Long-term monitoring chlorophyll-a concentration using HJ-1 A/B imagery and machine learning algorithms in typical lakes, a cold semi-arid region.

Chlorophyll a (Chl-a) in lakes serves as an effective marker for assessing algal biomass and the nutritional level of lakes, and its observation is feasible through remote sensing methods. HJ-1 (Huanjing-1) satellite, deployed in 2008, incorporates a CCD capable of a 30 m resolution and has a revisit interval of 2 days, rendering it a superb choice or supplemental sensor for monitoring trophic state of lakes. For effective long-term and regional-scale mapping, both the imagery and the evaluation of machine learning algorithms are essential. The several typical machine learning algorithms, i.e., Support Vector Regression (SVR), Gradient Boosting Decision Trees (GBDT), XGBoost (XGB), Random Forest (RF), K-Nearest Neighbor (KNN), Kernel Ridge Regression (KRR), and Multi-Layer Perception Network (MLP), were developed using our in-situ measured Chl-a. A cross-validation grid to identify the most effective hyperparameter combinations for each algorithm was used, as well as the selected optimal superparameter combinations. In Chl-a mapping of three typical lakes, the R2 of GBDT, XGB, RF, and KRR all reached 0.90, while XGB algorithm also exhibited stable performance with the smallest error (RMSE = 3.11 µg/L). Adjustments were made to align the Chl-a spatial-temporal patterns with past data, utilizing HJ1-A/B CCD images mapping through XGB algorithm, which demonstrates its stability. Our results highlight the considerable effectiveness and utility of HJ-1 A/B CCD imagery for evaluation and monitoring trophic state of lakes in a cold arid region, providing the application cases contribute to the ongoing efforts to monitor water qualities.

Identification and diagnostic potential of hsa_circ_101303 in colorectal cancer: unraveling a regulatory network.

BACKGROUND: The role of novel circular RNAs (circRNAs) in colorectal cancer (CRC) remains to be determined. This study aimed to identify a novel circRNA involved in CRC pathogenesis, assess its diagnostic value, and construct a regulatory network. METHODS: Differential expression analysis was conducted using circRNA datasets to screen for differentially expressed circRNAs. The expression of selected circRNAs was validated in external datasets and clinical samples. Diagnostic value of plasma circRNA levels in CRC was assessed. A competing endogenous RNA (ceRNA) network was constructed for the circRNA using TCGA dataset. RESULTS: Analysis of datasets revealed that hsa_circ_101303 was significantly overexpressed in CRC tissues compared to normal tissues. The upregulation of hsa_circ_101303 in CRC tissues was further confirmed through the GSE138589 dataset and clinical samples. High expression of hsa_circ_101303 was associated with advanced N stage, M stage, and tumor stage in CRC. Plasma levels of hsa_circ_101303 were markedly elevated in CRC patients and exhibited moderate diagnostic ability for CRC (AUC = 0.738). The host gene of hsa_circ_101303 was also found to be related to the TNM stage of CRC. Nine miRNAs were identified as target miRNAs for hsa_circ_101303, and 27 genes were identified as targets of these miRNAs. Subsequently, a ceRNA network for hsa_circ_101303 was constructed to illustrate the interactions between the nine miRNAs and 27 genes. CONCLUSIONS: The study identifies hsa_circ_101303 as a highly expressed circRNA in CRC, which is associated with the progression of the disease. Plasma levels of hsa_circ_101303 show promising diagnostic potential for CRC. The ceRNA network for hsa_circ_101303 provides valuable insights into the regulatory mechanisms underlying CRC.

Phylogenetic Analysis of the PR-4 Gene Family in Euphorbiaceae and Its Expression Profiles in Tung Tree (Vernicia fordii).

