Transatmospheric ileal stoma manometry can be applied for the early detection of stoma outlet obstruction

BackgroundStoma outlet obstruction (SOO) is a common complication of diverting ileostomy and usually detected at the advanced stage when the intestine is obviously obstructed. The objective of this study is to explore the efficacy of transatmospheric ileal stoma manometry (TISM) in early detection of SOO before the manifestation of intestinal obstruction.MethodsA single-center prospective study was performed in patients scheduled to undergo reversal ileostomy and laparoscopic anterior rectal resection and diverting ileostomy in Second Affiliated Hospital of Zhejiang University School of Medicine from 1st July 2022 to 31st December 2022. The stoma pressure was measured by TISM at different time points.ResultsThe mean stoma pressure of the 30 patients before reversal ileostomy was 5.21 cmH2O which was considered as normal standard of stoma pressure, and ranged from 1.2 to 8.56 cmH2O. After excluding two patients with anastomotic leakage, a total of 38 patients who were subjected to laparoscopic anterior rectal resection and diverting ileostomy were further included in this study. The incidence of anastomotic leakage was 5% and that of SOO was 12.5%. The mean postoperative obstruction time was 5.2 (3-7) days and the mean time from elevated stoma pressure to diagnosed as SOO was 2.8 (2-4) days in the five patients who developed SOO. The pressure measured at the third stoma manometry time point (second day after return of gut function) (10.23 vs. 6.04 cmH2O, p<0.001) and the postoperative hospital stay (10 vs. 8.49 days, p=0.028) showed significantly difference between the SOO and non-SOO groups. The pressures measured at the first time point (before return of gut function) (4 vs. 4.49 cmH2O, p=0.585), the second time point (the day of return of gut function) (6.8 vs. 5.62 cmH2O, p=0.123), and the fourth time point (discharge day) (5.88 vs. 5.9 cmH2O, p=0.933) showed no significant difference in both groups.ConclusionTISM can be utilized for early detection of SOO and can be incorporated as a novel diagnostic method together with abdominal CT scan to realize the goal of ERAS

Systems Pharmacology-Based Research on the Mechanism of Tusizi-Sangjisheng Herb Pair in the Treatment of Threatened Abortion

Threatened abortion (TA) is a common complication with high incidence in the first trimester of pregnancy, which will end in miscarriage if not treated properly. The Chinese herbs Cuscutae Semen (Tusizi in Chinese) and Herba Taxilli (Sangjisheng in Chinese) first recorded in the ancient classic medical book Shennong Bencao Jing are effective and widely used as an herb pair for the treatment of TA, while the active ingredients and the functional mechanism of Tusizi-Sangjisheng herb pair treating TA are still unknown. In order to exploit the relationship between those two herbs and TA, systems pharmacology analysis was carried out in this study. A total of 75 ingredients of Tusizi-Sangjisheng were collected from Traditional Chinese Medicine System Pharmacology Database and Analysis Platform (TCMSP). 12 bioactive compounds were screened, and 153 directly related targets were predicted by systematic models. Besides, Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were used to systematically explore the potential mechanisms of Tusizi-Sangjisheng treating TA. Meanwhile, Compound-Target (C-T), Target-Disease (T-D), and Target-Pathway (T-P) networks were constructed to further quest the underlying functional mechanisms of Tusizi-Sangjisheng. As a result, 31 targets and 3 key pathways were found to be directly related to TA that includes mitogen-activated protein kinases (MAPKs), phosphatidylinositol-3-kinase/protein kinase B (PI3K-Akt), and transforming growth factor-β (TGF-β) signaling pathways. The results in this study may provide some valuable clues about the molecular mechanisms of the efficient Chinese herb pair Tusizi-Sangjisheng in the treatment of TA

Urchin-like Fe₃O₄@Bi₂S₃ Nanospheres Enable the Destruction of Biofilm and Efficiently Antibacterial Activities

Biofilm-associated infections (BAIs) have been considered a major threat to public health, which induce persistent infections and serious complications. The poor penetration of antibacterial agents in biofilm significantly limits the efficiency of combating BAIs. Magnetic urchin-like core–shell nanospheres of Fe3O4@Bi2S3 were developed for physically destructing biofilm and inducing bacterial eradication via reactive oxygen species (ROS) generation and innate immunity regulation. The urchin-like magnetic nanospheres with sharp edges of Fe3O4@Bi2S3 exhibited propeller-like rotation to physically destroy biofilm under a rotating magnetic field (RMF). The mild magnetic hyperthermia improved the generation of ROS and enhanced bacterial eradication. Significantly, the urchin-like nanostructure and generated ROS could stimulate macrophage polarization toward the M1 phenotype, which could eradicate the persistent bacteria with a metabolic inactivity state through phagocytosis, thereby promoting the recovery of implant infection and inhibiting recurrence. Thus, the design of magnetic-driven sharp-shaped nanostructures of Fe3O4@Bi2S3 provided enormous potential in combating biofilm infections

Urchin-like Fe₃O₄@Bi₂S₃ Nanospheres Enable the Destruction of Biofilm and Efficiently Antibacterial Activities

Biofilm-associated infections (BAIs) have been considered a major threat to public health, which induce persistent infections and serious complications. The poor penetration of antibacterial agents in biofilm significantly limits the efficiency of combating BAIs. Magnetic urchin-like core–shell nanospheres of Fe3O4@Bi2S3 were developed for physically destructing biofilm and inducing bacterial eradication via reactive oxygen species (ROS) generation and innate immunity regulation. The urchin-like magnetic nanospheres with sharp edges of Fe3O4@Bi2S3 exhibited propeller-like rotation to physically destroy biofilm under a rotating magnetic field (RMF). The mild magnetic hyperthermia improved the generation of ROS and enhanced bacterial eradication. Significantly, the urchin-like nanostructure and generated ROS could stimulate macrophage polarization toward the M1 phenotype, which could eradicate the persistent bacteria with a metabolic inactivity state through phagocytosis, thereby promoting the recovery of implant infection and inhibiting recurrence. Thus, the design of magnetic-driven sharp-shaped nanostructures of Fe3O4@Bi2S3 provided enormous potential in combating biofilm infections

Butyrate ameliorates quinolinic acid–induced cognitive decline in obesity models

Obesity is a risk factor for neurodegenerative disease associated with cognitive dysfunction, including Alzheimer’s disease. Low-grade inflammation is common in obesity, but the mechanism between inflammation and cognitive impairment in obesity is unclear. Accumulative evidence shows that quinolinic acid (QA), a neuroinflammatory neurotoxin, is involved in the pathogenesis of neurodegenerative processes. We investigated the role of QA in obesity-induced cognitive impairment and the beneficial effect of butyrate in counteracting impairments of cognition, neural morphology, and signaling. We show that in human obesity, there was a negative relationship between serum QA levels and cognitive function and decreased cortical gray matter. Diet-induced obese mice had increased QA levels in the cortex associated with cognitive impairment. At single-cell resolution, we confirmed that QA impaired neurons, altered the dendritic spine’s intracellular signal, and reduced brain-derived neurotrophic factor (BDNF) levels. Using Caenorhabditis elegans models, QA induced dopaminergic and glutamatergic neuron lesions. Importantly, the gut microbiota metabolite butyrate was able to counteract those alterations, including cognitive impairment, neuronal spine loss, and BDNF reduction in both in vivo and in vitro studies. Finally, we show that butyrate prevented QA-induced BDNF reductions by epigenetic enhancement of H3K18ac at BDNF promoters. These findings suggest that increased QA is associated with cognitive decline in obesity and that butyrate alleviates neurodegeneration