Dynamics of key gut microbiome taxa in piglets under the influence of an isotonic protein mixture

Gut morphology and gene expression in obesity: Short review and perspectives

The intestinal microbiota has been implicated in the pathogenesis of complications following colorectal surgery, yet perioperative changes in gut microbiome composition are poorly understood. The objective of this study was to characterize the perioperative gut microbiome in patients undergoing colonoscopy and colorectal surgery and determine factors influencing its composition. Using Illumina amplicon sequencing coupled with targeted metabolomics, we characterized the fecal microbiota in: (A) patients (n = 15) undergoing colonoscopy who received mechanical bowel preparation, and (B) patients (n = 15) undergoing colorectal surgery who received surgical bowel preparation, composed of mechanical bowel preparation with oral antibiotics, and perioperative intravenous antibiotics. Microbiome composition was characterized before and up to six months following each intervention. Colonoscopy patients had minor shifts in bacterial community composition that recovered to baseline at a mean of 3 (1–13) days. Surgery patients demonstrated substantial shifts in bacterial composition with greater abundances of Enterococcus, Lactobacillus, and Streptococcus. Compositional changes persisted in the early postoperative period with recovery to baseline beginning at a mean of 31 (16–43) days. Our results support surgical bowel preparation as a factor significantly influencing gut microbial composition following colorectal surgery, while mechanical bowel preparation has little impact.

BACKGROUNDEndoscopic mucosa resection (EMR) is an important minimally invasive surgical method for treating early digestive tract tumors. In recent years, the crucial role of intestinal microbiota in disease occurrence and development has attracted increasing attention. However, the changes in intestinal microbiota after EMR and the effect of dietary fiber intervention on microbiota recovery remain insufficiently elucidated.AIMTo investigate the effects of dietary fiber intervention on intestinal microbiota recovery in patients undergoing EMR and evaluate its potential to improve postoperative outcomes and intestinal microecological balance.METHODSThis retrospective study analyzed intestinal microbiota sequencing and dietary fiber intervention in patients with EMR. Patients who underwent EMR surgery between 2020 and 2023 were selected and divided into a routine follow-up group and a dietary fiber intervention group. High-throughput 16S rRNA gene sequencing was performed to detect changes in patient intestinal microbiota, and microbiota diversity, structure, and function in different intervention groups were compared and analyzed.RESULTSA total of 86 patients with EMR were included in the study. Results showed that: (1) Intestinal microbiota diversity significantly decreased after EMR surgery, with notable changes in the proportion of Gram-negative bacilli and anaerobic bacteria; (2) The microbiota recovery rate in the dietary fiber intervention group was significantly higher than that in the control group, with a significantly higher microbiota diversity index (P < 0.05); and (3) The abundance of lactobacilli and bifidobacteria in the intervention group increased substantially, and intestinal barrier-related functional gene expression was upregulated.CONCLUSIONDietary fiber intervention can effectively promote intestinal microbiota recovery in patients with EMR, improve intestinal microecological balance, and provide a new intervention strategy for clinical post-EMR patient rehabilitation.

The Effectiveness of a Human Patient Simulator in the ATLS Shock Skills Station

The antidiabetic drug metformin has been proposed to affect non-alcoholic fatty liver disease (NAFLD) through its effects on intestinal microbiota and barrier function. However, so far most studies focused on long-term effects and more progressed disease stages. The aim of this study was to assess in two experimental settings, if the onset of NAFLD is associated with changes of intestinal microbiota and barrier function and to determine effects of metformin herein. C57Bl/6J mice were fed a liquid control diet (C) or fat-, fructose- and cholesterol-rich diet (FFC) for four days or six weeks ±300 mg/kg BW/day metformin (Met). Markers of liver health, intestinal barrier function and microbiota composition were assessed. Metformin treatment markedly attenuated FFC-induced NAFLD in both experiments with markers of inflammation and lipidperoxidation in livers of FFC + Met-fed mice being almost at the level of controls. Metformin treatment attenuated the loss of tight junction proteins in small intestine and the increase of bacterial endotoxin levels in portal plasma. Changes of intestinal microbiota found in FFC-fed mice were also significantly blunted in FFC + Met-fed mice. Taken together, protective effects of metformin on the onset of NAFLD are associated with changes of intestinal microbiota composition and lower translocation of bacterial endotoxins.

