Growing evidence indicated that the gut microbiota was the intrinsic and essential component of the cancer microenvironment, which played vital roles in the development and progression of colorectal cancer (CRC). In our present study, we investigated the alterations of fecal abundant microbiota with real‐time quantitative PCR and the changes of indicators of gut mucosal barrier from 53 early‐stage CRC patients and 45 matched healthy controls. We found that the traditional beneficial bacteria such as Lactobacillus and Bifidobacterium decreased significantly and the carcinogenic bacteria such as Enterobacteriaceae and Fusobacterium nucleatum were significantly increased in CRC patients. We also found gut mucosal barrier dysfunction in CRC patients with increased levels of endotoxin (LPS), D‐lactate, and diamine oxidase (DAO). With Pearson’s correlation analysis, D‐lactate, LPS, and DAO were correlated negatively with Lactobacillus and Bifidobacterium and positively with Enterobacteriaceae and F. nucleatum. Our present study found dysbiosis of the fecal microbiota and dysfunction of the gut mucosal barrier in patients with early‐stage CRC, which implicated that fecal abundant bacteria and gut mucosal barrier indicators could be used as targets to monitor the development and progression of CRC in a noninvasive and dynamic manner.

Acetaminophen is a widely used antipyretic and analgesic drug, and its overdose is the leading cause of drug-induced acute liver failure. This study aimed to investigate the effect and mechanism of Lacticaseibacillus casei Shirota (LcS), an extensively used and highly studied probiotic, on acetaminophen-induced acute liver injury. C57BL/6 mice were gavaged with LcS suspension or saline once daily for 7 days before acute liver injury was induced via intraperitoneal injection of 300 mg/kg acetaminophen. The results showed that LcS significantly decreased acetaminophen-induced liver and ileum injury, as demonstrated by reductions in the increases in aspartate aminotransferase, total bile acids, total bilirubin, indirect bilirubin, and hepatic cell necrosis. Moreover, LcS alleviated acetaminophen-induced intestinal mucosal permeability, decreased serum IL-1α and lipopolysaccharide levels, and elevated serum eosinophil chemokine (eotaxin) and hepatic glutathione levels. Furthermore, analysis of the gut microbiota and metabolome showed that LcS reduced the acetaminophen-enriched levels of Cyanobacteria , Oxyphotobacteria , long-chain fatty acids, cholesterol, and sugars in the gut. Additionally, the transcriptomic and proteomic results showed that LcS mitigated the decrease in metabolic and immune pathways as well as glutathione formation during acetaminophen-induced acute liver injury. This is the first study showing that pretreatment with LcS alleviates acetaminophen-enriched acute liver injury, and it provides a reference for the application of LcS. IMPORTANCE: Acetaminophen is the most frequently used antipyretic analgesic worldwide. As a result, overdoses easily occur and lead to drug-induced acute liver injury, which quickly progresses to liver failure with a mortality of 60%–80% if not corrected in time. The current emergency treatment for overused acetaminophen needs to be administered within 8 hours to avoid liver injury or even liver failure. Therefore, developing preventive strategies for liver injury during planned acetaminophen medication is particularly important, preferably nonpharmacological methods. Lacticaseibacillus casei Shirota (LcS) is a famous probiotic that has been used for many years. Our study found that LcS significantly alleviated acetaminophen-induced acute liver injury, especially acetaminophen-induced liver injury toward fulminant hepatic failure. Here, we elucidated the function and potential mechanisms of LcS in alleviating acetaminophen-induced acute liver injury, hoping it will provide preventive strategies to people during acetaminophen treatment.

