• acupuncture
• gut microbiota
• microbiota-gut-brain-axis
• post-stroke cognitive impairment
• traditional Chinese medicine

• gut microbiota
• gut microbiota–brain axis
• immune
• intracerebral hemorrhage
• neuroinflammation
• nlrp3 protein
• stroke
• therapeutics
• white matter injury

• Dysbiosis
• Gut-brain axis
• Major depressive disorder
• Microbiota
• Prebiotic
• Probiotics

• Probiotics/therapeutic use
• Prebiotics/administration & dosage
• Humans
• Depressive Disorder, Major/therapy
• Depressive Disorder, Major/diet therapy
• Gastrointestinal Microbiome
• Brain-Gut Axis/physiology
• Animals

Jianpi-Huatan-Huoxue-Anshen formula [Tzu-Chi cancer-antagonizing & life-protecting II decoction (TCCL)] is a Chinese medical formula that has been clinically shown to reduce the gastrointestinal side effects of chemotherapy in cancer patients and improve their quality of life. However, its effect and mechanism on the intestinal microecology after chemotherapy are not yet clear.

To discover the potential mechanisms of TCCL on gastrointestinal inflammation and microecological imbalance in chemotherapy-treated mice transplanted with hepatocellular carcinoma (HCC).

Ninety-six mice were inoculated subcutaneously with HCC cells. One week later, the mice received a large dose of 5-fluorouracil by intraperitoneal injection to establish a HCC chemotherapy model. Thirty-six mice were randomly selected before administration, and feces, ileal tissue, and ileal contents were collected from each mouse. The remaining mice were randomized into normal saline, continuous chemotherapy, Yangzheng Xiaoji capsules-treated, and three TCCL-treated groups. After treatment, feces, tumors, liver, spleen, thymus, stomach, jejunum, ileum, and colon tissues, and ileal contents were collected. Morphological changes, serum levels of IL-1β, IL-6, IL-8, IL-10, IL-22, TNF-α, and TGF-β, intestinal SIgA, and protein and mRNA expression of ZO-1, NF-κB, Occludin, MUC-2, Claudin-1, and IκB-α in colon tissues were documented. The effect of TCCL on the abundance and diversity of intestinal flora was analyzed using 16S rDNA sequencing.

TCCL treatment improved thymus and spleen weight, thymus and spleen indexes, and body weight, decreased tumor volumes and tumor tissue cell density, and alleviated injury to gastric, ileal, and colonic mucosal tissues. Among proteins and genes associated with inflammation, IL-10, TGF-β, SIgA, ZO-1, MUC-2, and Occludin were upregulated, whereas NF-κB, IL-1β, IL-6, TNF-α, IL-22, IL-8, and IκB-α were downregulated. Additionally, TCCL increased the proportions of fecal Actinobacteria, AF12, Adlercreutzia, Clostridium, Coriobacteriaceae, and Paraprevotella in the intermediate stage of treatment, decreased the proportions of Mucipirillum, Odoribacter, RF32, YS2, and Rikenellaceae but increased the proportions of p_Deferribacteres and Lactobacillus at the end of treatment. Studies on ileal mucosal microbiota showed similar findings. Moreover, TCCL improved community richness, evenness, and the diversity of fecal and ileal mucosal flora.

TCCL relieves pathological changes in tumor tissue and chemotherapy-induced gastrointestinal injury, potentially by reducing the release of pro-inflammatory factors to repair the gastrointestinal mucosa, enhancing intestinal barrier function, and maintaining gastrointestinal microecological balance. Hence, TCCL is a very effective adjuvant to chemotherapy.

• Chinese medicine
• Chemotherapy
• H22 hepatocellular carcinoma
• Intestinal barrier function
• Intestinal microecological balance

• broiler chickens
• cecal microbiota
• dietary lycopene
• feed additive
• growth performance

• ZDYF2020090 Key Research and Development Program of Hainan Province

• gut microbiota
• intestinal immunity
• intestinal microenvironment
• neuroinflammation
• stroke
• treatment

• Humans
• Stroke/drug therapy
• Brain
• Gastrointestinal Microbiome/physiology
• Intestines
• Inflammation