Objectives • To assess the intensity of labor pain and outcome of labor among the control group. • To assess the effectiveness of ambulation on intensity of labor pain and outcome of labor among the experimental group. • To assess the usefulness of ambulation by opinionnaire among experimental group. • To compare the effectiveness of ambulation on the intensity of labor pain and outcome of labor among experimental and control groups. • To find an association between the intensity of labor pain with selected demographic variables. Materials and methods An experimental research approach was used for the study. Random sampling technique was used to allocate the subjects into experimental and control groups. Visual analog scale was used to assess the intensity of pain and observational check list was used to assess the outcome of labor. The study comprised of 40 primigravida mothers and they were grouped as experimental and control through randomization. One group received ambulation treatment, the other did not. The researcher then observed the groups to determine the effect of the treatment. Results The collected data was analyzed by descriptive and inferential statistics. The intensity of pain revealed that 40% in the experimental and 55% in the control groups experienced severe pain. The labor augmentation revealed that both oxytocin and cerviprime gel was used for 30% in the experimental and 35% in the control groups. On the mode of delivery, majority of mothers (60%) had normal vaginal delivery both in experimental and control groups. On the duration of the first stage of labor revealed that 50% in the experimental and 20% in the control groups were between 10 to 12 hours. Second stage of labor revealed that majority were between 1 and 2 hours in both the control and experimental groups. The opinion of experimental group mothers on ambulation revealed that half of the mothers (50%) agreed for recommending the ambulation for their neighbors and friends and less than half (35%) of them have agreed for comfort during first stage of labor and 40% of them have agreed for ambulation should be made as a routine in labor room. In the experimental group, mean pain score (6.8) is less than the control group (7.5). The calculated Mann-Whitney Z-value (2.045) is greater than the Z α-value of 1.960 at 0.05 level of significance. In the experimental group, the mean duration of first stage of labor score (3.95) is significantly higher than the control group mean score (3.00). The mean outcome of labor in experimental group (13.95) is greater than the control group. Conclusion There was a significant difference in the duration of first stage of labor between the experimental and control groups. But, there was no significant difference in the overall outcome of labor between experimental and control groups. There was no significant association between intensity of labor pain with selected demographic variables. This may be because of small sample size. How to cite this article Savitha V, Nayak S, Paul S. Effect of Ambulation during First Stage of Labor on Labor Pain and Outcome of Labor among the Primigravida Mothers in a Selected Hospital, Mangalore. J South Asian Feder Obst Gynae 2013;5(1):1-3.

Aims The underlying mechanisms involved in Vitamin A- (VA-) related changes in glucose metabolic disorders remain unclear. Recent evidence suggests that intestinal microbiota is closely linked to the metabolic syndrome. Here, we explored whether and how intestinal microbiota affects glucose homeostasis in VA-deficient diet-fed mice. Methods Six-week-old male C57BL/6 mice were randomly placed on either a VA-sufficient (VAS) or VA-deficient (VAD) diet for 10 weeks. Subsequently, a subclass of the VAD diet-fed mice was switched to a VA-deficient rescued (VADR) diet for an additional 8 weeks. The glucose metabolic phenotypes of the mice were assessed using glucose tolerance tests and immunohistochemistry staining. Changes in intestinal microbiota were assessed using 16S gene sequencing. The intestinal morphology, intestinal permeability, and inflammatory response activation signaling pathway were assessed using histological staining, western blots, quantitative-PCR, and enzyme-linked immunosorbent assays. Results VAD diet-fed mice displayed reduction of tissue VA levels, increased area under the curve (AUC) of glucose challenge, reduced glucose-stimulated insulin secretion, and loss of β cell mass. Redundancy analysis showed intestinal microbiota diversity was significantly associated with AUC of glucose challenge and β cell mass. Redundancy analysis showed intestinal microbiota diversity was significantly associated with AUC of glucose challenge and κB signaling pathway activation. Reintroduction of dietary VA to VAD diet-fed mice restored tissue VA levels, endocrine hormone profiles, and inflammatory response, which are similar to those observed following VAS-controlled changes in intestinal microbiota. Conclusions We found intestinal microbiota effect islet function via controlling intestinal inflammatory phenotype in VAD diet-fed mice. Intestinal microbiota influences could be considered as an additional mechanism for the effect of endocrine function in a VAD diet-driven mouse model.