Both schizophrenia (SZ) and multiple sclerosis (MS) affect millions of people worldwide and impose a great burden on society. Recent studies indicated that MS elevated the risk of SZ and vice versa, whereas the underlying pathological mechanisms are still obscure. Considering that fecal microbiota played a vital role in regulating brain functions, the fecal microbiota and serum cytokines from 90 SZ patients and 71 age‐, gender‐, and BMI‐matched cognitively normal subjects (referred as SZC), 22 MS patients and 33 age‐, gender‐, and BMI‐matched healthy subjects (referred as MSC) were analyzed. We found that both diseases demonstrated similar microbial diversity and shared three differential genera, including the down‐regulated Faecalibacterium, Roseburia, and the up‐regulated Streptococcus. Functional analysis indicated that the three genera were involved in pathways such as “carbohydrate metabolism” and “amino acid metabolism.” Moreover, the variation patterns of serum cytokines associated with MS and SZ patients were a bit different. Among the six cytokines perturbed in both diseases, TNF‐α increased, while IL‐8 and MIP‐1α decreased in both diseases. IL‐1ra, PDGF‐bb, and RANTES were downregulated in MS patients but upregulated in SZ patients. Association analyses showed that Faecalibacterium demonstrated extensive correlations with cytokines in both diseases. Most notably, Faecalibacterium correlated negatively with TNF‐α. In other words, fecal microbiota such as Faecalibacterium may contribute to the coexistence of MS and SZ by regulating serum cytokines. Our study revealed the potential roles of fecal microbiota in linking MS and SZ, which paves the way for developing gut microbiota‐targeted therapies that can manage two diseases with a single treat.

Background: Intestinal barrier injury contributes to multiple diseases such as obesity and diabetes, whereas no treatment options are available.Methods: Due to close interactions between mucosal microbiome and intestinal barrier, we evaluated the potential of mucosal bacteria in providing targets for high‐fat diet (HFD)–related intestinal barrier injury. Whole‐genome metagenomics was used to evaluate mucosal microbiome, while intestinal barrier injury was estimated using serum LPS, FITC‐dextran intensity, and ZO‐1 protein.Results: We found that HFD induced significant fat accumulation in epididymal tissue at weeks 4 and 12, while ALT, LDL, and TC increased at week 12. Intestinal barrier injury was confirmed by elevated serum LPS at both weeks, upregulated FITC‐dextran intensity, and decreased ZO‐1 protein at week 12. Fourteen species such as Phocaeicola vulgatus differed in HFD‐fed mice. The co‐occurrence network of mucosal microbiome shifted from scale‐free graph in controls to nearly random graph in HFD‐fed mice. Besides, 10 hub bacteria especially Bacteroides ovatus decreased drastically in both mucosal and fecal samples of HFD‐fed mice, correlated with intestinal permeability, ALT, and KEGG pathways such as “Mitochondrial biogenesis” and “metabolism”. Moreover, Bacteroides ovatus has been confirmed to improve intestinal barrier function in a recent study.Conclusion: Mucosal hub bacteria can provide potential targets for improving HFD‐related intestinal barrier function.

Ammonia(NH₃) is the most abundant alkaline gas in the atmosphere. It is the root cause of the formation of most secondary particulates in PM2.5 and the accelerator of the haze pollution formation in the atmosphere. Therefore the monitoring of the NH₃ concentration is very important to the environmental protection. In this paper, the principle of NH₃ concentration detection based on Lambert-Beer law has been introduced. A dual-channel modulated ultraviolet photoelectric signal detection circuit for NH₃ concentration has been designed and its performance index has been studied. And then a precision detection circuit is designed, which is composed of a trans-impedance amplifier and a lock-in amplifier, with which the output of the UV photoelectric detector can be amplified to a suitable voltage range, and the DC noise of the pre-stage amplifier is effectively removed by the lock-in amplifier. The designed circuit has been tested for the NH3 concentration quantitative measuring in the laboratory, with the exchange calibration method being used to ensure the consistency of the two channels. It can be drawn from the test results that the designed circuit is of high SNR, measuring accuracy and a large dynamic range. The NH₃ concentration detection limit of vehicle emissions can reach 2ppm, while the detection precision is ±19ppm.