• Cervical screening
• Colposcopy
• Fluorescent imaging probe
• GAL7

• 2024J08310 Natural Science Foundation of Fujian Province
• 2024GGB28 Fujian Provincial Health Technology Project
• 2024GZL-GG48 Xiamen health high quality development science and technology project
• U24A20731, 82272111, 92159303, 62027901 National Natural Science Foundation of China
• 2023YFC3402804, SQ2024AAA030653 The National Key R&D Program of China
• 7252292 Beijing Natural National Science Foundation
• 22JHQ088 Shaanxi Fundamental Science Research Project for Chemistry and Biology
• 2023ZD0501700 Science and Technology Innovation 2030
• The National Key R&D Program of China

• 18F-fluorodeoxyglucose
• Immune cell infiltration
• Methyltransferase-like protein 3
• Soft tissue sarcomas

• Humans
• Fluorodeoxyglucose F18/metabolism
• Female
• Male
• Methyltransferases/metabolism
• Methyltransferases/genetics
• Middle Aged
• Sarcoma/diagnostic imaging
• Sarcoma/metabolism
• Sarcoma/pathology
• Sarcoma/genetics
• Adult
• Prognosis
• Aged
• Positron-Emission Tomography/methods
• Young Adult
• Biomarkers, Tumor/metabolism
• Radiopharmaceuticals
• Gene Expression Regulation, Neoplastic

• 2024-BS-164 Natural Science Foundation of Liaoning Province, China
• 2023DF036 Dalian Medical Science research project

• Gut microbiota
• Infant
• Longitudinal study
• Mother–child pair
• Older sibling
• Similarity

• Humans
• Gastrointestinal Microbiome
• Child, Preschool
• Japan
• Female
• Infant
• Male
• Infant, Newborn
• Longitudinal Studies
• Feces/microbiology
• Adult
• East Asian People

• JP18gm0710009 Japan Agency for Medical Research and Development
• 16H01781 Japan Society for the Promotion of Science
• 17K00577 Japan Society for the Promotion of Science
• JPMJOP1831 Japan Science and Technology Agency
• Chiba Foundation for Health Promotion and Disease Prevention
• Yakult Bio-Science Foundation

• Alhagi-honey
• Gut microbiota
• Heat stress
• Liver damage

• 32072815 Natural Sciences Foundation of China
• 2022YFD1300200 Chongqing Municipal Key Research and Development Program of China
• 2023-YBNY-140 the General Project of the Key R & D Plan of Shaanxi Province
• TG20221184 Horizontal Research Funding from Ningbo Second Hormone Factory
• the General Project of the Key R & D Plan of Shaanxi Province

• fatty
• nafld
• sex

• Humans
• Saudi Arabia/epidemiology
• Male
• Female
• Social Stigma
• Non-alcoholic Fatty Liver Disease/psychology
• Non-alcoholic Fatty Liver Disease/epidemiology
• Middle Aged
• Adult
• Surveys and Questionnaires
• Cost of Illness

• University Grants Commission

• anaesthesia
• climate change
• gastrointestinal endoscopy
• healthcare
• sustainability

• Humans
• Carbon Footprint/standards
• Climate Change
• Conservation of Natural Resources
• Delivery of Health Care/organization & administration
• Delivery of Health Care/standards
• Endoscopy, Gastrointestinal/standards
• Global Warming
• Greenhouse Effect/prevention & control
• Greenhouse Gases
• Intensive Care Units/organization & administration
• Intensive Care Units/standards
• Operating Rooms/organization & administration
• Operating Rooms/standards

• cardiac procedures
• morbidity
• mortality
• risk prediction

• Humans
• End Stage Liver Disease
• Liver Cirrhosis/complications
• Morbidity
• Severity of Illness Index
• Treatment Outcome

• Constipation
• Enteric neurotransmitter
• High-fat diet
• LimosiLactobacillus pentosus CQZC02
• Oxidative stress

• Mice
• Female
• Animals
• Mustard Plant
• Diet, High-Fat/adverse effects
• Constipation/chemically induced
• Constipation/drug therapy
• Intestine, Small/metabolism
• Neurotransmitter Agents

• Crohn’s disease
• biomarker
• fibrosis
• immune cells
• ssGSEA

• Animals
• Rats
• Crohn Disease/diagnosis
• Crohn Disease/genetics
• Matrix Metalloproteinase 2
• CD8-Positive T-Lymphocytes
• Fibroblast Growth Factor 2
• Computational Biology

• Acute pancreatitis
• Diabetes
• Fasting hyperglycaemia
• Impaired fasting glucose
• Risk factors
• Triglycerides

• 82170651 National Natural Science Foundation of China
• 81870442 National Natural Science Foundation of China

• Academic gastroenterology
• COVID-19
• Coronavirus
• Gastroenterology clinical service
• Gastroenterology fellowship
• Pandemic
• SARS

