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With increasing attention to diabetes remission, various special dietary patterns have been found to be effective in achieving diabetes remission. The effect of a single dietary pattern on lowering blood glucose is clear, but studies on the synergistic effects of different dietary patterns are limited. This article describes the types of intermittent fasting and ketogenic diets, potential mechanisms, contraindications of combination diets, recommendations for combination diets, and their health outcomes. This paper aims to illustrate the evidence for intermittent fasting combined with a ketogenic diet on outcomes of diabetes remission and effect on blood glucose control. Knowledge of these findings can help doctors and patients determine dietary patterns for achieving diabetes remission and understanding their application.
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BACKGROUND: Helicobacter pylori (H. pylori) infection is related to various extragastric diseases including type 2 diabetes mellitus (T2DM). However, the possible mechanisms connecting H. pylori infection and T2DM remain unknown. AIM: To explore potential molecular connections between H. pylori infection and T2DM. METHODS: We extracted gene expression arrays from three online datasets (GSE60427, GSE27411 and GSE115601). Differentially expressed genes (DEGs) commonly present in patients with H. pylori infection and T2DM were identified. Hub genes were validated using human gastric biopsy samples. Correlations between hub genes and immune cell infiltration, miRNAs, and transcription factors (TFs) were further analyzed. RESULTS: A total of 67 DEGs were commonly presented in patients with H. pylori infection and T2DM. Five significantly upregulated hub genes, including TLR4, ITGAM, C5AR1, FCER1G, and FCGR2A, were finally identified, all of which are closely related to immune cell infiltration. The gene-miRNA analysis detected 13 miRNAs with at least two gene cross-links. TF-gene interaction networks showed that TLR4 was coregulated by 26 TFs, the largest number of TFs among the 5 hub genes. CONCLUSION: We identified five hub genes that may have molecular connections between H. pylori infection and T2DM. This study provides new insights into the pathogenesis of H. pylori-induced onset of T2DM.
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Aims: This study aims to describe the clinical characteristics, laboratory data and complications of hospitalized COVID-19 patients with type 2 diabetes mellitus (T2DM) since epidemic prevention and control optimization was adjusted in December 2022 in China. Methods: This retrospective multicenter study included 298 patients with confirmed type 2 diabetes mellitus with or without COVID-19. We collected data from the first wave of the pandemic in The Fifth Affiliated Hospital of Guangzhou Medical University, Loudi Central Hospital and The First People's Hospital of Xiangtan from December 1, 2022 to February 1, 2023. We extracted baseline data, clinical symptoms, acute complications, laboratory findings, treatment and outcome data of each patient from electronic medical records. Results: For among 298 hospitalized patients with type 2 diabetes, 136 (45.6%) were COVID-19 uninfected, and 162 (54.4%) were COVID-19 infected. We found that the incidence of cough, fatigue, fever, muscle soreness, sore throat, shortness of breath, hyposmia, hypogeusia and polyphagia (all p<0.01) were significantly higher in the exposure group. They showed higher levels of ketone (p=0.04), creatinine (p<0.01), blood potassium (p=0.01) and more diabetic ketoacidosis (p<0.01). Patients with COVID-19 less use of metformin (p<0.01), thiazolidinediones (p<0.01) and SGLT2 (p<0.01) compared with patients without COVID-19. Conclusion: COVID-19 patients with diabetes showed more severe respiratory and constitutional symptoms and an increased proportion of hyposmia and hypogeusia. Moreover, COVID-19 patients with diabetes have a higher incidence of acute complications, are more prone to worsening renal function, and are more cautious about the use of antidiabetic drugs.
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Ageusia , COVID-19 , Diabetes Mellitus Tipo 2 , Humanos , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/epidemiología , Estudios Retrospectivos , Anosmia , COVID-19/complicaciones , COVID-19/epidemiología , China/epidemiologíaRESUMEN
A broken-gap heterojunction is a bright approach for designing tunneling field-effect transistors (TFETs) due to its distinct quantum tunneling mechanisms. In this study, we investigate the electronic structure and transport characteristics of a SiC/Ti2CO2 heterojunction, as well as the impacts of electric field and strain on the electronic properties via density functional theory. We determine that the interfacial atoms of the heterojunction are covalently bonded, forming a type-III heterojunction with a broken-gap. There exists band-to-band tunneling (BTBT) from the valence band (VB) of SiC to the conduction band (CB) of Ti2CO2. The creation of the heterojunction also enhances the carrier mobility arising from the large elastic modulus and the decrease of deformation potential. The current-voltage (I-V) characteristics of the device demonstrate a pronounced negative differential resistance (NDR) effect, along with a current that is about ten times greater than that of the vdW type-III heterojunction. Moreover, the tunneling window of SiC/Ti2CO2 is only slightly altered when subjected to an external electric field and vertical strain, demonstrating the remarkable stability of its type-III band alignments. Our results indicate that the SiC/Ti2CO2 heterojunction is useful to construct high-performance TFETs, and also introduces new ideas to design TFETs by using type-III covalent-bond heterojunctions.