Pathogenesis-related protein-4 (PR-4) is generally believed to be involved in physiological processes. However, a comprehensive investigation of this protein in tung tree (Vernicia fordii) has yet to be conducted. In this study, we identified 30 PR-4 genes in the genomes of Euphorbiaceae species and investigated their domain organization, evolution, promoter cis-elements, expression profiles, and expression profiles in the tung tree. Sequence and structural analyses indicated that VF16136 and VF16135 in the tung tree could be classified as belonging to Class II and I, respectively. Phylogenetic and Ka/Ks analyses revealed that Hevea brasiliensis exhibited a significantly expanded number of PR-4 genes. Additionally, the analysis of promoter cis-elements suggested that two VfPR-4 genes may play a role in the response to hormones and biotic and abiotic stress of tung trees. Furthermore, the expression patterns of VfPR-4 genes and their responses to 6-BA, salicylic acid, and silver nitrate in inflorescence buds of tung trees were evaluated using qRT-PCR. Notably, the expression of two VfPR-4 genes was found to be particularly high in leaves and early stages of tung seeds. These results suggest that VF16136 and VF16135 may have significant roles in the development of leaves and seeds in tung trees. Furthermore, these genes were found to be responsive to 6-BA, salicylic acid, and silver nitrate in the development of inflorescence buds. This research provides valuable insights for future investigation into the functions of PR-4 genes in tung trees.

Liver metabolomic characteristics in three different rat models of deficiency based on ultra-performance liquid chromatography coupled to quadrupole time-of-flight mass spectrometry.

OBJECTIVE: To investigate the mechanism of deficiency syndrome (YDS) by analyzing the liver metabolomic characteristics of three different deficiency rat models METHODS: Following the TCM etiology, for clinical features and pathological manifestations of modern medicine, three kinds of animal models of deficiency were induced and replicated. Totally 48 Sprague-Dawley (SD) male rats were randomly divided into blank group, irritation induced model group, Fuzi-Ganjiang induced model group, and thyroxine-reserpine induced model group. After successful development of model, the ultra-performance liquid chromatography coupled to quadrupole time-of-flight mass spectrometry was carried out to detect metabolites in each group. The metabolites of rat liver were analyzed for the characteristics of their biomarkers. The pathway enrichment analysis and metabolic network construction were performed through various online databases including Metabolite Biology Role, Human Metabolome Database, MetaboAnalyst, and Kyoto Encyclopedia of Genes and Genomes. RESULTS: The SD rats in the experimental group showed symptoms like less weight gain, reduced diet and water intake, high body temperature, increased liver and kidney indexes, and abnormal liver and kidney tissue morphology. Moreover, the rats showed high increased levels of serum cyclic adenosine monophosphate, estradiol, alanine transaminase, and aspartate aminotransferase and decreased levels of cyclic guanosinc monophosphate and testosterone. We found four key interrelated metabolic pathways in the liver tissue metabolomics, including the biosynthesis of pantothenic acid and coenzyme A, and metabolism of alpha-linolenic acid metabolism, glycerophospholipid metabolism, and sphingolipid. CONCLUSION: The liver and kidney YDS is closely related to the biosynthesis of pantothenic acid and CoA and abnormal metabolism of α-linolenic acid, glycerophospholipid, and sphingolipid in SD rats.

Identification of Blood Exosomal miRNA-1246, miRNA-150-5p, miRNA-5787 and miRNA-8069 as Sensitive Biomarkers for Hepatitis B Virus Infection.

BACKGROUND: There is a big difference in the expression of miRNAs of plasma exosomes of patients with HBV infection. This study aims to analyze four molecular markers of peripheral blood plasma exosomes to evaluate their potential diagnostic values in HBV infection. METHODS: A total of 55 cases of patients with chronic hepatitis B were in Experimental Group 1; 49 cases of hepatitis B carriers were in Experimental Group 2, and 46 cases were in the healthy control group. The total RNA of the plasma exosome was used to analyze the specificity and sensitivity and draw ROC curves. RESULTS: There was a significant difference in the expression of miRNA-1246, miRNA-150-5p, miRNA-5787, and miRNA-8069 down-regulated by plasma exosomes in Experimental Group 1 and Group 2 and Control Group, with a p value of less than 0.05. CONCLUSIONS: The molecular markers down-regulated were miRNA-1246, miRNA-150-5p, miRNA-5787, and miRNA-8069. The four miRNAs were initially identified as new markers of miRNAs of peripheral blood plasma exosomes after HBV infection. It is better to use multiple markers for combined diagnosis.