• Humans
• COVID-19
• Gastroenterology
• Internship and Residency
• Schools, Medical
• Fellowships and Scholarships
• Pandemics
• Endoscopy, Gastrointestinal
• Hospitals, Teaching

• LPS
• accumulation
• arsenic
• intestinal microbiota
• tight junction

• 5-methylcytosine
• RNA methylation
• colorectal cancer
• immune infiltrates
• precision medicine
• tumor microenvironment

Acinar-to-ductal metaplasia (ADM) is a recently recognized, yet less well-studied, precursor lesion of pancreatic ductal adenocarcinoma (PDAC) developed in the setting of chronic pancreatitis. Through digital spatial mRNA profiling, we compared ADM and adjacent PDAC tissues from patient samples to unveil the bridging genes during the malignant transformation of pancreatitis. By comparing the bridging genes with the 7-methylguanosine (m7G)-seq dataset, we screened 19 m7G methylation genes for a subsequent large sample analysis. We constructed the “m7G score” model based on the RNA-seq data for pancreatic cancer in The Cancer Genome Atlas (TCGA) database and The Gene Expression Omnibus (GEO) database. Tumors with a high m7G score were characterized by increased immune cell infiltration, increased genomic instability, higher response rate to combined immune checkpoint inhibitors (ICIs), and overall poor survival. These findings indicate that the m7G score is associated with tumor invasiveness, immune cell infiltration, ICI treatment response, and overall patients’ survival. We also identified FN1 and ITGB1 as core genes in the m7Gscore model, which affect immune cell infiltration and genomic instability not only in pancreatic cancer but also in pan-cancer. FN1 and ITGB1 can inhibit immune T cell activition by upregulation of macrophages and neutrophils, thereby leading to immune escape of pancreatic cancer cells and reducing the response rate of ICI treatment.

• Carcinoma, Pancreatic Ductal/genetics
• Carcinoma, Pancreatic Ductal/metabolism
• Carcinoma, Pancreatic Ductal/therapy
• Genomic Instability
• Humans
• Immunotherapy
• Metaplasia
• Pancreatic Neoplasms/genetics
• Pancreatic Neoplasms/metabolism
• Pancreatic Neoplasms/therapy
• Prognosis

• National Natural Science Foundation of China

• Core/periphery network
• Inflammatory bowel disease
• Mucosal microbiome
• Species co-occurrence network
• Species diversity
• Ulcerative colitis

• Deciduous teeth
• Illumina MiSeq
• Preschool children
• Probiotics
• Salivary microbial community

• bacterial overgrowth syndrome
• dyspepsia
• functional dyspepsia

• Bacterial Infections
• Breath Tests
• Dyspepsia/diagnosis
• Dyspepsia/epidemiology
• Humans
• Irritable Bowel Syndrome
• Lactulose
• Prevalence
• Russia

• Helicobacter pylori
• apoptosis
• autophagy
• carcinogenesis
• gastric epithelial cell

• HCV
• antiviral therapy
• interferon alfa
• polymerase inhibitors
• protease inhibitors
• ribavirin

• PI3K
• antigen presentation
• dendritic cell
• phospholipids
• toll like receptors

• Adaptive Immunity
• Animals
• Antigen Presentation
• Autoimmune Diseases/metabolism
• Dendritic Cells/immunology
• Humans
• Immunity, Innate
• Inflammation/metabolism
• Neoplasms/metabolism
• Phosphatidylinositol 3-Kinases/metabolism
• Protein Isoforms/metabolism
• Receptors, Pattern Recognition/metabolism
• Signal Transduction

• MR/M023230/1 Medical Research Council

• Helicobacter pylori
• cytoprotection
• eradication
• peptic ulcer
• rebamipide

• Adult
• Alanine/administration & dosage
• Alanine/adverse effects
• Alanine/analogs & derivatives
• Alanine/therapeutic use
• Amoxicillin/administration & dosage
• Amoxicillin/therapeutic use
• Anti-Infective Agents/administration & dosage
• Anti-Infective Agents/therapeutic use
• Anti-Ulcer Agents/administration & dosage
• Anti-Ulcer Agents/adverse effects
• Anti-Ulcer Agents/therapeutic use
• Clarithromycin/administration & dosage
• Clarithromycin/therapeutic use
• Drug Administration Schedule
• Drug Therapy, Combination
• Female
• Helicobacter Infections/complications
• Helicobacter Infections/drug therapy
• Helicobacter Infections/microbiology
• Helicobacter pylori/drug effects
• Humans
• Male
• Omeprazole/administration & dosage
• Omeprazole/therapeutic use
• Peptic Ulcer/complications
• Peptic Ulcer/drug therapy
• Peptic Ulcer/microbiology
• Prospective Studies
• Quinolones/administration & dosage
• Quinolones/adverse effects
• Quinolones/therapeutic use
• Treatment Outcome