SUMMARY Fifty nine 3-day-old gnotobiotic pigs were randomly assigned to 4 experimental groups: 14 pigs were orally inoculated with rotavirus (rv), 14 were orally inoculated with enterotoxigenic Escherichia coli (etec), 18 were orally inoculated with both agents, and 13 were controls. Pigs inoculated with rv plus etec were given the rv inoculum at 3 days of age and then, 24 hours later, were given the etec inoculum. Three pigs inoculated only with rv, 3 pigs inoculated only with etec, 4 pigs inoculated with rv plus etec, and 3 pigs in the control group were euthanatized at 5 and 7 days of age. Two pigs in each of the 4 experimental groups also were euthanatized at 9 days of age. Intestinal segments from 6 sites in the small intestine were examined by virologic, bacteriologic, and histologic procedures. For 10 days after inoculation, the remaining pigs in each group were observed clinically to monitor severity and duration of diarrhea, mortality, and shedding of rv or etec. Pigs inoculated with the combined rv plus etec inoculum developed more severe diarrhea, compared with pigs inoculated with the single agents; all dually inoculated pigs died between 3 and 6 days after inoculation. There was no mortality in pigs inoculated with either rv or etec. Lesions were restricted to the small intestine in pigs inoculated with rv plus etec and in pigs inoculated with rv or etec. There was no difference in the severity of the villus atrophy between the dually inoculated pigs and pigs inoculated only with rv. The pigs inoculated only with etec at 5 days of age had villus atrophy in the distal half of the small intestine, which progressed proximally to involve all segments except the duodenum in pigs euthanatized at 9 days of age. Escherichia coli organisms were observed in all segments of the small intestine by light microscopy and in Gram-stained intestinal smears from pigs inoculated only with etec or dually inoculated with rv plus etec. The etec organisms in the proximal half of the small intestine were not adherent to intestinal villi, but were prevalent in the lumen of the small intestine, and a few expressed K99 antigen. In the distal half of the small intestine of the dually inoculated pigs or of the pigs inoculated only with etec, E coli organisms were adherent to villous epithelial cells of the small intestine, expressed K99 antigen, and were most numerous in the terminal aspect of the ileum. The concentration of bacteria (colony-forming units per centimeter of intestine) in the jejunum and ileum was significantly (P ≤ 0.01) higher in the dually inoculated pigs euthanatized at 7 and 9 days, compared with bacterial counts from similar specimens from pigs inoculated only with etec. The more severe clinical disease and mortality in the pigs inoculated with rv plus etec were attributed to a combined malabsorption and hypersecretory diarrhea, which resulted in excessive dehydration and loss of flesh not found in pigs inoculated with only one agent. We concluded that the combined inoculum induced an additive, but not a synergistic effect, because lesions were no more severe in the dually inoculated pigs, compared with those in the single agent-inoculated pigs. Rotavirus did not consistently enhance the growth of E coli in the small intestine of the dually inoculated pigs.

