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BACKGROUND: The modified pancreatitis activity scoring system (mPASS) was proposed to assess the activity of acute pancreatitis (AP) while it doesn't include indicators that directly reflect pathophysiology processes and imaging characteristics. OBJECTIVES: To determine the threshold of admission mPASS and investigate radiomics and laboratory parameters to construct a model to predict the activity of AP. METHODS: AP inpatients at institution 1 were randomly divided into training and validation groups based on a 5:5 ratio. AP inpatients at Institution 2 were served as test group. The cutoff value of admission mPASS scores in predicting severe AP was selected to divide patients into high and low level of disease activity group. LASSO was used in screening features. Multivariable logistic regression was used to develop radiomics model. Meaningful laboratory parameters were used to construct combined model. RESULTS: There were 234 (48 years ± 10, 155 men) and 101 (48 years ± 11, 69 men) patients in two institutions. The threshold of admission mPASS score was 112.5 in severe AP prediction. The AUC of the radiomics model was 0.79, 0.72, and 0.76 and that of the combined model incorporating rad-score and white blood cell were 0.84, 0.77, and 0.80 in three groups for activity prediction. The AUC of the combined model in predicting disease without remission was 0.74. CONCLUSIONS: The threshold of admission mPASS was 112.5 in predicting severe AP. The model based on CECT radiomics has the ability to predict AP activity. Its ability to predict disease without remission is comparable to mPASS. CRITICAL RELEVANCE STATEMENT: This work is the first attempt to assess the activity of acute pancreatitis using contrast-enhanced CT radiomics and laboratory parameters. The model provides a new method to predict the activity and prognosis of AP, which could contribute to further management. KEY POINTS: Radiomics features and laboratory parameters are associated with the activity of acute pancreatitis. The combined model provides a new method to predict the activity and prognosis of AP. The ability of the combined model is comparable to the modified Pancreatitis Activity Scoring System.
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BACKGROUND: The circadian clock, also known as the circadian rhythm, is responsible for predicting daily and seasonal changes in the environment, and adjusting various physiological and developmental processes to the appropriate times during plant growth and development. The circadian clock controls the expression of the Lhcb gene, which encodes the chlorophyll a/b binding protein. However, the roles of the Lhcb gene in tea plant remain unclear. RESULTS: In this study, a total of 16 CsLhcb genes were identified based on the tea plant genome, which were distributed on 8 chromosomes of the tea plant. The promoter regions of CsLhcb genes have a variety of cis-acting elements including hormonal, abiotic stress responses and light response elements. The CsLhcb family genes are involved in the light response process in tea plant. The photosynthetic parameter of tea leaves showed rhythmic changes during the two photoperiod periods (48 h). Stomata are basically open during the day and closed at night. Real-time quantitative PCR results showed that most of the CsLhcb family genes were highly expressed during the day, but were less expressed at night. CONCLUSIONS: Results indicated that CsLhcb genes were involved in the circadian clock process of tea plant, it also provided potential references for further understanding of the function of CsLhcb gene family in tea plant.
Subject(s)
Camellia sinensis , Circadian Rhythm , Photosynthesis , Photosynthesis/genetics , Camellia sinensis/genetics , Camellia sinensis/physiology , Circadian Rhythm/genetics , Gene Expression Regulation, Plant , Plant Proteins/genetics , Plant Proteins/metabolism , Genes, Plant , Multigene Family , Chlorophyll Binding Proteins/genetics , Chlorophyll Binding Proteins/metabolism , PhotoperiodABSTRACT
Lignin is an important component of plant cell walls and plays crucial roles in the essential agronomic traits of tea quality and tenderness. However, the molecular mechanisms underlying the regulation of lignin biosynthesis in tea plants remain unclear. CsWRKY13 acts as a negative regulator of lignin biosynthesis in tea plants. In this study, we identified a GRAS transcription factor, phytochrome A signal transduction 1 (CsPAT1), that interacts with CsWRKY13. Silencing CsPAT1 expression in tea plants and heterologous overexpression in Arabidopsis demonstrated that CsPAT1 positively regulates lignin accumulation. Further investigation revealed that CsWRKY13 directly binds to the promoters of CsPAL and CsC4H and suppresses transcription of CsPAL and CsC4H. CsPAT1 indirectly affects the promoter activities of CsPAL and CsC4H by interacting with CsWRKY13, thereby facilitating lignin biosynthesis in tea plants. Compared with the expression of CsWRKY13 alone, the co-expression of CsPAT1 and CsWRKY13 in Oryza sativa significantly increased lignin biosynthesis. Conversely, compared with the expression of CsPAT1 alone, the co-expression of CsPAT1 and CsWRKY13 in O. sativa significantly reduced lignin accumulation. These results demonstrated the antagonistic regulation of the lignin biosynthesis pathway by CsPAT1 and CsWRKY13. These findings improve our understanding of lignin biosynthesis mechanisms in tea plants and provide insights into the role of the GRAS transcription factor family in lignin accumulation.