• Pancreatic Club
• consensus
• endocrine pancreatic insufficiency
• exocrine pancreatic insufficiency
• pancreatic surgery

• Blood Glucose/analysis
• Consensus
• Exocrine Pancreatic Insufficiency/diagnosis
• Exocrine Pancreatic Insufficiency/etiology
• Exocrine Pancreatic Insufficiency/therapy
• Feces/chemistry
• Glycated Hemoglobin/analysis
• Hormone Replacement Therapy/methods
• Lipase/therapeutic use
• Nutritional Status
• Pancreas/enzymology
• Pancreas/physiopathology
• Pancreas/surgery
• Pancreatectomy
• Pancreatic Elastase/analysis
• Russia

• Treg/Th17 balance
• berberine
• gut microbiota
• inflammation
• ulcerative colitis

Magnolol (MG) is a kind of lignin isolated from Magnolia officinalis, which serves several different biological functions, such as antifungal, anticancer, antioxidant, and hepatoprotective functions. This study aimed to evaluate the protective effect of MG against oleic acid (OA)-induced hepatic steatosis and inflammatory damage in HepG2 cells and in a tyloxapol (Ty)-induced hyperlipidemia mouse model. Our findings indicated that MG can effectively inhibit OA-stimulated tumor necrosis factor α (TNF-α) secretion, reactive oxygen species generation, and triglyceride (TG) accumulation. Further study manifested that MG significantly suppressed OA-activated mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways and that these inflammatory responses can be negated by pretreatment with inhibitors of extracellular regulated protein kinase and c-Jun N-terminal kinase (U0126 and SP600125, respectively). In addition, MG dramatically upregulated peroxisome proliferator-activated receptor α (PPARα) translocation and reduced sterol regulatory element-binding protein 1c (SREBP-1c) protein synthesis and excretion, both of which are dependent upon the phosphorylation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), acetyl-CoA carboxylase, and AKT kinase (AKT). However, MG suspended the activation of PPARα expression and was thus blocked by pretreatment with LY294002 and compound c (specific inhibitors of AKT and AMPK). Furthermore, MG clearly alleviated serum TG and total cholesterol release; upregulated AKT, AMPK, and PPARα expression; suppressed SREBP-1c generation; and alleviated hepatic steatosis and dyslipidemia in Ty-induced hyperlipidemia mice. Taken together, these results suggest that MG exerts protective effects against steatosis, hyperlipidemia, and the underlying mechanism, which may be closely associated with AKT/AMPK/PPARα activation and MAPK/NF-κB/SREBP-1c inhibition.

• AMPK
• hyperlipidemia
• inflammatory responses
• magnolol
• peroxisome proliferator-activated receptor α
• steatosis

• gut microbiota
• gut–brain axis
• immune stress
• immune–brain axis
• intestinal inflammation
• lipopolysaccharide
• mental health
• neuropeptide Y

To estimate annual direct and indirect costs for patients diagnosed with irritable bowel syndrome (IBS) and subtypes.

Patients completed a standardized questionnaire concerning usage of healthcare resources, travel costs, meals, and productivity loss of patients when seeking treatment for IBS. Total annual costs per patient were calculated as the sum of direct (including medical and nonmedical) and indirect costs. Total annual costs per patient among various IBS subtypes were compared. Analysis of variance and bootstrapped independent sample t-tests were performed to determine differences between groups after controlling for IBS subtypes.

A total of 105 IBS patients (64.80% female), mean age of 57.12 years ± 10.31 years), mean disease duration of 4.31 years ± 5.40 years, were included. Total annual costs per patient were estimated as CNY18262.84 (USD2933.08). Inpatient and outpatient healthcare use were major cost drivers, accounting for 46.41%and 23.36% of total annual costs, respectively. Productivity loss accounted for 25.32% of total annual costs. The proportions of direct and indirect costs were similar to published studies in other countries. Nationally, the total costs of managing IBS would amount to CNY123.83 billion (USD1.99 billion). Among the IBS subtypes, total annual costs per patient of IBS-M was highest at CNY18891.18 (USD3034). Furthermore, there was significant difference in productivity loss among IBS subtypes (P = 0.031).

IBS imposes a huge economic burden on patients and healthcare systems, which could account for 3.3% of the total healthcare budget for the entire Chinese nation. More than two-thirds of total annual costs of IBS consist of inpatient and outpatient healthcare use. Among the subtypes, IBS-M patients appear to have the greatest economic burden but require further confirmation.