• 2019YFC0840709 National Key Research and Development Program of China
• 81774059 National Natural Science Foundation of China
• 81973626 National Natural Science Foundation of China
• 82204906 National Natural Science Foundation of China
• 2021099 Tianjin Health Committee
• 21JCYBJC01620 Tianjin Municipal Science and Technology Commission of China
• National Key Research and Development Program of China
• National Natural Science Foundation of China

• CXCL11
• DNA methylation
• Escherichia coli
• pig

The intestinal mucosa is a highly compartmentalized structure that forms a direct barrier between the host intestine and the environment, and its dysfunction could result in a serious disease. As T cells, which are important components of the mucosal immune system, interact with gut microbiota and maintain intestinal homeostasis, they may be involved in the process of intestinal barrier dysfunction. P2X7 receptor (P2X7R), a member of the P2X receptors family, mediates the effects of extracellular adenosine triphosphate and is expressed by most innate or adaptive immune cells, including T cells. Current evidence has demonstrated that P2X7R is involved in inflammation and mediates the survival and differentiation of T lymphocytes, indicating its potential role in the regulation of T cell function. In this review, we summarize the available research about the regulatory role and mechanism of P2X7R on the intestinal mucosa-derived T cells in the setting of intestinal barrier dysfunction.

• Intestinal barrier dysfunction
• P2X7 receptor
• T lymphocyte

• Adenosine Triphosphate
• Humans
• Inflammation
• Intestinal Mucosa
• Intestines
• Receptors, Purinergic P2X7

Autism spectrum disorders (ASDs) represent a diagnostic challenge with a still partially uncertain etiology, in which genetic and environmental factors have now been assessed. Among the hypotheses underlying the involvement of biological and environmental factors, the gut–brain axis is of particular interest in autism spectrum disorders. Several studies have highlighted the related incidence of particular gastrointestinal symptoms (GISs) in children suffering from ASDs. Probiotics have shown success in treating several gastrointestinal dysbiotic disorders; therefore, it is plausible to investigate whether they can alleviate behavioral symptoms as well. On these bases, a randomized double-blind crossover study with a placebo was conducted, evaluating the effects of a mixture of probiotics in a group of 61 subjects aged between 24 months and 16 years old with a diagnosis of ASD. Behavioral evaluation was performed through the administration of a questionnaire including a Parenting Stress Index (PSI) test and the Vineland Adaptive Behavior Scale (VABS). The Psycho-Educational Profile and the Autism Spectrum Rating Scale (ASRS) were also evaluated. Microbial composition analyses of fecal samples of the two groups was also performed. The study showed significant improvements in GISs, communication skills, maladaptive behaviors, and perceived parental stress level after the administration of probiotics. Microbiome alpha diversity was comparable between treatment arms and no significant differences were found, although beta diversity results were significantly different in the treatment group between T0 and T1 time points. Streptococcus thermophilus, Bifidobacterium longum, Limosilactobacillus fermentum, and Ligilactobacillus salivarius species were identified as some of the most discriminant taxa positively associated with T1 samples. This preliminary study corroborates the relationship between intestinal microbiota and ASD recently described in the literature.

• Parkinson's disease
• air pollution
• diesel exhaust
• neurodegeneration

• Air Pollutants/toxicity
• Air Pollution/adverse effects
• Humans
• Inflammation/chemically induced
• Neurodegenerative Diseases
• Parkinson Disease/complications
• Parkinson Disease/etiology

• R01 ES031106 NIEHS NIH HHS
• T32 ES015457 NIEHS NIH HHS

Vasoactive intestinal peptide (VIP) plays an important role in the neuro-endocrine-immune system. Mast cells (MCs) are important immune effector cells. This study was conducted to investigate the protective effect of L. casei ATCC 393 on Enterotoxigenic Escherichia coli (ETEC) K88-induced intestinal mucosal immune barrier injury and its association with VIP/MC signaling by in vitro experiments in cultures of porcine mucosal mast cells (PMMCs) and in vivo experiments using VIP receptor antagonist (aVIP) drug. The results showed that compared with the ETEC K88 and lipopolysaccharides (LPS)-induced model groups, VIP pretreatment significantly inhibited the activation of MCs and the release of β-hexosaminidase (β-hex), histamine and tryptase. Pretreatment with aVIP abolished the protective effect of L. casei ATCC 393 on ETEC K88-induced intestinal mucosal immune barrier dysfunction in C57BL/6 mice. Also, with the blocking of VIP signal transduction, the ETEC K88 infection increased serum inflammatory cytokines, and the numbers of degranulated MCs in ileum, which were decreased by administration of L. casei ATCC 393. In addition, VIP mediated the regulatory effect of L. casei ATCC 393 on intestinal microbiota in mice. These findings suggested that VIP may mediate the protective effect of L.casei ATCC 393 on intestinal mucosal immune barrier dysfunction via MCs.