Subject(s)
Camellia sinensis , Gene Expression Regulation, Plant , Lignin , Plant Proteins , Transcription Factors , Lignin/metabolism , Lignin/biosynthesis , Transcription Factors/metabolism , Transcription Factors/genetics , Plant Proteins/genetics , Plant Proteins/metabolism , Camellia sinensis/genetics , Camellia sinensis/metabolism , Arabidopsis/genetics , Arabidopsis/metabolism , Plants, Genetically Modified , Promoter Regions, Genetic/geneticsABSTRACT
Tea plants (Camellia sinensis (L.) O. Kuntze) belong to Theaceae family, in the section Thea. Tea plants are widely distributed in subtropical and tropical regions in the word. α-carotene and ß-carotene in the tea leaves belong to carotenoids, which are associated with the aroma and color of the tea. Phytoene synthase (PSY) is a rate-limiting enzyme in carotenoids biosynthesis. We identified three CsPSY genes in 'Shuchazao', named CsPSY1, CsPSY2, and CsPSY3. Structural analysis of three CsPSY genes showed that CsPSY1 had a longer intro structure. The cis-acting elements of CsPSYs promoter were mainly associated with light-responsiveness, abiotic stress-responsiveness, and hormone-responsiveness. CsPSY1 exhibited expression in all tissues of the tea plants, whereas CsPSY2 and CsPSY3 were trace expression levels in all tissues. The positive expression of CsPSY1 under hormonal and abiotic stresses suggested its role in plant development and defense responses. The amino acid sequence of CsPSY1 was highly conserved in eight tea cultivars. The recombinant vector pCAMBIA1301-CsPSY1 was constructed to stabilize the overexpression of CsPSY1 in carrot. The contents of α-carotene and ß-carotene in transgenic carrot callus were significantly increased. This study provides a foundational basis for further research on the function of CsPSYs and carotenoids accumulation in tea plants.
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MATERIALS: Patients with alcoholic acute pancreatitis in our hospital were recruited from Jan 2019 to July 2022 and divided into IAAP and RAAP groups. All patients underwent Contrast-Enhanced Computerized Tomography (CECT) or Magnetic Resonance Imaging (MRI) after administration. Imaging manifestations, local complications, severity scores on the Modified CT/MR Severity Index (MCTSI/MMRSI), Extrapancreatic Inflammation on CT/MR (EPIC/M), clinical severity [Bedside Index for Severity in Acute Pancreatitis (BISAP) Acute Physiology and Chronic Health Evaluation (APACHE-II)], and clinical prognosis were compared between the two groups.Results: 166 patients were recruited for this study, including 134 IAAP (male sex 94%) and 32 RAAP patients (male sex 100%). On CECT or MRI, IAAP patients were more likely to develop ascites and Acute Necrosis collection (ANC) than RAAP patients (ascites:87.3%vs56.2%; P = .01; ANC:38%vs18.7%; P < .05). MCTSI/MMRSI and EPIC/M scores were higher in IAAP than in RAAP patients(MCTSI/MMRSI:6.2vs5.2; P < .05; EPIC/M:5.4vs3.8; P < .05).Clinical severity scores (APACHE-II and BISAP), length of stay, and systemic complications [Systemic Inflammatory Response Syndrome (SIRS), respiratory failure] were higher in the IAAP group than in the RAAP group (P < .05). No mortality outcomes were reported in either group while hospitalized.Conclusions: Patients with IAAP had more severe disease than those with RAAP. These results may be helpful for differentiating care paths for IAAP and RAAP, which are essential for management and timely treatment in clinical practice.