• Irritable bowel syndrome
• Burden of illness
• Direct and indirect medical and nonmedical costs
• Irritable bowel syndrome subtype
• Productivity loss

• Absenteeism
• Aged
• Ambulatory Care/economics
• China/epidemiology
• Cost of Illness
• Efficiency
• Female
• Health Care Costs
• Health Expenditures
• Health Resources/economics
• Health Resources/statistics & numerical data
• Hospital Costs
• Humans
• Irritable Bowel Syndrome/diagnosis
• Irritable Bowel Syndrome/economics
• Irritable Bowel Syndrome/epidemiology
• Irritable Bowel Syndrome/therapy
• Male
• Meals
• Middle Aged
• Prospective Studies
• Sick Leave/economics
• Time Factors
• Transportation/economics

Progressive familial intrahepatic cholestasis (PFIC) is a heterogeneous group of autosomal recessive genetic diseases with a major clinical manifestation of severe intrahepatic cholestasis and an incidence rate of 1/10000 to 1/5000. PFIC is usually first diagnosed in infancy or childhood and eventually develops into liver failure and death. Based on clinical manifestations, laboratory tests, and genetic defects in liver tissue, PFIC is roughly divided into three types: PFIC-1, PFIC-2 and PFIC-3. Studies have demonstrated that all three types of PFIC are associated with the mutations of bile transport system genes in the liver. Promoting transporter expression has important clinical significance for the treatment of PFIC. In this paper, we summarize the etiology and treatment status of PFIC and discuss the treatment of PFIC by promoting the expression of transporters.

• Transporter
• Expression
• Progressive familial intrahepatic cholestasis

Hepatocellular carcinoma (HCC) is a major health problem worldwide, representing one of the leading causes of death. Chronic hepatitis B virus (HBV) infection (CHB) is the most important etiologic factor of this tumor, accounting for the development of more than 50% of the cases in the world. Primary prevention of HCC is possible by hepatitis B vaccination conferring protection from HBV infection. However, according to the World Health Organization Hepatitis B Fact sheet N° 204 (update of July 2014) globally there exists a large pool of > 240 million people chronically infected with HBV who are at risk for development of HCC. These individuals represent a target population for secondary prevention both of cirrhosis and of HCC. Since ongoing HBV replication in CHB is linked with the progression of the underlying liver disease to cirrhosis as well as with the development of HCC, effective antiviral treatment in CHB has also been evaluated in terms of secondary prevention of HCC. Currently, most patients with active CHB are subjected to long term treatment with the first line nucleos(t)ide analogues entecavir and tenofovir. These compounds are of high antiviral potency and have a high barrier to HBV resistance compared to lamivudine, adefovir dipivoxil and even telbivudine. Many studies have shown that patients under antiviral treatment, especially those in virological remission, develop less frequently HCC compared to the untreated ones. However, the risk for development of HCC cannot be eliminated. Therefore, surveillance for the development of HCC of patients with chronic hepatitis B must be lifelong or until a time in the future when new treatments will be able to completely eradicate HBV from the liver particularly in the early stages of CHB infection. In this context, the aim of this review is to outline the magnitude of the risk for development of HCC among patients with CHB, in the various phases of the infection and in relation to virus, host and environmental factors as evaluated in the world literature. Moreover, the benefits of antiviral treatment of CHB with nucleos/tide analogs, which have changed the natural history of the disease and have reduced but not eliminated the risk of HCC are also reviewed.

• Chronic hepatitis B
• Cirrhosis
• Hepatocellular carcinoma
• Hepatitis B virus
• Treatment
• Interferon
• Lamivudine
• Adefovir
• Entecavir
• Tenofovir
• Virological remission
• Nucleos(t)ide analogues

• Complex regional pain syndrome
• Crohn’s disease
• Cure
• Lymphangiomatosis
• Mycobacterium avium paratuberculosis

• Adult
• Antitubercular Agents/therapeutic use
• Bacteriological Techniques
• Biopsy
• Child
• Colonoscopy
• Combined Modality Therapy
• Complex Regional Pain Syndromes/diagnosis
• Complex Regional Pain Syndromes/microbiology
• Complex Regional Pain Syndromes/therapy
• Crohn Disease/diagnosis
• Crohn Disease/microbiology
• Crohn Disease/therapy
• Female
• Humans
• Male
• Mycobacterium avium subsp. paratuberculosis/drug effects
• Mycobacterium avium subsp. paratuberculosis/isolation & purification
• Mycobacterium avium subsp. paratuberculosis/radiation effects
• Paratuberculosis/diagnosis
• Paratuberculosis/microbiology
• Paratuberculosis/therapy
• Paratuberculosis/transmission
• Remission Induction
• Treatment Outcome
• Ultraviolet Therapy/methods
• Young Adult

The purpose of this article review is to update what is known about the role of diet on non-alcoholic fatty liver disease (NAFLD). NAFLD is the most common cause of chronic liver disease in the developed world and is considered to be a spectrum, ranging from fatty infiltration of the liver alone (steatosis), which may lead to fatty infiltration with inflammation known as non alcoholic steatohepatitis While the majority of individuals with risk factors like obesity and insulin resistance have steatosis, only few people may develop steatohepatitis. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Weight loss alone by dietary changes has been shown to lead to histological improvement in fatty liver making nutrition therapy to become a cornerstone of treatment for NAFLD. Supplementation of vitamin E, C and omega 3 fatty acids are under consideration with some conflicting data. Moreover, research has been showed that saturated fat, trans-fatty acid, carbohydrate, and simple sugars (fructose and sucrose) may play significant role in the intrahepatic fat accumulation. However, true associations with specific nutrients yet to be clarified.