This study aimed to evaluate the effectiveness of combining Lactobacillus reuteri with racecadotril in treating pediatric rotavirus enteritis, focusing on its impact on intestinal mucosa and immune function. Eighty-five children diagnosed with pediatric rotavirus enteritis were randomly divided into two groups: the control group (43 cases) receiving racecadotril alone and the observation group (42 cases) treated with both Lactobacillus reuteri and racecadotril. Evaluation of the RV conversion rate and treatment efficacy was conducted at 3d, 5d, and 7d post-treatment. The study also assessed changes in intestinal mucosal barrier function, immune response, and intestinal microbiota. The observation group exhibited significantly higher RV conversion rates at 3d, 5d, and 7d post-treatment compared to the control group (P<0.05), reaching 61.90%, 76.19%, and 92.86%, respectively. Following treatment, the observation group showed improvements in mucosal barrier function, increased CD4+ levels, decreased AGEs, D-lactic acid, endotoxins, and CD8+ levels. There were notable changes in intestinal microbiota, with elevated Lactobacillus and Bifidobacterium levels and decreased Escherichia coli. Combining Lactobacillus reuteri and racecadotril in treating pediatric rotavirus enteritis demonstrated efficacy in regulating intestinal microbiota, alleviating mucosal barrier dysfunction, improving immune function, and enhancing treatment effectiveness.

Monascus purpureus M-32 fermented soybean meal improves the growth, immunity parameters, intestinal morphology, disease resistance, intestinal microbiota and metabolome in Pacific white shrimp (Litopenaeus vannamei)

Objective To investigate the effects of probiotics on the survival of sepsis mice and their mechanism. Methods A total of 60 male C57BL6 mice were randomly divided into 3 groups, respectively, the sham operation group (n = 20), the control group (n = 20) and the experimental group (n = 20). After feeding 2 d, mice in the experimental group were given 200 μL probiotics solution daily; mice in the control and sham operation groups were given 200 μL NaCl solution, with continuous intragastric administration for 4 weeks. Cecal ligation and puncture (CLP) was performed on the mice in the experimental and control groups, while mice in the sham operation group were performed with the same procedures of CLP except for cecal puncture. Ten mice in each group were used to observe their activity and survival of 7 d, and the blood and colon tissues were taken in the other 10 mice in each group after 24 hours. The expression levels of serum inflammatory factor interleukin 22 (IL-22), IL-2 and tumor necrosis factor alpha (TNF-α) were detected by enzyme-linked immunosorbent assay, the colon tissues were measured by the hematoxylin and eosin (HE) staining method, and the expression of colonic mucosa (Occludin) in each group was observed by the immunohistochemical method. Results Mice in the sham operation group grew well, mice in the control group curled up in a corner of the cage and trembled, and mice in the experimental group were more active than the experimental group, without obvious tremor. At 7 d, there were still 3 survived mice in the experimental group which were given euthanasia; the 7 d survival was significantly higher than that of the control group (P = 0.020). At 7 d, 10 mice in the sham operation group all survived and were given euthanasia. The expressions of serum IL-22 [(103 ± 23) ng/L vs. (27 ± 9) ng/L, t = 7.590, P < 0.001], IL-2 [(328 ± 27) ng/L vs. (77 ± 21) ng/L, t = 21.368, P < 0.001] and TNF-α [(94 ± 22) ng/L vs. (56 ± 9) ng/L, t = 4.734, P < 0.001] in the control group were significantly different as compared to the sham operation group. Meanwhile, the expressions of serum IL-22 [(75 ± 33) ng/L vs. (27 ± 9) ng/L, t = 3.755, P = 0.001], IL-2 [(217 ± 30) ng/L vs. (77 ± 21) ng/L, t = 10.850, P < 0.001] and TNF-α [(107 ± 20) ng/L vs. (56 ± 9) ng/L, t = 5.956, P < 0.001] in the experimental and sham operation groups all showed statistically significant differences. Compared with the control group, the expressions of serum IL-22 [(103 ± 23) ng/L vs. (75 ± 33) ng/L, t = 2.185, P = 0.042] and IL-2 [(328 ± 27) ng/L vs. (217 ± 30) ng/L, t = 8.371, P < 0.001] in the experimental group were significantly different, while the TNF-α [(94 ± 22) ng/L vs. (107 ± 20) ng/L, t = 1.363, P = 0.188] expression showed no statistically significant difference. In the sham operation group, the colonic mucosa was intact and the glands were regularly arranged with little or no inflammatory cell infiltration. However, mice in the control group appeared derangement, deformation and lack of colonic mucosal epithelial glands, fuzzy connected structures of enterocytes, and extensive infiltration of inflammatory cells some of which had crypt abscess. The colonic epithelia of mice in the experimental group were basically complete without erosion and loss, glands were normally arranged, and the infiltration of inflammatory cells decreased more as compared to the control group. The results of immunohistochemistry showed that mice in the sham operation group had complete acinar structures of colonic epithelial cells and more Occludin proteins. The acinar structures of colonic epithelial cells in the control group were destructed and disappeared, and there were infiltration of inflammatory cells and less Occludin proteins. The acinar structures of colonic epithelial cells in the experimental group were complete with widened interacinar gaps, and the expression of Occludin protein increased as compared to the control group. Conclusion Probiotics can inhibit the reduction of Occludin of intestinal epithelial cells and stabilize barrier structures of intestinal mucosas, thus effectively improving the survival of septic mice. Key words: Probiotics; Sepsis; Occludin