Subject(s)
Pancreatitis , Humans , Male , Pancreatitis/diagnostic imaging , Pancreatitis/complications , Cross-Sectional Studies , Retrospective Studies , Severity of Illness Index , Acute Disease , Ascites/complications , Predictive Value of Tests , PrognosisABSTRACT
Statins play an important role in the treatment of diabetic nephropathy. Increasing attention has been given to the relationship between statins and insulin resistance, but many randomized controlled trials confirm that the therapeutic effects of statins on diabetic nephropathy are more beneficial than harmful. However, further confirmation of whether the beneficial effects of chronic statin administration on diabetic nephropathy outweigh the detrimental effects is urgently needed. Here, we find that long-term statin administration may increase insulin resistance, interfere with lipid metabolism, leads to inflammation and fibrosis, and ultimately fuel diabetic nephropathy progression in diabetic mice. Mechanistically, activation of insulin-regulated phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway leads to increased fatty acid synthesis. Furthermore, statins administration increases lipid uptake and inhibits fatty acid oxidation, leading to lipid deposition. Here we show that long-term statins administration exacerbates diabetic nephropathy via ectopic fat deposition in diabetic mice.
Subject(s)
Diabetes Mellitus, Experimental , Diabetic Nephropathies , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Hypercholesterolemia , Insulin Resistance , Animals , Mice , Diabetes Mellitus, Experimental/complications , Diabetes Mellitus, Experimental/metabolism , Diabetic Nephropathies/chemically induced , Diabetic Nephropathies/drug therapy , Diabetic Nephropathies/metabolism , Fatty Acids , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Lipids , MammalsABSTRACT
Auxin affects all aspects of plant growth and development, including morphogenesis and adaptive responses. Auxin transmembrane transport is promoted by PIN formation (PIN) and a structurally similar PIN-like (PILS) gene family, which jointly controls the directional transport of the auxin between plant cells, and the accumulation of intracellular auxin. At present, there is no study investigating the roles of CslPIN and CslPILS gene family in root development in the tea plant (Camellia sinensis). In this study, 8 CslPIN and 10 CslPILS genes were identified in the tea plant, and their evolutionary relationships, physical and chemical properties, conserved motifs, cis-acting elements, chromosome location, collinearity, and expression characteristics were analyzed. The mechanism of CslPIN and CslPILS in the formation of tea adventitious roots (ARs) was studied by the AR induction system. Through functional verification, the regulation of CslPIN3 gene on root growth and development of tea plant was studied by over-expression of CslPIN3 in Arabidopsis thaliana and in situ hybridization in Camellia sinensis. The results confirmed CslPIN3 was involved in the regulation of root growth and development as well as auxin accumulation. This study provides a better insight into the regulatory mechanism of CslPIN and CslPILS gene family on the formation of AR in tea plant.
Subject(s)
Arabidopsis Proteins , Arabidopsis , Camellia sinensis , Camellia sinensis/genetics , Indoleacetic Acids/metabolism , Arabidopsis Proteins/metabolism , Arabidopsis/genetics , Tea/metabolism , Gene Expression Regulation, Plant , Plant Roots/metabolism , Plant Proteins/genetics , Plant Proteins/metabolismABSTRACT
Aims: The genes targeted by miRNAs have been well studied. However, little is known about the feedback mechanisms to control the biosynthesis of miRNAs that are essential for the miRNA feedback networks in the cells. In this present study, we aimed at examining how hydrogen sulfide (H2S) promotes angiogenesis by regulating miR-192 biosynthesis. Results: H2S promoted in vitro angiogenesis and angiogenesis in Matrigel plugs embedded in mice by upregulating miR-192. Knockdown of the H2S-generating enzyme cystathionine γ-lyase (CSE) suppressed in vitro angiogenesis, and this suppression was rescued by exogenous H2S donor NaHS. Plakophilin 4 (PKP4) served as a target gene of miR-192. H2S up-regulated miR-192 via the VEGFR2/Akt pathway to promote the splicing of primary miR-192 (pri-miR-192), and it resulted in an increase in both the precursor- and mature forms of miR-192. H2S translocated YB-1 into the nuclei to recruit Drosha to bind with pri-miR-192 and promoted its splicing. NaHS treatment promoted angiogenesis in the hindlimb ischemia mouse model and the skin-wound-healing model in diabetic mice, with upregulated miR-192 and downregulated PKP4 on NaHS treatment. In human atherosclerotic plaques, miR-192 levels were positively correlated with the plasma H2S concentrations. Innovation and Conclusion: Our data reveal a role of YB-1 in recruiting Drosha to splice pri-miR-192 to mediate the proangiogenic effect of H2S. CSE/H2S/YB-1/Drosha/miR-192 is a potential therapeutic target pathway for treating diseases, including organ ischemia and diabetic complications. Antioxid. Redox Signal. 36, 760-783. The Clinical Trial Registration number is 2016-224.