• Diet
• Non-alcoholic fatty acids
• Fatty acids
• Obesity
• Insulin resistance

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

Over the last two decades, the rise in the prevalence rates of overweight and obesity explains the emergence of nonalcoholic fatty liver disease (NAFLD) as the leading cause of chronic liver disease worldwide. As described in adults, children and adolescents with fatty liver display insulin resistance, glucose intolerance, and dyslipidemia. Thus NAFLD has emerged as the hepatic component of the metabolic syndrome (MetS) and a strong cardiovascular risk factor even at a very early age. Several studies, including pediatric populations, have reported independent associations between NAFLD and markers of subclinical atherosclerosis including impaired flow-mediated vasodilation, increased carotid artery intima-media thickness, and arterial stiffness, after adjusting for cardiovascular risk factors and MetS. Also, it has been shown that NAFLD is associated with cardiac alterations, including abnormal left ventricular structure and impaired diastolic function. The duration of these subclinical abnormalities may be important, because treatment to reverse the process is most likely to be effective earlier in the disease. In the present review, we examine the current evidence on the association between NAFLD and atherosclerosis as well as between NAFLD and cardiac dysfunction in the pediatric population, and discuss briefly the possible biological mechanisms linking NAFLD and cardiovascular changes. We also address the approach to treatment for this increasingly prevalent disease, which is likely to have an important future global impact on the burden of ill health, to prevent not only end-stage liver disease but also cardiovascular disease.

• Nonalcoholic fatty liver disease
• Children
• Atherosclerosis
• Cardiac structure
• Cardiac function

• Adolescent
• Age Factors
• Cardiovascular Diseases/diagnosis
• Cardiovascular Diseases/epidemiology
• Cardiovascular Diseases/metabolism
• Cardiovascular Diseases/physiopathology
• Cardiovascular Diseases/prevention & control
• Child
• Heart/physiopathology
• Humans
• Non-alcoholic Fatty Liver Disease/diagnosis
• Non-alcoholic Fatty Liver Disease/epidemiology
• Non-alcoholic Fatty Liver Disease/metabolism
• Non-alcoholic Fatty Liver Disease/therapy
• Prevalence
• Prognosis
• Risk Factors
• Risk Reduction Behavior

Alcohol is one of the main factors of liver damage. The evaluation of the degree of liver fibrosis is of great value for therapeutic decision making in patients with alcoholic liver disease (ALD). Staging of liver fibrosis is essential to define prognosis and management of the disease. Liver biopsy is a gold standard as it has high sensitivity and specificity in fibrosis diagnostics. Taking into account the limitations of liver biopsy, there is an exigency to introduce non-invasive serum markers for fibrosis that would be able to replace liver biopsy. Ideal serum markers should be specific for the liver, easy to perform and independent to inflammation and fibrosis in other organs. Serum markers of hepatic fibrosis are divided into direct and indirect. Indirect markers reflect alterations in hepatic function, direct markers reflect extracellular matrix turnover. These markers should correlate with dynamic changes in fibrogenesis and fibrosis resolution. The assessment of the degree of liver fibrosis in alcoholic liver disease has diagnostic and prognostic implications, therefore noninvasive assessment of fibrosis remains important. There are only a few studies evaluating the diagnostic and prognostic values of noninvasive biomarkers of fibrosis in patients with ALD. Several noninvasive laboratory tests have been used to assess liver fibrosis in patients with alcoholic liver disease, including the hyaluronic acid, FibroTest, FibrometerA, Hepascore, Forns and APRI indexes, FIB4, an algorithm combining Prothrombin index (PI), α-2 macroglobulin and hyaluronic acid. Among these tests, Fibrotest, FibrometerA and Hepascore demonstrated excellent diagnostic accuracy in identifying advanced fibrosis and cirrhosis, and additionally, Fibrotest was independently associated with survival. Therefore, the use of biomarkers may reduce the need for liver biopsy and permit an earlier treatment of alcoholic patients.