Corrigendum: Inflammatory Stress Potentiates Emodin-Induced Liver Injury in Rats.

[This corrects the article DOI: 10.3389/fphar.2015.00233.].

Interlaboratory Assessment of Dried Blood Spot Fatty Acid Compositions.

Dried blood spots for fatty acid profiling are increasing in popularity; however, variability in results between laboratories has not been characterized. Whole blood from two subjects (low and high n-3 polyunsaturated fatty acid [PUFA] status) was collected, 25 µL applied to butylated hydroxytoluene (BHT)-treated chromatography strips, dried in air, and shipped to five laboratories. Results were reported as "routine" (typical fatty acids for each laboratory) or "standardized" (a set of 19 fatty acids), and outliers and variability (%CV) were determined. Five and eight outliers of a possible 91 measures each were identified by routine and standardized reporting, respectively, including eicosapentaenoic acid (EPA, 20:5n-3) in the low n-3 PUFA sample and arachidonic acid in the high n-3 PUFA sample. By standardized reporting, no outliers were identified for EPA or docosahexaenoic acid (DHA, 22:6n-3), and %CV decreased from 8.6% to 6.0% and 9.1% to 6.6% for EPA and 10.5% to 7.2% and 10.5% to 6.6% for DHA in the low and high n-3 PUFA sample, respectively. In conclusion, fatty acid profiles yielded few outliers, and standardization of reporting reduced the variability between laboratories.

Influence of Sensitization Patterns on Fractional Exhaled Nitric Oxide in Asthmatic Children.

Fractional exhaled nitric oxide (FeNO) has been suggested as a non-invasive biomarker of airway inflammation, which is increased in atopic subjects. Whether sensitization to particular allergens is a predictive factor for increased FeNO levels is not yet fully understood. We conducted a retrospective cross-sectional study. From October to December in 2015, the medical documents of 127 mild, steroid-naive asthmatic children and 34 healthy age-matched children were enrolled in this study. The results of the FeNO measurements, skin prick test, and the spirometry were collected for analysis. Sensitization patterns to the 18 aeroallergens (5 categories: mites, molds, animal dander, pollen, and other) were determined in study population. A significant increase in FeNO level was observed in poly-sensitized asthmatic children (34.7 part per billion, (ppb) [28.3-41.1 p.p.b]), compared with mono-sensitized asthmatics (30.7 p.p.b [18.3-43.2 p.p.b]) and with non-sensitized asthmatics (17.3 p.p.b [10.8-24.5 p.p.b]). With sensitization to perennial allergens (mites, mold, and animal dander), blood eosinophil counts were significantly associated with increased FeNO (p<0.05 for all). The highest FeNO level was identified in children sensitized to a combination of the perennial, seasonal, and other allergens, when compared with those sensitized to one category of allergen alone (p=0.004). Our study showed that variations in FeNO level were associated with individuals' sensitization patterns. Being sensitized to some particular allergens might contribute to prompt the airway inflammation.

Untargeted Metabolomics Reveals Intervention Effects of Total Turmeric Extract in a Rat Model of Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common forms of chronic liver disease. Currently, there are no recognized medical therapies effective for NAFLD. Previous studies have demonstrated the effects of total turmeric extract on rats with NAFLD induced by high-fat diet. In this study, serum metabolomics was employed using UHPLC-Q-TOF-MS to elucidate the underlying mechanisms of HFD-induced NAFLD and the therapeutic effects of TE. Supervised orthogonal partial least-squares-discriminant analysis was used to discover differentiating metabolites, and pathway enrichment analysis suggested that TE had powerful combined effects of regulating lipid metabolism by affecting glycerophospholipid metabolism, glycerolipid metabolism, and steroid hormone biosynthesis signaling pathways. In addition, the significant changes in glycerophospholipid metabolism proteins also indicated that glycerophospholipid metabolism might be involved in the therapeutic effect of TE on NAFLD. Our findings not only supply systematic insight into the mechanisms of NAFLD but also provide a theoretical basis for the prevention or treatment of NAFLD.