This randomized-controlled trial demonstrates that an exercise consultation, based on the transtheoretic model of exercise behavior change, significantly improves short-term adherence to exercise.

Lead (Pb) is a hazardous pollutant in water environments that can cause significant damage to aquatic animals and humans. In this study, crucian carp (Carassius auratus) were exposed to waterborne Pb for 96 h; then, histopathological analysis, quantitative qPCR analysis, and 16S high-throughput sequencing were performed to explore the effects of Pb on intestinal bioaccumulation, structural damage, oxidative stress, immune response, and microbiota imbalance of C. auratus. After Pb exposure, the intestinal morphology was obviously damaged, including significantly increasing the thickness of the intestinal wall and the number of goblet cells and reducing the depth of intestinal crypts. Pb exposure reduced the mRNA expressions of Claudin-7 and villin-1 while significantly elevated the level of GST, GSH, CAT, IL-8, IL-10, IL-1, and TNF-α. Furthermore, 16S rRNA analysis showed that the Shannon and Simpson indices decreased at 48 h after Pb exposure, and the abundance of pathogenic bacteria (Erysipelotrichaceae, Weeksellaceae, and Vibrionaceae) increased after Pb exposure. In addition, the correlation network analysis found that Proteobacteria were negatively correlated with Firmicutes and positively correlated with Bacteroidetes. Functional prediction analysis of bacteria speculated that the change in intestinal microbiota led to the PPAR signaling pathway and peroxisome function of the intestine of crucian carp was increased, while the immune system and membrane transport function were decreased. Finally, canonical correlation analysis (CCA) found that there were correlations between the intestinal microbiota, morphology, antioxidant factors, and immune factors of crucian carp after Pb exposure. Taken together, our results demonstrated that intestinal flora dysbiosis, morphological disruption, oxidative stress, and immune injury are involved in the toxic damage of Pb exposure to the intestinal structure and function of crucian carp. Meanwhile, Pb exposure rapidly increased the abundance of pathogenic bacteria, leading to intestinal disorders, further aggravating the damage of Pb to intestinal structure and function. These findings provide us a basis for the link between gut microbiome changes and heavy metal toxicity, and gut microbiota can be used as biomarkers for the evaluation of heavy metal pollution in future.

