Xinyu Huang

Background: Food addiction and an impulsive personality can increase overeating, which can lead to weight gain. The amygdala and nucleus accumbens (NAcc) are critical for regulating obesogenic behaviour. However, whether the amygdala or the NAcc acts as the neural basis for the regulation of food addiction, impulsive personality, and body weight remains unclear.Methods: We examined the differences in the volume of the amygdala and NAcc, especially the lateralization index (LI), between 33 obese participants and 39 age- and sex-matched healthy controls. The associations of the LI of each brain region with clinical variables and body mass index (BMI) were identified using network analysis. Finally, we explored the relationships among the LIs of brain regions, impulsive personality, food addiction, and BMI through a multiple chain mediation model.Results: We observed a significant decrease in the LI of the amygdala in the obese group compared with the healthy group (F = 20.276, p < 0.001), which indicates that the right amygdala was larger than the left amygdala in the obese group. Network analysis revealed that the LI of the amygdala was very closely associated with nonplanning impulsivity, food addiction and BMI. The results of the mediation analysis indicated that increased nonplanning impulsiveness could lead to weight gain through increased food addiction (β = 0.069, SE = 0.043, 95% CI [0.014, 0.184]). Moreover, in this symptom chain, the LI of the amygdala can mediate the relationship between food addiction and BMI (β = 0.018, SE = 0.014, 95% CI [0.002, 0.061]).Conclusion: Our observations indicate a substantial reduction in the LI of the amygdala among individuals with obesity, suggesting a structural predisposition. The findings reveal a potential neural mechanism that can help explain the interplay between impulsivity, food addiction, and obesity.

Background: Preoperative prediction of severe cholecystitis (SC), including acute gangrenous cholecystitis (AGC) and acute purulent cholecystitis (APC), as opposed to acute exacerbation of chronic cholecystitis (ACC), is of great significance, as SC is associated with high mortality rate.Methods: In this study, we retrospectively investigated medical records of 114 cholecystitis patients, treated in Shanghai No. 6 People’s Hospital from February 2009 to July 2020. Gallbladder wall thickness (GBWT), indexes of blood routine examination, including white blood cell (WBC), alkaline phosphatase (ALP), the percentage of neutrophil, alanine transaminase (ALT), aspartate aminotransferase (AST), fibrinogen (FIB), gamma-glutamyl transferase, prothrombin time and total bilirubin were evaluated. One-way analysis of variance (ANOVA) was used to evaluate significant differences between a certain kind of SC and ACC to select a prediction index for each kind of SC. Receiver operating characteristic (ROC) curve analysis was conducted to identify the prediction effectiveness of these indexes and their optimal cut-off values.Results: Higher WBC and lower ALP were associated with AGC diagnosis (P < 0.05). Higher percentage of neutrophils was indicative of APC and AGC, while higher GBWT was significantly associated with APC diagnosis (P < 0.05) The optimal cut-off values for these indexes were established at 11.1*10⁹/L (OR: 5.333, 95% CI 2.576–10.68,P < 0.0001, sensitivity: 72.73%, specificity: 66.67%), 79.75% (OR: 5.735, 95% CI 2.749–12.05,P < 0.0001, sensitivity: 77.92%, specificity: 61.9%) and 5.5 mm (OR: 22, 95% CI 4.757–83.42,P < 0.0001, sensitivity: 78.57%, specificity: 85.71%), respectively.Conclusion: We established a predictive model for the differentiations of APC and AGC from ACC using clinical indexes, such as GBWT, the percentage of neutrophil and WBC, and determined cut-off values for these indexes based on ROC curves. Index values exceeding these cut-off values will allow to diagnose patients as APC and AGC, as opposed to a diagnosis of ACC.