• Lactobacillus casei ATCC 393
• intestinal barrier
• mast cells
• mucosal immune
• probiotic
• vasoactive intestinal peptide

With the continuous development of duck farming and the increasing breeding density, the incidence of duck hepatitis A virus type 1 (DHAV-1) has been on the rise, seriously endangering the development of duck farming. To reduce the use of antibiotics in duck breeding, susceptibility risks and mortality, and avoid virulence recovery and immune failure risk, this study aims to develop a new type of mucosal immune probiotics and make full use of molecular biology techniques, on the level of genetic engineering, to modify Lactococcus lactis (L. lactis). In this study, a secretory recombinant L. lactis named MG1363-VP1 with an enhanced Green Fluorescent Protein (eGFP) and translation enhancer T7g10L was constructed, which could express the VP1-eGFP fusion protein of DHAV-1. The animal experiment in ducklings was performed to detect the immune response and protection effect of oral microecologics by recombinant L. lactis. The results showed that oral L. lactis MG1363-VP1 significantly induced the body’s humoral immune system and mucosal immune system to produce specific anti-VP1 IgG antibodies and mucosal secretory immunoglobulin A (sIgA) for DHAV-1 in ducklings, and cytokines including interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-10 (IL-10), and interferon gamma (IFN-γ). The mortality rate was monitored simultaneously by the natural infestation in the process of production and breeding; notably, the ducklings vaccinated with L. lactis MG1363-VP1 were effectively protected against the nature infection of DHAV-1. The recombinant L. lactis MG1363-VP1 constructed in this study provides a new means of preventing and controlling DHAV-1 infection in the future.

• Lactococcus lactis
• VP1 protein
• duck hepatitis A virus type 1
• mucosal immune

• Lycopene
• antioxidant capacity
• finishing pigs
• inflammatory
• intestinal mucosal morphology

• DNA sequencing
• Organophosphorus pesticides
• inflammation
• lipid profiles
• microbiome

• Animals
• Gastrointestinal Microbiome/drug effects
• Gastrointestinal Microbiome/genetics
• Gastrointestinal Tract/drug effects
• Gastrointestinal Tract/metabolism
• Gastrointestinal Tract/microbiology
• Hormones/blood
• Lipids/blood
• Male
• Organophosphates/toxicity
• Organothiophosphates/toxicity
• Pesticides/toxicity
• RNA, Ribosomal, 16S
• Rats, Wistar
• Triazoles/toxicity
• Rats

Irritable bowel syndrome (IBS) and functional dyspepsia (FD) are common functional gastrointestinal disorders (FGIDs) and account for a large proportion of consulting patients. These 2 disorders overlap with each other frequently. The pathogenesis of IBS or FD is complicated and multi-factors related, in which infectious or non-infectious inflammation and local or systemic immune response play significant roles. There are few studies focusing on the mechanism of inflammation in patients with overlap syndrome of irritable bowel syndrome and functional dyspepsia (IBS-FD). This review focuses on current advances about the role of inflammation in the pathogenesis of IBS and FD and the possible mechanism of inflammation in IBS-FD.

• Dyspepsia
• Inflammation
• Irritable bowel syndrome

The human microbiota has a broad range of functions contributing to metabolic processes and the activities of our immune system. Its influence on health, well-being and chronic diseases are discussed in various studies. The intestinal microbiota and the mucosal integrity are influenced by diet, environment and other lifestyle factors, including physical activity. There are correlations between cardiorespiratory fitness and important markers of intestinal health. However, data linking endurance exercise to microbiota composition are sparse. Many endurance athletes take probiotics to reduce gastrointestinal symptoms linked to exercise or immunosuppression, but the longitudinal data is insufficient.

This randomised, controlled cross-over pilot study will examine the impact of specific endurance training and probiotic supplementation on the intestinal microbiota and mucosa in healthy, athletic students.

The aim of this pilot study is to elucidate the impact of physical activity on the intestinal microbiota and mucosa with regard to the effects of a probiotic supplementation.