Inflammatory stress potentiates emodin-induced liver injury in rats.

Herbal medicines containing emodin, widely used for the treatment of hepatitis in clinic, have been reported with hepatotoxicity in individuals. A modest inflammatory stress potentiating liver injury has been linked to the idiosyncratic drug-induced liver injury (IDILI). In this study, we investigated the hypothesis that lipopolysaccharide (LPS) interacts with emodin could synergize to cause liver injury in rats. Emodin (ranging from 20, 40, to 80 mg/kg), which is in the range of liver protection, was administered to rats, before LPS (2.8 mg/kg) or saline vehicle treatment. The biochemical tests showed that non-toxic dosage of LPS coupled with emodin caused significant increases of plasma ALT and AST activities as compared to emodin alone treated groups (P < 0.05). In addition, with LPS or emodin alone could not induce any changes in ALT and AST activity, as compared with the control group (0.5% CMC-Na treatment). Meanwhile, the plasma proinflammatory cytokines, TNF-α, IL-1ß, and IL-6 increased significantly in the emodin/LPS groups compared to either emodin groups or the LPS (P < 0.05). Histological analysis showed that liver damage was only found in emodin/LPS cotreatmented rat livers samples. These results indicate that non-toxic dosage of LPS potentiates the hepatotoxicity of emodin. This discovery raises the possibility that emodin and herbal medicines containing it may induce liver injury in the inflammatory stress even in their therapeutic dosages.

[Comparison of processed and crude Polygoni Multiflori Radix induced rat liver injury and screening for sensitive indicators].

To investigate the difference of liver injury in rats gavaged with crude and processed Polygoni Multiflori Radix. The 75% ethanol extract of crude and processed Polygoni Multiflori Radix (50 g · kg(-1) crude medicine weight/body weight) were continuous oral administered to rats for 6 weeks. Serum biochemical indicators were dynamically detected, the change of liver histopathology was assessed 6 weeks later. Principal component analysis (PCA) was adopted to screen sensitive indicator of the liver damage induced by polygoni multiflori radix. Biochemical tests showed that the crude Polygoni Multiflori Radix group had significant increase of serum ALT, AST, ALP, DBIL and TBIL (P < 0.01 or P < 0.05) and significant decreases of serum IBIL and TBA (P < 0.01 or P < 0.05), while the processed Polygoni Multiflori Radix group showed no obvious changes, compared to the untreated normal group. Histopathologic analysis revealed that crude Polygoni Multiflori Radix group exhibited significant inflammatory cells infiltration in portal area around the blood vessels, tissue destruction and local necrosis of liver cells. There were not obvious pathological changes in processed Polygoni Multiflori Radix group. The results demonstrated that the injury effect of processed Polygoni Multiflori Radix on liver injury of rats was significantly lower than that of unprocessed, and that processing can effectively reduce the hepatotoxicity of Polygoni Multiflori Radix. Traditional transaminase liver function indicators were not sensitive for crude Polygoni Multiflori Radix induced liver damage. The serum content of DBIL and TBIL can reflect the liver damage induced by crude Polygoni Multiflori Radix early and can be sensitive indicators for clinical monitoring the usage of it.

[The idiosyncratic hepatotoxicity of Polygonum multiflorum based on endotoxin model].