Subject(s)
Diabetes Mellitus, Experimental , Hydrogen Sulfide , MicroRNAs , Animals , Cystathionine gamma-Lyase/metabolism , Hydrogen Sulfide/metabolism , Ischemia , Mice , MicroRNAs/genetics , MicroRNAs/metabolism , Transcription FactorsABSTRACT
Diabetes (especially Type II) is one of the primary threats to cardiovascular health. Wound healing defects and vascular dysfunction are common in diabetic patients, and the primary cause of deterioration is sustained high plasma glucose. microRNA, a noncoding RNA, has regulatory functions that are critical to maintaining homeostasis. MicroRNA (miR)-126-3p is a potential diabetes biomarker and a proangiogenic factor, and its plasma level decreases in diabetic patients. Previous studies have revealed the proangiogenic character of the gasotransmitter hydrogen sulfide (H2S). However, little is known about the relationship between H2S and miR-126-3p when the extracellular glucose level is high, let alone their influences on deteriorated endothelial cell migration, a key component of angiogenesis, which is crucial for wound healing. Human umbilical vein endothelial cells (HUVECs) were treated with high glucose (33.3 mmol/L) or normal glucose (5.5 mmol/L) for 48 h. Affymetrix miRNA profiling and real-time PCR were used to validate the miRNA expression. An H2S probe (HSip-1) was used to detect endogenous H2S. Scratch wound-healing assays were used to evaluate HUVEC migration. The protein levels were quantified by Western blot. Both exogenous and endogenous H2S could upregulate the miR-126-3p levels in HUVECs or muscle tissue. High glucose decreased the H2S level and the protein expression of the H2S-producing enzyme cystathionine γ-lyase (CSE) in HUVECs; however, the DNA methyltransferase 1 (DNMT1) protein level was upregulated. CSE overexpression not only increased the miR-126-3p level by decreasing the DNMT1 protein level but also rescued the deteriorated cell migration in HUVECs treated with high glucose. DNMT1 overexpression decreased the miR-126-3p level and inhibited the migration of HUVECs, whereas silencing DNMT1 improved cell migration. High glucose decreased the endogenous H2S and miR-126-3p levels and increased the DNMT1 expression, thus inducing the migration dysfunction of HUVECs. Treatment with exogenous H2S or the overexpression of the endogenously produced enzyme CSE would rescue this migration dysfunction through H2S-DNMT1-miR-126-3p.
Subject(s)
Diabetes Mellitus, Type 2/drug therapy , Hydrogen Sulfide/pharmacology , MicroRNAs/genetics , Neovascularization, Physiologic/drug effects , Animals , Blood Vessels/drug effects , Blood Vessels/growth & development , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/genetics , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/pathology , Cell Movement/drug effects , Cystathionine gamma-Lyase/genetics , DNA (Cytosine-5-)-Methyltransferase 1/genetics , Diabetes Mellitus, Type 2/genetics , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/pathology , Disease Models, Animal , Gene Expression Regulation/drug effects , Glucose/metabolism , Glucose/toxicity , Human Umbilical Vein Endothelial Cells/drug effects , Humans , Hydrogen Sulfide/metabolism , Mice , Neovascularization, Physiologic/genetics , Signal Transduction/drug effects , Wound Healing/drug effectsABSTRACT
Tibetan monks have a special way of life and food habits, however, little is known about their dyslipidemia. This study aimed to investigate the prevalence of dyslipidemia and risk factors of this population. A cross-sectional study of dyslipidemia was conducted in 876 Tibetan monks and 912 local residents in the same area. All subjects underwent interviews and physical examinations. The total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) of the subjects were analyzed. Compared to local residents, the overall prevalence of dyslipidemia in monks was 29.5%, which was significantly lower (p<0.05). It was increased with higher age and BMI, but reduced with higher educational level (p<0.05). The typical forms of dyslipidemia in monks were elevated TG and low HDL-C, while it was lower HDL-C in residents (p<0.05). Our study demonstrated that monks in Gannan Tibetan autonomous district had a lower prevalence of dyslipidemia. It suggested that the relatively healthy lifestyle and food habits of monks were mainly responsible of the lower prevalence of dyslipidemia.