In this pilot study, thirty non-specifically trained student athletes will participate in an intervention consisting of a two-week rest (baseline) period, a four-week exercise programme and a four-week probiotic intervention using SymbioLactComp®. The exercise programme consists of three 60-min running workouts per week at 70–85% of the peak heart rate (HRpeak). Primary endpoint of this pilot study is the feasibility and practicality of the intervention as well as a sample size estimation. Furthermore, anthropometric measurements and information on nutrition and lifestyle will be obtained. The peak oxygen uptake (VO₂peak) and peak heart rate (HRpeak) (determined during a shuttle run test) as well as selected blood and saliva parameters (haemogram, cytokines) will be evaluated. Changes to the intestinal microbiota will be analysed by stool diagnostics (KyberKompaktPRO®, KyberPlus®). The potential changes may include microbiota composition, bacterial metabolites and mucosa- and immune markers.

Results will be used for the design of a main randomised controlled trial with a larger collective based on feasibility, validity and sample size estimation as well as the potential effects of endurance exercise on intestinal microbiota and mucosa. Evidence-based information of an exercise-altered microbiota could be of importance for the prevention and therapy of intestinal or immune disorders.

German Clinical Trials Register: DRKS00011108. Retrospectively registered on 28 November 2016.

The online version of this article (10.1186/s40814-019-0459-9) contains supplementary material, which is available to authorized users.

• Cardiorespiratory fitness
• Exercise
• Intestinal health
• Intestinal microbiota
• Physical activity
• Probiotics

• DNA sequencing
• endocrine system
• hormones
• inflammation
• microbiome

• Animals
• Body Weight/drug effects
• Cytokines/blood
• Endocrine System/drug effects
• Gastrointestinal Microbiome/drug effects
• Gastrointestinal Tract/drug effects
• Hormones/blood
• Immune System/drug effects
• Inflammation/blood
• Lipids/blood
• Male
• Metabolome
• Organophosphates/toxicity
• Pesticides/toxicity
• Rats, Wistar

• Allergic March
• allergic rhinitis
• asthma
• atopic dermatitis
• extra-intestinal manifestations
• gastrointestinal tract
• non-IgE mediated

• Intestinal barrier dysfunction
• Multiple organ dysfunction syndrome
• Traumatic brain injury

• gut bacteria
• mechanism
• microbiome
• nanotoxicity
• silver nanoparticle

• LPS
• amplification
• amyloid
• blood clotting
• inflammation
• iron dysregulation

• Animals
• Chronic Disease
• Gastrointestinal Microbiome
• Humans
• Inflammation/etiology
• Iron/metabolism

• BB/L025752/1 Biotechnology and Biological Sciences Research Council

• Autoimmune Diseases/epidemiology
• Autoimmune Diseases/metabolism
• Autoimmune Diseases/microbiology
• Blood Group Antigens/metabolism
• Cardiovascular Diseases/epidemiology
• Cardiovascular Diseases/metabolism
• Cardiovascular Diseases/microbiology
• Diabetes Mellitus/epidemiology
• Diabetes Mellitus/metabolism
• Diabetes Mellitus/microbiology
• Gastrointestinal Microbiome
• Humans
• Inflammation/epidemiology
• Inflammation/metabolism
• Inflammation/microbiology
• Obesity/epidemiology
• Obesity/metabolism
• Obesity/microbiology

• U24 DK097193 NIDDK NIH HHS

The gut microbiome consists of over 10³–10⁴ microorganism inhabitants that together possess 150 times more genes that the human genome and thus should be considered an “organ” in of itself. Such communities of bacteria are in dynamic flux and susceptible to changes in host environment and body condition. In turn, gut microbiome disturbances can affect health status of the host. Gut dysbiosis might result in obesity, diabetes, gastrointestinal, immunological, and neurobehavioral disorders. Such host diseases can originate due to shifts in microbiota favoring more pathogenic species that produce various virulence factors, such as lipopolysaccharide. Bacterial virulence factors and metabolites may be transmitted to distal target sites, including the brain. Other potential mechanisms by which gut dysbiosis can affect the host include bacterial-produced metabolites, production of hormones and factors that mimic those produced by the host, and epimutations. All animals, including humans, are exposed daily to various environmental chemicals that can influence the gut microbiome. Exposure to such chemicals might lead to downstream systemic effects that occur secondary to gut microbiome disturbances. Increasing reports have shown that environmental chemical exposures can target both host and the resident gut microbiome. In this review, we will first consider the current knowledge of how endocrine disrupting chemicals (EDCs), heavy metals, air pollution, and nanoparticles can influence the gut microbiome. The second part of the review will consider how potential environmental chemical-induced gut microbiome changes might subsequently induce pathophysiological responses in the host, although definitive evidence for such effects is still lacking. By understanding how these chemicals result in gut dysbiosis, it may open up new remediation strategies in animals, including humans, exposed to such chemicals.