The liver injury induced by Polygonum multiflorum Thunb. (PM) was investigated based on idiosyncratic hepatotoxicity model co-treated with lipopolysaccharide (LPS) at a non-hepatotoxic dose. Sprague-Dawley (SD) rats were intragastrically administered with three doses (18.9, 37.8, 75.6 g crude drug per kg body weight) of 50% alcohol extracts of PM alone or co-treated with non-toxic dose of LPS (2.8 mg·kg(-1)) via tail vein injection. The plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were assayed and the isolated livers were evaluated for histopathological changes. The dose-toxicity relationships of single treatment of PM or co-treatment of LPS were investigated comparatively to elucidate the idiosyncratic hepatotoxicity of PM. The results showed that no significant alterations of plasma ALT and AST activities were observed in the groups of solo-administration of LPS (2.8 mg·kg(-1), i.v.) or different dosage (18.9, 37.8 and 75.6 g·kg(-1), i.g.) of PM, compared to normal control group (P > 0.05); while significant elevations were observed in the co-administration groups of PM and LPS. Treatment with LPS alone caused slight infiltration of inflammatory cells in portal area but no evident hepatocytes injury. Co-treatment with LPS and PM (75.6 g·kg(-1), i.g.) caused hepatocyte focal necrosis, loss of central vein intima and a large number of inflammatory cell infiltration in portal areas. When further reduce the dosage of PM, significant increases of plasma ALT and AST activities (P < 0.05) were still observed in co-administration groups of LPS and PM (1.08 or 2.16 g·kg(-1)), but not in LPS or PM solo-administration groups. Nevertheless, the co-treatment of low dosage of PM (0.54 g·kg(-1)) with LPS did not induce any alteration of plasma ALT and AST. In conclusion, intragastric administration with 75.6 g·kg(-1) of PM did not induce liver injury in normal rats model; while the 2 folds of clinical equivalent dose of PM (1.08 g·kg(-1)) could result in liver injury in the LPS-based idiosyncratic hepatotoxicity model, which could be used to evaluate the idiosyncratic hepatotoxicity of PM.

Pulmonary artery reconstruction using autologous pericardium or azygos venae substitute for surgical treatment of central non-small cell lung cancer.

We evaluated the clinico-surgical significance of pulmonary artery (PA) reconstruction using a patch of autologous pericardium/azygos venae substitute to treat central non-small cell lung cancer in 62 patients with pulmonary arteries invaded by tumor. According to TNM-classification, four patients were stage IIb, 46 were stage IIIa, and 12 were stage IIIb. Depending on tumor infiltration, surgical procedures included partial PA tangential resections/reconstructions by a patch of autologous azygos venae, a patch of autologous pericardium and complete PA sleeve resection and reconstruction by a custom-made autologous pericardial conduit interposition. 47 patients received postoperative chemotherapy and 19 received radiotherapy. There were 2 (3.2%) postoperative early deaths due to bronchial anastomotic leakage. Postoperative complications occurred in 17.7% (11/62) patients and all recovered uneventfully. Mean follow-up time after surgical resection was 49.5 (6-12) months and overall ≤1-, 3-, 5-, and ≥10-year survival rates were 80.2, 44.7, 31.4, and 23.1%, respectively. It was concluded that autologous pericardial patch and azygos vein patch reconstruction of PA were safe and effective. Regarding extended circumferential defects after sleeve resection in which end-to-end anastomosis is not feasible, autologous pericardial conduit interposition may be useful for reconstruction when a tumor extensively infiltrates full circumference of the PA.

Upregulated mRNA expression of major histocompatibility complex class I chain-related gene A in colon and activated natural killer cells of Chinese patients with ulcerative colitis.

