apoptosis via ROS, but independent of sirtuin1, in the human gastric cancer cell line SGC7901.