• air pollution
• arsenic
• endocrine disrupting chemicals
• gastrointestinal system
• gut-microbiome-brain axis
• heavy metals
• lead
• nanoparticles

• Aggregatibacter/drug effects
• Animals
• Bacteroides/drug effects
• Brain/drug effects
• Brain/physiopathology
• Clostridium/drug effects
• Corynebacterium/drug effects
• Dysbiosis/chemically induced
• Dysbiosis/microbiology
• Dysbiosis/physiopathology
• Feces/microbiology
• Gastrointestinal Microbiome/drug effects
• Gastrointestinal Microbiome/genetics
• Gastrointestinal Tract/drug effects
• Gastrointestinal Tract/physiopathology
• Humans
• Metal Nanoparticles/administration & dosage
• Metal Nanoparticles/adverse effects
• Peptococcus/drug effects
• Rats
• Rats, Sprague-Dawley

• T32 OD011126 NIH HHS

• Animal Feed/analysis
• Animal Nutritional Physiological Phenomena
• Animals
• Behavior, Animal
• Cattle/physiology
• Cecum/metabolism
• Diet/veterinary
• Dietary Supplements
• Drinking
• Eating
• Fermentation
• Inflammation
• Male
• Plant Leaves
• Rumen/metabolism

• DOHaD
• Peromyscus
• bacteria
• california mice
• endocrine disrupting chemicals
• estrogens
• metabolic pathway

• cognition
• enteric infections
• environmental enteropathy
• intestinal microbiome
• malnutrition

• brain-gut axis
• gender
• intestinal barrier
• irritable bowel syndrome
• microbiome
• sex steroids
• stress

• Depression
• Gluten sensitivity
• IgG hypersensitivity
• Inflammatory theory of depression
• Leaky gut
• Zonulin

• FUNCTIONAL BOWEL DISORDER
• FUNCTIONAL DYSPEPSIA
• IRRITABLE BOWEL SYNDROME
• MAST CELLS
• NERVE - GUT INTERACTIONS

Daily exposure of humans to nanoparticles from edible plants is inevitable, but significant advances are required to determine whether edible plant nanoparticles are beneficial to our health. Additionally, strategies are needed to elucidate the molecular mechanisms underlying any beneficial effects. Here, as a proof of concept, we used a mouse model to show that orally given nanoparticles isolated from ginger extracts using a sucrose gradient centrifugation procedure resulted in protecting mice against alcohol-induced liver damage. The ginger-derived nanoparticle (GDN)–mediated activation of nuclear factor erythroid 2-related factor 2 (Nrf2) led to the expression of a group of liver detoxifying/antioxidant genes and inhibited the production of reactive oxygen species, which partially contributes to the liver protection. Using lipid knock-out and knock-in strategies, we further identified that shogaol in the GDN plays a role in the induction of Nrf2 in a TLR4/TRIF-dependent manner. Given the critical role of Nrf2 in modulating numerous cellular processes, including hepatocyte homeostasis, drug metabolism, antioxidant defenses, and cell-cycle progression of liver, this finding not only opens up a new avenue for investigating GDN as a means to protect against the development of liver-related diseases such as alcohol-induced liver damage but sheds light on studying the cellular and molecular mechanisms underlying interspecies communication in the liver via edible plant–derived nanoparticles.