• Liver fibrosis markers
• Alcoholic liver disease

• Biomarkers/blood
• Biopsy
• Disease Progression
• Humans
• Liver/metabolism
• Liver/pathology
• Liver Cirrhosis, Alcoholic/blood
• Liver Cirrhosis, Alcoholic/diagnosis
• Liver Cirrhosis, Alcoholic/mortality
• Liver Cirrhosis, Alcoholic/pathology
• Liver Function Tests
• Predictive Value of Tests
• Prognosis
• Severity of Illness Index

Nonalcoholic fatty liver disease (NAFLD) refers to the accumulation of fat (mainly triglycerides) within hepatocytes. Approximately 20%-30% of adults in the general population in developed countries have NAFLD; this trend is increasing because of the pandemicity of obesity and diabetes, and is becoming a serious public health burden. Twenty percent of individuals with NAFLD develop chronic hepatic inflammation [nonalcoholic steatohepatitis (NASH)], which can be associated with the development of cirrhosis, portal hypertension, and hepatocellular carcinoma in a minority of patients. And thus, the detection and diagnosis of NAFLD is important for general practitioners. Liver biopsy is the gold standard for diagnosing NAFLD and confirming the presence of NASH. However, the invasiveness of this procedure limits its application to screening the general population or patients with contraindications for liver biopsy. The development of noninvasive diagnostic methods for NAFLD is of paramount importance. This review focuses on the updates of noninvasive diagnosis of NAFLD. Besides, we review clinical evidence supporting a strong association between NAFLD and the risk of cardiovascular disease because of the cross link between these two disorders.

• Nonalcoholic fatty liver disease
• Noninvasive diagnosis
• Laboratory biochemistry
• Image assessment
• Cardiovascular disease

• Biomarkers/blood
• Biopsy
• Cardiovascular Diseases/epidemiology
• Diagnostic Imaging/methods
• Disease Progression
• Elasticity Imaging Techniques
• Humans
• Inflammation Mediators/blood
• Liver/diagnostic imaging
• Liver/metabolism
• Liver/pathology
• Magnetic Resonance Imaging
• Non-alcoholic Fatty Liver Disease/blood
• Non-alcoholic Fatty Liver Disease/diagnosis
• Non-alcoholic Fatty Liver Disease/epidemiology
• Predictive Value of Tests
• Prognosis
• Risk Assessment
• Risk Factors
• Severity of Illness Index
• Time Factors

AIM: To investigate the correlation between the appearance of skin lesions and concentration of interleukin (IL)-17A, IL-23 and interferon-γ (IFN-γ) in Crohn’s disease (CD) patients during anti-tumor necrosis factor-α (TNF-α) therapy

METHODS: A prospective study included 30 adult patients with CD of Caucasian origin (19 men and 11 women; mean age ± SD 32.0 ± 8.6 years) during biological therapy with anti-TNF-α antibodies from January 2012 to March 2013. Eighteen patients were treated with infliximab, seven with adalimumab and five with certolizumab. Inclusion criteria were exacerbation of the underlying disease, Crohn’s Disease Activity Index over 300 and the ineffectiveness of previously used non-biological therapies. Patients with a history of psoriasis, atopic dermatitis and other autoimmune skin lesions were excluded from the study. The control group consisted of 12 healthy subjects. A diagnostic survey was carried out, blood tests and careful skin examination were performed, and the serum levels of IL-17, IL-23 and IFN-γ were measured using an enzyme-linked immunosorbent assays technique. Dermatoses that have developed in the course of biological therapy in patients who had no pre-existing skin lesions of similar character were qualified as skin lesions induced by anti-TNF-α therapy.

RESULTS: Skin manifestations occurred in 18 of CD patients during the anti-TNF-α therapy (60%), in the average time of 10.16 ± 3.42 mo following the beginning of the 52-wk treatment cycle. Skin lesions observed in CD patients during biological therapy included psoriasiform lesions (44.4%), and eczema forms lesions (22.2%). In CD patients with drug induced skin lesions significantly higher levels of hemoglobin (13.3 ± 1.5 g/dL vs 10.8 ± 1.9 g/dL, P = 0.018) and hematocrit (39.9% ± 4.5% vs 34.3% ± 5.4%, P = 0.01), as well as a significantly lower level of platelets (268 ± 62 × 10³/μL vs 408 ± 239 × 10³/μL, P = 0.046) was observed compared with CD patients without skin manifestations. The concentrations of IL-17A and IL-23 in CD patients with skin lesions developed under anti-TNF-α therapy were significantly higher compared to those in patients without lesions (IL-17A: 39.01 ± 7.03 pg/mL vs 25.71 ± 4.90 pg/mL, P = 0.00004; IL-23: 408.78 ± 94.13 pg/mL vs 312.15 ± 76.24 pg/mL, P = 0.00556).

CONCLUSION: Skin lesions in CD patients during biological therapy may result from significantly increased concentrations of IL-17A and IL-23, which are strongly associated with TNF-α/Th1 immune pathways.