OBJECTIVE: To explore the expression of major histocompatibility complex class I chain-related gene A (MICA) and its ligand in colonic mucosa and the role of MICA-natural killer (NK) group 2D (NKG2D) interaction in activating NK cells in ulcerative colitis (UC) patients. METHODS: Intestinal mucosal biopsies were obtained from patients with UC and the controls. The expression of major histocompatibility complex class I-related gene (MIC) genes was determined by a reverse transcription polymerase chain reaction (RT-PCR) and the imaging of MICA expressed on colonic mucosa was measured by confocal microscopy resonance scanning. NKG2D and intracellular interferon (IFN)-γ expressions on NK cells were assayed by flow cytometry. RESULTS: The relative amount of MICA mRNA in the colonic mucosa of UC patients was significantly higher than in that of the controls (3.5408 ± 2.6658 vs 1.0477 ± 0.7201, P = 0.001), as were the major histocompatibility complex class I chain-related gene B (MICB) (8.9879 ± 3.2893 vs 4.6293 ± 1.2616, P < 0.001) and NKG2D mRNA expression (2.4395 ± 0.8147 vs 1.1624 ± 0.3954, P < 0.001). Confocal microscopy resonance scanning had shown that MICA was localized predominantly on the basolateral membranes of the epithelium. Further flow cytometry confirmed that the percentage of IFN-γ producer NK cells that expressed NKG2D in peripheral blood lymphocytes was higher in UC patients than in the healthy controls (45.36% ± 12.47% vs 27.45% ± 9.30%, P < 0.001). CONCLUSION: MICA, MICB and NKG2D were upregulated in the colonic mucosa of UC and were associated with activating NK cells with promoted NKG2D and IFN-γ production.

[CTLA-4 gene polymorphism regulates CTLA-4 mRNA stability and protein level in patients with ulcerative colitis].

OBJECTIVE: To investigate the effect of (AT)n repeat polymorphism of the 3'untranslated region in cytotoxic T-lymphocyte associated antigen 4 (CTLA-4) gene on CTLA-4 mRNA stability and full length (flCTLA-4) and soluble CTLA4 (sCTLA-4) expression in ulcerative colitis (UC). METHODS: flCTLA-4 mRNA in colonic biopsies and sCTLA-4 mRNA stability in peripheral blood mononuclear cells of UC patients were measured by quantitative PCR and half-life, respectively. The protein expression of flCTLA-4 in colonic biopsies and sCTLA-4 in sera of UC patients were determined by immunohistochemistry and enzyme-linked immunosorbent assay, respectively. The polymorphism of CTLA-4 (AT)n repeats in 300 UC and 700 age and sex matched healthy controls was genotyped by fluorescent PCR. RESULTS: Among the UC patients, sCTLA-4 mRNA expression levels were decreased in active disease compared to non-active disease (P= 0.004). Carriers of the longer alleles of the (AT)n repeats expressed lower levels of flCTLA-4 and sCTLA-4 mRNA and sCTLA-4 protein than those of the shorter alleles in UC (all P< 0.01), and mRNA with long (AT)n repeat alleles has shorter half-life than mRNA with short alleles and, hence, are unstable. The frequency of long allele carriers of CTLA-4 (AT)n repeats was significantly higher in UC patients than in the healthy controls (22.0% vs. 6.3%, P< 0.01, OR= 4.21, 95% CI: 2.79-6.33), and associated with extensive colitis (P= 0.008). CONCLUSION: CTLA-4 gene expression levels were associated with (AT)n repeat polymorphisms in UC patients. The expression of CTLA-4 mRNA and protein were decreased in carriers of the longer alleles of the (AT)n repeats of CTLA-4 gene. This study suggests that CTLA-4 plays an important role in genetic risk and pathophysiology for UC in central China.

Effect of cytotoxic T lymphocyte-associated molecule 4 1661 gene polymorphism on its expression and transcription in ulcerative colitis.