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AIMS: This study aims to investigate the pathophysiological role and mechanism of pigment epithelium-derived factor (PEDF) deletion in ovarian damage. METHODS: Female PEDF-knockout mice and their wild-type littermates were used in this study. Relevant tests were performed at 8-10â¯weeks or 32â¯weeks of age. KEY FINDINGS: Compared to the wild-type mice, the PEDF-knockout mice showed diminished ovarian reserve (DOR), worse ovum quality after injection to induce controlled ovarian stimulation, increased serum follicle stimulating hormone (FSH) level and an follicle stimulating hormone/luteinizing hormone (FSH/LH) ratio. Moreover, severe ovarian oxidative damage was found in ovaries of PEDF-knockout mice that mainly manifested as an accumulation of reactive oxygen species (ROS), NFE2-related factor 2 (Nrf2) pathway activation, significantly upregulated expression of ROS-generating genes. Correspondingly, the PEDF-knockout mice exhibited lipid metabolism disorder and insulin resistance, which mainly manifested as obesity, abdominal fat accumulation, adipocyte enlargement, severe ectopic fat deposition, dyslipidemia, changes in adipokine levels, hyperglycemia, hyperinsulinemia, impaired glucose tolerance, impaired insulin tolerance and significantly declined protein kinase B (Akt) phosphorylation levels. SIGNIFICANCE: Loss of PEDF leads to ovarian oxidative damage accompanied by DOR in mice, this is related to PEDF deficiency induced severe insulin resistance and lipid metabolism disorder. Therefore, PEDF may be a potential target for the treatment of diseases related to ovarian oxidative damage.
Subject(s)
Eye Proteins/genetics , Nerve Growth Factors/genetics , Ovarian Reserve/physiology , Ovary/physiopathology , Oxidative Stress/physiology , Reactive Oxygen Species/metabolism , Serpins/genetics , Abdominal Fat/metabolism , Animals , Eye Proteins/metabolism , Female , Insulin Resistance/genetics , Insulin Resistance/physiology , Lipid Metabolism/genetics , Lipid Metabolism/physiology , Mice , Mice, Inbred C57BL , Mice, Knockout , Nerve Growth Factors/metabolism , Obesity/pathology , Ovarian Reserve/genetics , Oxidative Stress/genetics , Serpins/metabolism , Up-RegulationABSTRACT
Primary hepatocellular carcinoma (PHC) includes hepatocellular carcinoma, intrahepatic cholangiocarcinoma and other pathological types and is characterized by rapid progression. Most of the clinical diagnoses are made at late stage or when distant metastasis occurs, increasing the difficulty of treatment and resulting in a poor prognosis. Therefore, the early diagnosis of PHC plays an important role in timely treatment and the improvement of prognosis. The gold standard for the diagnosis of primary liver cancer is liver biopsy, but it has limitations as an invasive examination. Presently, imaging has become the first choice for the diagnosis of liver cancer. We here summarize the new methods and techniques of imaging in diagnosis and evaluation of primary liver cancer in recent years, including ultrasonography, computed tomography perfusion imaging, diffusion-weighted imaging technology-voxel incoherent motion, diffusion tensor imaging, iterative decomposition of water and fat with echo asymmetry and least squares estimation-iron quantification, dynamic enhanced magnetic resonance imaging and hepatocyte-specific contrast medium imaging. Imaging diagnosis can not only evaluate the degree of differentiation, blood supply and perfusion, and invasiveness of the lesion, but also predict the prognosis, evaluate liver function, and provide references for clinical diagnosis and treatment.