• Nrf2 detoxic effect
• TLR4/TRIF pathway
• alcoholic liver injury
• ginger nanoparticles
• shogaol

• Animals
• Autism Spectrum Disorder/diet therapy
• Autism Spectrum Disorder/immunology
• Autism Spectrum Disorder/microbiology
• Dysbiosis/diet therapy
• Dysbiosis/immunology
• Dysbiosis/microbiology
• Gastrointestinal Microbiome/physiology
• Gastrointestinal Tract/immunology
• Gastrointestinal Tract/microbiology
• Humans
• Microbiota/physiology
• Prebiotics/administration & dosage
• Probiotics/administration & dosage

T helper cell 17 (Th17) cells are identified as a new subset of T helper cells. Their differentiation is associated with a variety of cytokines and transcription factors, and they can secrete a variety of cytokines, such as interleukin (IL)-17 and IL-22, both of which can promote inflammation in the intestinal mucosa barrier and have a protective effect on organs. Probiotics

have been confirmed to have anti-inflammatory effects in the intestinal tract, the role of which may be associated with inhibiting Th17 cell activity. However, the stable number of Th17 cells requires the presence of intestinal symbiotic microbita. This paper will review the differentiation of Th17 cells and their role in intestinal mucosal immunity.

• T helper cell 17 cells
• Interleukin-17
• Intestinal mucosal immunity
• Probiotics
• Gut microbiota
• Immunonutrition

The interface between the intestinal lumen and the mucosa is the location where the majority of ingested immunogenic particles face the scrutiny of the vast gastrointestinal immune system. Upon regular physiological conditions, the intestinal micro-flora and the epithelial barrier are well prepared to process daily a huge amount of food-derived antigens and non-immunogenic particles. Similarly, they are ready to prevent environmental toxins and microbial antigens to penetrate further and interact with the mucosal-associated immune system. These functions promote the development of proper immune responses and oral tolerance and prevent disease and inflammation. Brain-gut axis structures participate in the processing and execution of response signals to external and internal stimuli. The brain-gut axis integrates local and distant regulatory networks and super-systems that serve key housekeeping physiological functions including the balanced functioning of the intestinal barrier. Disturbance of the brain-gut axis may induce intestinal barrier dysfunction, increasing the risk of uncontrolled immunological reactions, which may indeed trigger transient mucosal inflammation and gut disease. There is a large body of evidence indicating that stress, through the brain-gut axis, may cause intestinal barrier dysfunction, mainly via the systemic and peripheral release of corticotropin-releasing factor. In this review, we describe the role of stress and corticotropin-releasing factor in the regulation of gastrointestinal permeability, and discuss the link to both health and pathological conditions.

• Corticotropin-releasing factor
• Inflammation
• Permeability
• Stress

AIM: To explore the feasibility of using in vivo cerebral microdialysis and high performance liquid chromatography (HPLC) to determine the contents of glutamate (Glu), glycine (Gly), γ-aminobutyric acid (γ-GABA) and taurine (Tau), and to observe the protein expression of γ-aminobutyric acid receptor A (GABA_Aα1) in irritable bowel syndrome with diarrhea (IBS-D) and irritable bowel syndrome with constipation (IBS-C) to investigate the preliminary pathogenesis of these two subtypes.

METHODS: Using in vitro relative recovery and in vivo relative loss ratio as monitoring indicators, the feasibility of using cerebral microdialysis and HPLC to determine the contents of Glu, Gly, Tau and γ-GABA was first explored. IBS-C was induced by cold water administration and IBS-D by folium sennae combined with restraint. Cerebral microdialysis and HPLC were then used to determine the contents of Glu, Gly, Tau and γ-GABA in the rat brain. Western blot was used to detect the expression of GABA_Aα1 protein in brain tissue.

RESULTS: In vivo cerebral microdialysis and HPLC were feasible for determining the contents of Glu and γ-GABA; the in vitro relative recovery rates were 21.6% and 24.5%, respectively; in vivo relative loss rates were 41.8% and 32.5%. Compared with rats in the normal group, the ratio of Glu/γ-GABA in the IBS-C and IBS-D groups significantly increased (P < 0.05). GABA_Aα1 protein expression in both IBS-C and IBS-D groups were significantly higher than that in the normal group (P < 0.05). In addition, GABA_Aα1 protein expression in the IBS-D group was significantly higher than that in the IBS-C group (P < 0.05).

CONCLUSION: The pathogenesis of IBS-C and IBS-D may be related with Glu/GABA ratio and GABA_Aα1 in the brain.

• Irritable bowel syndrome with diarrhea
• Irritable bowel syndrome with constipation
• Cerebral microdialysis-High performance liquid chromatography
• Amino acid neurotransmitter
• γ-aminobutyric acid receptor