Introduction: Aldehyde dehydrogenases (ALDH), particularly ALDH1B1 has been shown to have increased expression in both human and APCMin mice colorectal tumors. Studies have proposed the use of ALDH1B1 as a potential novel human colorectal tumor marker. Previous in vitro studies have shown that ALDH1B1 plays a critical role in colon carcinogenesis. The goal of this study is to understand the in vivo role of ALDH1B1 in colon carcinogenesis using a newly developed mouse model, APCMinAldh1b1−/− mice, through characterization of its phenotype in tumor growth and development, and elucidating the underlying potential molecular mechanisms. Methods: We generated APCMinAldh1b1−/-. At 12-14 weeks old, the experimental group APCMinAldh1b1−/- (n=6) and control group APCMinAldh1b1+/+ (n=7) were euthanized. Tumor counts, size and burden for each intestinal segments were recorded. H&amp;E staining was performed and observed for tumor types and counts. Immunohistochemistry using the markers Ki-67 (proliferation), Cleave Caspase 3 (apoptosis), KRT20 (differentiation) were done in colon. IHC of retinoic acid binding proteins (anti-CRBP2 and anti-FABP5) were also performed Results: The experimental group had shown significantly higher total average intestinal tumor burden (6.8 fold) (p=0.0007) and total average tumor counts observed (3.6 fold) (p=0.02). In the colon, there was a 3.5-fold increase in average tumor burden (p=0.017) with a 2.7-fold increase in average tumor size (p=0.025)in the experimental group. We also noticed a trend of increased average tumor counts observed in the colon of the experimental group although statistically insignificant. Average tumor counts of ileum observed was 9-fold higher in experimental group with only 1 mice from control group showed observable small tumor growth which did not meet criteria for tumor size and tumor burden calculation. There were no significant differences in observable tumor counts, tumor size and tumor burden in jejunum. Histologically, all tumors were pedunculated adenocarcinomas. Many unobservable small tumors less than 1mm width and length were seen in the H&amp;E of both ileum and jejunum in the experimental and control group. In the control group, there was less observable tumors compared to the experimental group although the tumor counts on H&amp;E in both groups showed no major differences. This indicates that the tumor size in the experimental group was larger than the control group. On the contrary, average tumor counts of colon in H&amp;E were lower compared to tumor counts observed in both control and experimental groups, indicating low number of small unobservable tumors in colon. Although the tumor counts of colon on H&amp;E and observation between the two groups were statistically insignificant, we noticed a pattern of increased tumor counts in the experimental group suggesting a potential increase in tumor incidence. Immunohistochemical staining of colon is ongoing. Conclusion: ALDH1B1 reduced tumor growth rate in the ileum, and reduced tumor size in the colon suggesting its role in tumor promotion and progression. A larger number of experimental and control group is required to establish its potentially tumor-initiating role in the colon. Further characterization of ALDH1B1 in colon carcinogenesis is ongoing. We are also elucidating the role and regulation of retinoic acid signaling by ALDH1B1 in colorectal tumor growth. Citation Format: Wan Ying Tan, David. J. Orlicky, Ying Chen, Yatrik M. Shah, David C. Thompson, Vasilis Vasiliou. Role of aldehyde dehydrogenase 1B1 in colon carcinogenesis in a newly developed mouse model [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 6141.

Cystic fibrosis (CF) is frequently associated with gastrointestinal problems, including intestinal microbiota dysbiosis. Cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapies, such as elexacaftor-tezacaftor-ivacaftor (ELX/TEZ/IVA), have demonstrated improvements in lung function, abdominal symptoms, and quality of life in patients with CF. However, the impact of these modulators on the intestinal microbiota in the pediatric population remains incompletely understood. The objective of this study was to characterize the changes in the intestinal microbiota of pediatric patients with CF after 6 months of treatment with ELX/TEZ/IVA. Thirty-one patients with CF, aged 6-18 years, were recruited. Stool samples were collected before the initiation of treatment and approximately 6 months thereafter. Microbiota analysis was performed using 16S rRNA gene amplicon sequencing. Statistical analyses were employed to evaluate changes in alpha and beta diversity and variations in the relative abundance of different bacterial taxa. Clinical variables such as concomitant use of azithromycin and probiotics were considered. After 6 months of treatment, no significant changes in the alpha diversity were observed. However, alterations in bacterial composition were detected. A decrease in the abundance of potentially pathogenic bacteria, such as Enterobacteriaceae members (Escherichia/Shigella) was observed. The abundance of genus Blautia increased. Differential analysis according to antibiotic and probiotic consumption revealed specific changes in microbiota composition. ELX/TEZ/IVA therapy for 6 months induces changes in the intestinal microbiota composition of pediatric patients with CF, characterized by a reduction in potentially harmful bacteria and an increase in potentially beneficial bacteria. These findings suggest a modulation towards a healthier intestinal microbiota profile.