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PURPOSE: To study MRI findings of hemorrhage in acute pancreatitis (AP) and correlate the presence and extent of hemorrhage with the MR severity index (MRSI), Acute Physiology And Chronic Health Evaluation (APACHE) II scores, and clinical outcome. MATERIALS AND METHODS: This retrospective study included 539 patients with AP. Hemorrhage was defined as areas of hyperintensity in or outside the pancreas on liver imaging with volume acceleration flexible (LAVA-Flex). The presence of hemorrhage was classified into three areas: within the pancreatic parenchyma, retroperitoneal space, and sub-or intraperitoneal space. Involvement of each area was awarded 1 point resulting in the hemorrhage severity index (HSI) score. The predicted severity of AP was graded by MRSI and APACHE II score. The association between HSI, MRSI, and APACHE II scores was analyzed. The length of hospital stay and organ dysfunction was used as clinical outcome parameters. RESULTS: Among 539 AP patients, 62 (11.5%) had hemorrhage. The prevalence of hemorrhage was 1.1% (2/186), 13.9% (43/310), and 39.5% (17/43) in predicted mild, moderate, and severe AP, respectively, based on MRSI (χ2â¯=â¯55.3, pâ¯=â¯0.00); and 7.7% (21/273) and 19.2% (18/94) in predicted mild and severe AP, respectively, based on APACHE II (χ2â¯=â¯21.2, pâ¯=â¯0.00). HSI score significantly correlated with MRSI (râ¯=â¯0.36, pâ¯<â¯0.001) and APACHE II scores (râ¯=â¯0.21, pâ¯=â¯0.00). The prevalence of organ dysfunction was higher and length of hospital stay was longer in patients with hemorrhage than in those without hemorrhage (pâ¯<â¯0.01). CONCLUSIONS: Hemorrhage in AP is common. The presence of hemorrhage, rather than its extent, correlates with poor clinical outcome.
Subject(s)
Hemorrhage/diagnostic imaging , Hemorrhage/etiology , Magnetic Resonance Imaging/methods , Pancreatitis/complications , Pancreatitis/diagnostic imaging , APACHE , Acute Disease , Adolescent , Adult , Aged , Aged, 80 and over , Child , Female , Hemorrhage/epidemiology , Humans , Length of Stay , Liver/diagnostic imaging , Male , Middle Aged , Multiple Organ Failure/epidemiology , Multiple Organ Failure/etiology , Pancreas/diagnostic imaging , Pancreatitis/epidemiology , Prevalence , Retrospective Studies , Treatment Outcome , Young AdultABSTRACT
Tea plants [Camellia sinensis (L.) O. Kuntze] are an important leaf-type crop that are widely used for the production of non-alcoholic beverages in the world. Exposure to excessive amounts of heavy metals adversely affects the quality and yield of tea leaves. To analyze the molecular responses of tea plants to heavy metals, a reliable quantification of gene expression is important and of major importance herein is the normalization of the measured expression levels for the target genes. Ideally, stably expressed reference genes should be evaluated in all experimental systems. In this study, 12 candidate reference genes (i.e., 18S rRNA, Actin, CYP, EF-1α, eIF-4α, GAPDH, MON1, PP2AA3, TBP, TIP41, TUA, and UBC) were cloned from tea plants, and the stability of their expression was examined systematically in 60 samples exposed to diverse heavy metals (i.e., manganese, aluminum, copper, iron, and zinc). Three Excel-based algorithms (geNorm, NormFinder, and BestKeeper) were used to evaluate the expression stability of these genes. PP2AA3 and 18S rRNA were the most stably expressed genes, even though their expression profiles exhibited some variability. Moreover, commonly used reference genes (i.e., GAPDH and TBP) were the least appropriate reference genes for most samples. To further validate the suitability of the analyzed reference genes, the expression level of a phytochelatin synthase gene (i.e., CsPCS1) was determined using the putative reference genes for data normalizations. Our results may be beneficial for future studies involving the quantification of relative gene expression levels in tea plants.
Subject(s)
Camellia sinensis/genetics , Camellia sinensis/physiology , Gene Expression Profiling/standards , Genes, Plant/genetics , Metals/pharmacology , Stress, Physiological/drug effects , Stress, Physiological/genetics , Camellia sinensis/drug effects , Reference StandardsABSTRACT
The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production, and to identify the role of microRNA-455-3p (miR-455-3p) during those processes. In cultured human umbilical vein endothelial cells (HUVECs), the expression of miR-455-3p, eNOS protein and the NO production was detected after administration with 50 µM NaHS. The results indicated that H2S could augment the expression of miR-455-3p and eNOS protein, leading to the increase of NO level. We also found that overexpression of miR-455-3p in HUVECs increased the protein levels of eNOS whereas inhibition of miR-455-3p decreased it. Moreover, H2S and miR-455-3p could no longer increase the protein level of eNOS in the presence of proteasome inhibitor, MG-132. In vivo, miR-455-3p and eNOS expression were considerably increased in C57BL/6 mouse aorta, muscle and heart after administration with 50 µmol/kg/day NaHS for 7 days. We also identified that H2S levels and miR-455-3p expression increased in human atherosclerosis plaque while H2S levels decreased in plasma of atherosclerosis patients. Our data suggest that the stability of eNOS protein and the NO production could be regulated by H2S through miR-455-3p.