Background:Primary retroperitoneal liposarcoma (PRPLS) is the most common soft tissue sarcoma of the retroperitoneum with high recurrence rate and short overall survival (OS).Methods:A retrospective review of 51 patients with PRPLS, treated between September 1, 2009 and November 30, 2020, was conducted to evaluate clinical outcomes of PRPLS resection. Patient demographics, histopathologic subtypes, overall survival (OS), progression-free survival (PFS), disease recurrence rate, and tumor stage were reviewed and analyzed. Univariate analysis was done to identify factors potentially affecting OS and PFS of PRPLS patients. Multivariate Cox proportional hazards analysis was used to evaluate the impact of various clinicopathological factors on OS and PFS of PRPLS patients.Results:Fifty-one PRPLS patients (28 Males, 23 Females; mean age 56.25 years) were evaluated. There was no significant effect of age, gender, contiguous organ resection, degree of differentiation and tumor size on the OS and PFS of the patients. Univariate analysis showed that negative surgical margin and early tumor stage significantly correlated with OS and PFS (allP< 0.001). Multivariate analysis showed that tumor stage [hazard ratio (HR) = 1.177,P= 0.001] was an independent predictors of poor progression-free survival, and surgical margins [HR = 4.0674P= 0.038] and tumor stage [HR = 1.167P= 0.001] were identified as independent predictors of poor overall survival.Conclusion:Negative surgical margin is a prognostic factor of OS, and can prolong the postoperative survival time of PRPLS patients. Tumor stage is a prognostic factor for OS and PFS, and can influence the survival of PRPLS patients. Earlier tumor stages of PRPLS are associated with significantly better outcomes.

Post-surgery mesh infections are one of the most common complications of hernia repair at the interface of implant materials and tissue, because high doses of antimicrobial agents are toxic and low doses of antibacterial agents are ineffective, with no good clinical solution currently available. To reduce the infection rates after mesh implantation, we designed a “one-pot synthesized” mesoporous silica nanoplatform consisting of levofloxacin (Lev) and silver (Lev@MSN@Ag) composites with poly-L-lactide (PLLA) electrospun fibrous membranes via blending electrospinning. With advances in the combined antibacterial agents Lev and Ag at a low dosage for the treatment of drug-resistant bacterial infections (28 μg mL⁻¹ Lev and 12 μg mL⁻¹ Ag) with a concentration of 5 × 10⁵ CFU mL⁻¹, the composite electrospun fibers act as a carrier for drug-loading and have an antibacterial effect over 8 weeks. Lev@MSN@Ag–PLLA fibers showed a superior antibacterial effect on drug resistant strains in the in vitro test at low doses of antibacterial agents. Further, the in vivo study showed that Lev@MSN@Ag–PLLA fibers significantly inhibited bacterial growth and infection over 8 weeks through the combined effect of low dosage antibacterial drugs. In conclusion, the Lev@MSN@Ag–PLLA fibers provided an advanced combined antibacterial nanoplatform of low dosage for the treatment of drug-resistant bacterial infections.

Pancreatic cancer is susceptible to gemcitabine resistance, and patients receive less benefit from gemcitabine chemotherapy. Previous studies report that gambogic acid possesses antineoplastic properties; however, to our knowledge, there have been no specific studies on its effects in pancreatic cancer. Therefore, the purpose of this study was to explore whether increases the sensitivity of pancreatic cancer to gemcitabine, and determine the synergistic effects of gambogic acid and gemcitabine against pancreatic cancer. The effects of gambogic acid on cell viability, the cell cycle, and apoptosis were assessed using 4,5-dimethylthiazol-2-yl)-3,5-diphenylformazan (MTT) and flow cytometry in pancreatic cancer cell lines. Protein expression was detected by western blot analysis and mRNA expression was detected using q-PCR. A xenograft tumor model of pancreatic cancer was used to investigate the synergistic effects of gambogic acid and gemcitabine. Gambogic acid effectively inhibited the growth of pancreatic cancer cell lines by inducing S-phase cell cycle arrest and apoptosis. Synergistic activity of gambogic acid combined with gemcitabine was observed in PANC-1 and BxPC-3 cells based on the results of MTT, colony formation, and apoptosis assays. Western blot results demonstrated that gambogic acid sensitized gemcitabine-induced apoptosis by enhancing the expression of cleaved caspase-3, cleaved caspase-9, cleaved-PARP, and Bax, and reducing the expression of Bcl-2. In particular, gambogic acid reduced the expression of the ribonucleotide reductase subunit-M2 (RRM2) protein and mRNA, a trend that correlated with resistance to gemcitabine through inhibition of the extracellular signal-regulated kinase (ERK)/E2F1 signaling pathway. Treatment with gambogic acid and gemcitabine significantly repressed tumor growth in the xenograft pancreatic cancer model. Immunohistochemistry results demonstrated a downregulation of p-ERK, E2F1, and RRM2 in mice receiving gambogic acid treatment and combination treatment. These results demonstrate that gambogic acid sensitizes pancreatic cancer cells to gemcitabine in vitro and in vivo by inhibiting the activation of the ERK/E2F1/RRM2 signaling pathway. The results also indicate that gambogic acid treatment combined with gemcitabine might be a promising chemotherapy strategy for pancreatic cancer.