• Biological therapy
• Crohn’s disease
• Interleukin 17A
• Interleukin 23
• Interferon γ
• Tumor necrosis factor-α

• Adalimumab
• Adult
• Anti-Inflammatory Agents/adverse effects
• Antibodies, Monoclonal/adverse effects
• Antibodies, Monoclonal, Humanized/adverse effects
• Case-Control Studies
• Crohn Disease/blood
• Crohn Disease/diagnosis
• Crohn Disease/drug therapy
• Crohn Disease/immunology
• Cytokines/blood
• Drug Eruptions/diagnosis
• Drug Eruptions/etiology
• Drug Eruptions/immunology
• Female
• Gastrointestinal Agents/adverse effects
• Humans
• Infliximab
• Interferon-gamma/blood
• Interleukin-17/blood
• Interleukin-23/blood
• Male
• Prospective Studies
• Risk Factors
• Severity of Illness Index
• Skin/drug effects
• Skin/immunology
• Skin/pathology
• Time Factors
• Treatment Outcome
• Tumor Necrosis Factor-alpha/antagonists & inhibitors
• Young Adult

Gastric cancer (GC), which is mainly induced by Helicobacter pylori (H. pylori) infection, is one of the leading causes of cancer-related death in the developing world. Active inflammation initiated by H. pylori infection and maintained by inherent immune disorders promotes carcinogenesis and postoperative recurrence. However, the presence with H. pylori in tumors has been linked to a better prognosis, possibly due to the induction of antitumor immunity. Tumor infiltrations of tumor-associated macrophages, myeloid-derived suppressor cells, neutrophils, Foxp3⁺ regulatory T cells are correlated with poor prognosis. Tumor infiltrating CD8⁺ cytotoxic T lymphocytes, dendritic cells, and CD45RO T cells are generally associated with good prognosis of GC, although some subsets of these immune cells have inverse prognosis prediction values. High ratios of Foxp3⁺/CD4⁺ and Foxp3⁺/CD8⁺ in tumors are associated with a poor prognosis; whereas high Th1/Th2 ratio in tumors predicts a good prognosis. High levels of interleukin (IL)-6, IL-10, IL-32, and chemokine C-C motif ligands (CCL)7 and CCL21 in circulation, high expression of CXC chemokine receptor 4, chemokine C-C motif receptor (CCR)3, CCR4, CCR5, CCR7, hypoxia-inducible factor-1α, signal transducer activator of transcription-3, cyclooxygenase-2, and orphan nuclear receptor 4A2 in tumors are associated with an unfavorable prognosis. Increased serum levels of matrix metalloproteinases (MMP)-3, MMP-7, and MMP-11 and increased levels of MMP-9, MMP-12, and MMP-21 in tumors are consistently associated with poor survival of GC. Further emphasis should be put on the integration of these biomarkers and validation in large cohorts for personalized prediction of GC postoperative prognosis.

• Gastric cancer
• Inflammation
• Biomarker
• Prognosis

• Animals
• Biomarkers, Tumor/metabolism
• Cytokines/metabolism
• Gastritis/complications
• Gastritis/immunology
• Gastritis/metabolism
• Gastritis/microbiology
• Helicobacter Infections/complications
• Helicobacter Infections/immunology
• Helicobacter Infections/metabolism
• Helicobacter Infections/microbiology
• Helicobacter pylori/immunology
• Helicobacter pylori/pathogenicity
• Host-Pathogen Interactions
• Humans
• Inflammation Mediators/metabolism
• Lymphocytes, Tumor-Infiltrating/immunology
• Lymphocytes, Tumor-Infiltrating/metabolism
• Predictive Value of Tests
• Prognosis
• Risk Factors
• Signal Transduction
• Stomach Neoplasms/etiology
• Stomach Neoplasms/immunology
• Stomach Neoplasms/metabolism
• Stomach Neoplasms/microbiology
• Stomach Neoplasms/mortality
• Transcription Factors/metabolism
• Tumor Microenvironment

AIM: To observe the effect of Qingfei Chengqi granules on immune response in early severe acute pancreatitis (SAP) patients.

METHODS: Sixty-eight patients with early SAP were randomly assigned to either an observation group or a control group. The observation group received Western medicine treatment plus Qingfei Chengqi granules, while the control group received Western medicine therapy plus placebo. The expression rate of human leukocyte antigen DR [HLA-DR (%)], helper T lymphocytes 1/2 (Th1/Th2) and regulatory T lymphocytes (Tregs) in peripheral blood were determined on days 1, 3, 7 and 14.