Subject(s)
Gene Expression Regulation , Hydrogen Sulfide/metabolism , MicroRNAs/genetics , Nitric Oxide Synthase Type III/metabolism , Animals , Cell Movement/genetics , Cells, Cultured , Cullin Proteins/genetics , Female , Gene Expression Regulation/drug effects , Human Umbilical Vein Endothelial Cells , Humans , Hydrogen Sulfide/pharmacology , Mice , Nitric Oxide/metabolism , Nitric Oxide Synthase Type III/genetics , Plaque, Atherosclerotic/genetics , Plaque, Atherosclerotic/metabolism , Plaque, Atherosclerotic/pathology , Proteasome Endopeptidase Complex/metabolism , Protein Stability , RNA Interference , Ubiquitin/metabolismABSTRACT
BACKGROUND: To study the initial and follow up patterns of gastrointestinal tract involvement in acute pancreatitis (AP) using magnetic resonance imaging (MRI). METHODS: A total of 209 patients with AP undergoing abdominal MRI on 1.5 T MRI were compared to 100 control patients selected from our daily clinical caseload who underwent MRI over the same recruitment period and had no other disease which can cause abnormality of gastrointestinal tract. Initial and follow up MRI examinations of gastrointestinal tract abnormalities were noted for AP patients. The severity of AP was graded by the MRSI and APACHE II. Spearman correlation of gastrointestinal tract involvement with MRSI and APACHE II was analyzed. RESULTS: In 209 patients with AP, 63% of the AP patients on their initial MRI exams and 5% of control subjects had at least one gastrointestinal tract abnormality (P<0.05). In the control group, thirty-seven patients were normal on MRI, 24 patients with renal cysts, eighteen patients with liver cysts, eleven patients with liver hemangiomas, and ten patients with splenomegaly. The abnormalities of gastrointestinal tract observed in AP patients included thickened stomach wall (20%), thickened duodenum wall (27%), thickened ascending colon wall (11%), thickened transverse colon wall (15%), and thickened descending colon wall (26%), among others. Gastrointestinal tract abnormalities were correlated with the MRSI score (r=0.46, P<0.05) and APACHE II score (r=0.19, P<0.05). Among 62 patients who had follow up examinations, 26% of patients had gastrointestinal tract abnormality, which was significantly lower than that in the initial exams (P<0.05). Resolution of gastrointestinal tract abnormal MRI findings coincided with symptom alleviation in AP patients. CONCLUSIONS: Gastrointestinal tract abnormalities on MRI are common in AP and they are positively correlated with the severity of AP. It may add value for determining the severity of AP.
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Hydrogen sulfide (H2S)has emerged as pivotal signaling molecules since it is recognized as the third gasotransmitter together with nitric oxide and carbon monoxide. The development of detecting technologies contributed to the research in H2S biology.H2S plays significant roles in human body systems, such as the cardiovascular system, nervous system, respiratory system etc.. Alterations of H2S concentrations have been connected with many diseases. Hypertension, atherosclerosis, neurodegenerative disorder, asthma and many other diseases are found to be related with abnormal H2S metabolism. It has become a potential drug for therapeutic purposes. Understanding the mechanism of H2S biology, including a molecular switch contained in its "receptor", has deepened the research on how small molecules regulate big molecules, as well as providing new strategy for the therapeutic approaches for varies of diseases.