OBJECTIVE: Our aim was to investigate the expression of cytotoxic T lymphocyte-associated molecule 4 (CTLA-4) in ulcerative colitis (UC) and to evaluate the effect of CTLA-4 gene -1661A/G polymorphism on CTLA-4 expression and transcription. METHODS: A total of 20 UC patients and 22 healthy controls matched by age and sex were enrolled at Zhongnan Hospital of Wuhan University in central China. The CTLA-4 -1661A/G polymorphism was genotyped by the polymerase chain reaction-restriction fragment length polymorphism method. A Western blot analysis was performed to determine the full length CTLA-4 (flCTLA-4) protein expression in the peripheral blood of the UC patients. Serum-soluble CTLA-4 (sCTLA-4) levels were measured by enzyme-linked immunosorbent assay. CTLA-4-1661G mutant promoter transcription function was analyzed by site-directed PCR-based mutagenesis. RESULTS: CTLA-4 protein expression on CD4(+) T cells in UC patients was lower than that in the healthy controls (P < 0.001) while serum sCTLA-4 in the UC patients was significantly higher than that in the healthy controls (P < 0.001). No correlation was found between flCTLA-4 and sCTLA-4 expression levels and the -1661 A/G polymorphism of the CTLA-4 gene. Meanwhile, CTLA-4 -1661 allele A had no significant impact on the promoter activity compared with allele G (P > 0.05). CONCLUSION: CTLA-4 expressions were aberrant in UC patients compared with the healthy controls. CTLA-4 -1661A/G polymorphism had no significant impact on CTLA-4 expression and transcription in the peripheral CD4 T cells of UC patients.

[Association of cytotoxic T lymphocyte antigen-4 promoter C-658T polymorphism with ulcerative colitis in Chinese].

OBJECTIVE: To investigate the association of gene polymorphism of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) with ulcerative colitis (UC) in Chinese. METHODS: One hundred and seventeen patients with UC and 246 healthy controls were genotyped for the polymorphisms of C-658T in the promoter and C61T at the 3' untranslated region of the CTLA-4 gene using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), respectively. The genotype and allele frequencies of the two groups were calculated and compared by chi square test. RESULTS: The frequency of TT+CT genotype at the CTLA-4 gene C-658T in the promoter was significantly higher in UC patients than that in healthy controls (P=0.015). The frequency of the T allele at this locus was also significantly higher in UC patients than that in the controls (P=0.033). The frequencies of TT genotype and T allele at the C-658T locus were highly associated with extensive colitis in UC patients (P=0.037, and P=0.0067, respectively). CONCLUSION: The T allele of CTLA-4 promoter C-658T locus was highly associated with UC in Chinese Han of central China.

[An association between MICB 0106 allele and ulcerative colitis in Chinese Han in Hubei province].

OBJECTIVE: To investigate the association between the exon 2, 3, 4 of MHC class I chain-related gene-B (MICB) and ulcerative colitis (UC) in Chinese Han. METHODS: Using polymerase chain reaction single-stranded conformation polymorphism, allele frequency of MICB exon 2, 3 and 4 in 105 patients with UC and 213 age and sex matched healthy controls were genotyped. All of the studied individuals were Chinese Han. RESULTS: Allele frequency of MICB 0106 was increased in patients with UC as compared with normal controls (19.0% vs 8.9%, P = 0.000, Pc < 0.001, OR = 2.402, 95% CI: 1.488-3.879). The frequency of MICB 0106 was increased significantly in patients with extensive colitis (24.4% vs 8.9%, P = 0.000, Pc < 0.001, OR = 3.294, 95% CI: 1.800-6.027), moderate and severe disease (24.1% vs 8.9%, P = 0.000, Pc < 0.001, OR = 3.294, 95% CI: 1.893-5.576) and in those with extra intestinal manifestations (20.5% vs 8.9%, P = 0.002, Pc = 0.012, OR = 2.626, 95% CI: 1. 18 4. 61). Furthermore, MICB 0106 allele was higher in frequency in the male patients with UC (22. % vs 8. % P = 0. 01, Pc =0 . 06, OR =3 . 76, 95% CI:1 . 37 6. 78) and the patients more than4 0 years old (28.8% vs 8.3% P = 0.000, Pc <0 .001, OR= 4 .500, 95% I:2 . 81 8.504) as compared with healthy controls. CONCLUSION: MICB 0106 allele is positively associated with UC, especially with extensive colitis, moderate and severe disease, presence of extra intestinal manifestations, male gender and age of more than 40 years in Chinese Han in Hubei province.