RESULTS: Nine (13.24%) patients die within 28 days, including three (9.09%) in the observation group and six (17.14%) in the control group. Compared with the control group, HLA-DR (%) on days 7 and 14 (86.77% ± 17.39% vs 65.46% ± 28.72%, 85.43% ± 20.36% vs 73.32% ± 29.03%, P < 0.05 for both) and Tregs on days 1 and 3 (9.37% ± 5.61% vs 5.65% ± 3.75%, 9.10% ± 6.86% vs 7.09% ± 4.80%, P < 0.05 for both) were significantly increased, and Th1/Th2 on days 7 and 14 (3.58 ± 3.74 vs 4.62 ± 2.69, 3.54 ± 2.65 vs 5.64 ± 2.34, P < 0.05 for both) were significantly decreased in the observation group. Compared with pretreatment values in the observation group, HLA-DR (%) on days 7 and 14 (86.77% ± 17.39% vs 67.71% ± 28.63%, 85.43% ± 20.36% vs 67.71% ± 28.63%, P < 0.05 for both) and Tregs on days 1 and 3 (9.37% ± 5.61% vs 6.11% ± 4.08%, 9.10% ± 6.86% vs 6.11% ± 4.08%, P < 0.05) were significantly increased, and Th1/Th2 on days 7 and 14 (3.58 ± 3.74 vs 5.96 ± 6.12, 3.54 ± 2.65 vs 5.96 ± 6.12, P < 0.05 for both) were significantly decreased after treatment. Compared with pretreatment values in the control group, HLA-DR (%) on day 14 (73.32% ± 29.03% vs 61.71% ± 28.77%, P < 0.05) were significantly increased.

CONCLUSION: Qingfei Chengqi granules may enhance antigen presentation and immune response to reduce immune suppression in early SAP possibly by inducing high expression of Treg cells to promote the transition of Th1 to Th2 cells, thereby reducing inflammation damage and fatality rate.

• Severe acute pancreatitis
• Qingfei chengqi granules
• Human leukocyte antigen DR site
• The helper T lymphocyte 1/2
• The regulatory T lymphocyte

• Cirrhosis
• Hepatopulmonary syndrome
• Liver transplantation
• Pathophysiology

• Animals
• Hepatopulmonary Syndrome/diagnosis
• Hepatopulmonary Syndrome/etiology
• Hepatopulmonary Syndrome/physiopathology
• Hepatopulmonary Syndrome/surgery
• Humans
• Liver Cirrhosis/complications
• Liver Cirrhosis/diagnosis
• Liver Cirrhosis/surgery
• Liver Transplantation
• Patient Selection
• Predictive Value of Tests
• Prognosis
• Risk Assessment
• Risk Factors
• Waiting Lists

• Allergy
• Asthma
• Children
• Chronic idiopathic thrombocytopenic purpura
• Diabetes mellitus
• Growth retardation
• Helicobacter pylori
• Iron deficiency anemia

• Anemia, Iron-Deficiency/microbiology
• Asthma/microbiology
• Child
• Clinical Trials as Topic
• Diabetes Mellitus/microbiology
• Growth Disorders/microbiology
• Helicobacter Infections/diagnosis
• Helicobacter Infections/epidemiology
• Helicobacter pylori
• Humans
• Hypersensitivity/microbiology
• Purpura, Thrombocytopenic, Idiopathic/microbiology

AIM: To investigate whether autologous dendritic cell (DC)-cytokine-induced killer (CIK) cell therapy is able to improve the therapeutic efficacy of chemotherapy in colon cancer.

METHODS: We conducted a systematic review of published papers from the sources of MEDLINE, the Cochrane Central Register of Controlled Trials, EMBASE, the Wanfang Database, the China Science and Technology Periodical Database and China Journal Net. Published data were extracted independently by two authors using predefined database templates. The quality of the data from individual papers was also assessed. The effects of chemotherapy were compared with those of chemotherapy in combination with DC-CIK immunotherapy. The pooled analysis was performed using the data from random or fixed-effect models.

RESULTS: Seven trials matched our inclusion criteria (n = 533). The overall analysis showed significant survival benefit [one-year overall survival (OS), P < 0.0001; two-year OS, P = 0.009; three-year OS, P = 0.002] in favor of DC-CIK immunotherapy combined with chemotherapy. Disease-free survival (DFS) rate was improved after the combination of DC-CIK immunotherapy and chemotherapy (one-year DFS, P < 0.0001; two-year DFS, P = 0.002; three-year DFS, P = 0.02). An improved overall response rate (P = 0.009) was also observed in patients who received DC-CIK therapy. Furthermore, the analysis of T-lymphocyte subsets in peripheral blood indicated that the number of CD4⁺ T cells significantly increased in the DC-CIK plus chemotherapy group (P < 0.05).

CONCLUSION: The combination of DC-CIK immunotherapy and chemotherapy was superior in prolonging the survival time and enhancing immunological responses.

• Dendritic cells
• Cytokine-induced killer cells
• Meta-analysis
• Colon cancer
• Immunotherapy

• Antineoplastic Agents/therapeutic use
• Chemotherapy, Adjuvant
• China/epidemiology
• Colonic Neoplasms/epidemiology
• Colonic Neoplasms/immunology
• Colonic Neoplasms/mortality
• Colonic Neoplasms/therapy
• Cytokine-Induced Killer Cells/immunology
• Cytokine-Induced Killer Cells/transplantation
• Dendritic Cells/immunology
• Dendritic Cells/transplantation
• Humans
• Immunotherapy, Adoptive
• Survival Analysis
• Time Factors
• Treatment Outcome