Subject(s)
Hydrogen Sulfide/metabolism , Signal Transduction , Asthma , Atherosclerosis , Carbon Monoxide , Cardiovascular System , Humans , Hypertension , Nervous System , Neurodegenerative Diseases , Nitric Oxide , Respiratory SystemABSTRACT
BACKGROUND: Alzheimer's disease is a common neurodegenerative disorder in elderly. This study was aimed to systematically evaluate the association between tea intake and the risk of cognitive disorders by meta-analysis. METHODS AND FINDINGS: PubMed, Embase and Wanfang databases were systematically searched and a total of 26 observational studies were included in this study. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were calculated and pooled by using fixed or random effects models according to the degree of heterogeneity. RESULTS: The overall pooled analysis indicated that tea intake could significantly reduce the risk of cognitive disorders (OR = 0.65, 95%CI = 0.58-0.73). Subgroup analyses were conducted based on study design, population, frequency of tea drinking and type of cognitive disorders. The results showed that tea drinking was significantly associated with the reduced incidence of cognitive disorders in all of subgroups based on study design and frequency of tea drinking. In particular, tea drinking was inversely associated with the risk of cognitive impairment (CoI), mild cognitive impairment (MCI), cognitive decline and ungrouped cognitive disorders. Moreover, for population subgroups, the significant association was only found in Chinese people. CONCLUSION: Our study suggests that daily tea drinking is associated with decreased risk of CoI, MCI and cognitive decline in the elderly. However, the association between tea intake and Alzheimer's disease remains elusive.
Subject(s)
Cognition Disorders/prevention & control , Tea , Alzheimer Disease/epidemiology , Alzheimer Disease/prevention & control , Cognition Disorders/epidemiology , Humans , Risk FactorsABSTRACT
Many previous studies have provided evidence that the ADIPOQ +45T>G polymorphism (rs2241766) might cause metabolic syndrome (MS). As a cardiovascular manifestation of MS, the incidence of stroke is associated with adiponectin; however, the results remain controversial and inconsistent. Systematic searches of relevant studies published up to Dec 2014 and Jan 2016 on the ADIPOQ +45T>G polymorphism and the risk of MS and adiponectin levels and the risk of stroke, respectively, were conducted in MEDLINE and EMBASE. The odds ratio (OR) or risk ratio (RR) and their 95% confidence interval (95% CI) were extracted. Sixteen studies containing 4,113 MS cases and 3,637 healthy controls indicated a weak positive association between ADIPOQ +45 T>G and MS in the dominant genetic model (OR = 1.30, 95% CI = 1.03-1.65), which was also validated by stratified subgroup analyses. Twelve studies including 26,213 participants and 4,246 stroke cases indicated that 5 µg/ml increments in adiponectin level were not relevant to stroke risk (RR = 1.05, 95% CI = 1.00-1.10, P = 0.069). This study suggested a weak positive association of ADIPOQ +45T>G with MS and a strong association with metabolic-related disease. Additionally, adiponectin level was not a causal factor of increasing stroke risk.
Subject(s)
Adiponectin/genetics , Metabolic Diseases/genetics , Metabolic Syndrome/genetics , Polymorphism, Single Nucleotide , Stroke/genetics , Adiponectin/blood , Confidence Intervals , Female , Genetic Predisposition to Disease , Humans , Male , Metabolic Diseases/epidemiology , Metabolic Syndrome/epidemiology , Odds Ratio , Risk , Stroke/epidemiologyABSTRACT
Flavonoids are the main flavor components and functional ingredients in tea, and the shikimic acid pathway is considered as one of the most important pathways in flavonoid biosynthesis, but little was known about the function of regulatory genes in the metabolism phenolic compounds in tea plant (Camellia sinensis), especially related genes in shikimic acid pathway. The dynamic changes of catechin (predominant flavonoid) contents were analyzed in this study, and four genes (CsPPT, CsDAHPS, CsSDH and CsCS) involving in shikimic acid pathway in C. sinensis albino cultivar 'Baicha 1' were cloned and characterized. The full-length cDNA sequences of these genes were obtained using reverse transcription-PCR and rapid amplification of cDNA ends. At the albinistic stage, the amounts of all catechins decreased to the lowest levels, when epigallocatechin gallate was the highest, whereas gallocatechin-3-O-gallate the lowest. Gene expression patterns analyzed by qRT-PCR showed that CsPPT and CsDAHPS were highly expressed in flowers and buds, while CsSDH and CsCS showed high expression levels in buds and leaves. It was also found that the transcript abundance of shikimic acid biosynthetic genes followed a tightly regulated biphasic pattern, and was affected by albinism. The transcript levels of CsPPT and CsDAHPS were decreased at albinistic stage followed elevated expression, whereas CsSDH and CsCS were increased only at re-greening stage. Taken together, these findings suggested that these four genes in C. sinensis may play different roles in shikimic acid biosynthesis and these genes may have divergent functions.