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OBJECTIVES: Epidemiological studies have confirmed that low birth weight (BW) is related to neuroticism and they may have a common genetic mechanism based on phenotypic correlation research. We conducted our study on a European population with 159,208 neuroticism and 289,142 birth weight samples. In this study, we aimed to identify new neuroticism single nucleotide polymorphisms (SNPs) and pleiotropic SNPs associated with neuroticism and BW and to provide more theoretical basis for the pathogenesis of the disease. METHODS: We estimated the pleiotropic enrichment between neuroticism and BW in two independent Genome-wide association studies (GWAS) when the statistical thresholds were Conditional False Discovery Rate (cFDR) < 0.01 and Conjunctional Conditional False Discovery Rate (ccFDR) < 0.05. We performed gene annotation and gene functional analysis on the selected significant SNPs to determine the biological role of gene function and pathogenesis. Two-sample Mendelian Randomization (TSMR) analysis was performed to explore the causal relationship between the neuroticism and BW. RESULTS: The conditional quantile-quantile plots (Q-Q plot) indicated that neuroticism and BW have strong genetic pleiotropy enrichment trends. With the threshold of cFDR < 0.001, we identified 126 SNPs related to neuroticism and 172 SNPs related to BW. With the threshold of ccFDR < 0.05, we identified 62 SNPs related to both neuroticism and BW. Among these SNPs, rs8039305 and rs35755513 have eQTL (expressed quantitative trait loci) and meQTL (methylation quantitative trait loci) effects simultaneously. Through GO enrichment analysis we also found that the two pathways of positive regulation of "mesenchymal cell proliferation" and "DNA-binding transcription factor activity" were significantly enriched in neuroticism and BW. Mendelian randomization analysis results indicate that there is no obvious causal relationship between neuroticism and birth weight. CONCLUSION: We found 126 SNPs related to neuroticism, 172 SNPs related to BW and 62 SNPs associated with both neuroticism and BW, which provided a theoretical basis for their genetic mechanism and novel potential targets for treatment/intervention development.
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Estudio de Asociación del Genoma Completo , Polimorfismo de Nucleótido Simple , Humanos , Estudio de Asociación del Genoma Completo/métodos , Neuroticismo , Peso al Nacer/genética , Predisposición Genética a la EnfermedadRESUMEN
OBJECTIVE: In this study we aimed to predict the risk factors related to histopathologic upgrade after endoscopic submucosal dissection (ESD) in patients with pre-ESD esophageal squamous low-grade intraepithelial neoplasm (LGIN). METHODS: A training cohort of 201 patients with biopsy-confirmed esophageal squamous LGIN and underwent ESD at a tertiary medical center between January 2017 and July 2019 were included. Risk factors for histological upgrade were identified using the least absolute shrinkage and selection operator (LASSO) regression. A nomogram was then established. Internal validation was evaluated by discrimination, calibration plot, and decision-curve analysis. Another cohort of 48 patients were prospectively collected from July 2019 to June 2021 for external validation of the nomogram. RESULTS: The rate of histological upgrade was 34.8% (70/201) and 27.1% (13/48) in the training and validation sets, respectively. LASSO regression identified that tumor area (mm2 ) per biopsy, Lugol's staining pattern, background coloration, and the circumferential range of the lesion were significantly associated with histological upgrade. The final nomogram attained favorable prediction efficacy in the training cohort (area under the receiver operating curve [AUROC] 0.96, 95% confidence interval [CI] 0.94-0.98) and validation cohort (AUROC 0.92, 95% CI 0.79 -0.99). This model generated well-fitted calibration and clinical-decision curves in both cohorts. CONCLUSIONS: The nomogram may better guide clinical decision on whether performing EDS or follow-up for suspicious lesions in patients with biopsy-confirmed esophageal squamous LGIN.
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Carcinoma in Situ , Carcinoma de Células Escamosas , Resección Endoscópica de la Mucosa , Neoplasias Esofágicas , Carcinoma in Situ/patología , Carcinoma de Células Escamosas/cirugía , Neoplasias Esofágicas/patología , Neoplasias Esofágicas/cirugía , Humanos , Nomogramas , Estudios RetrospectivosRESUMEN
@#Objective - To optimize the extraction and quantification methods for the determination of S phenylmercapturic acid - Methods (SPMA) in urine with performance liquid chromatography mass spectrometry. The urine was hydrolyzed with 50.0% sulfuric acid. The hydrolysate was purified by solid phase extraction column. Purified samples were separated by C18 chromatographic column and detected by tandem mass spectrometry. The isotope labeled SPMA was used as the internal Results - standard. The internal standard curve was used for quantification. The linear range of SPMA was 0.50 50.00 μg/L with the correlation coefficient of 0.999 8. The detection limit and the lower limit of quantification were 0.05 and 0.17 μg/L, - - - - respectively. The recovery rate was 97.0% 102.0%. The within run and between run relative standard deviation were 0.6% 1.0% - and 1.7% 6.5%, respectively. The mass concentration of urinary SPMA in the occupational benzene exposure group was - vs P higher than the non occupational benzene exposure group by this method (median: 2.81 0.28 μg/g creatinine, <0.05). Conclusion Compared to the national standard method, this optimized method of solid phase extraction and internal standard for quantification eliminates the matrix effect. This method is accurate and precise, and is suitable for the determination of SPMA acid in urine.
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How to correctly and scientifically dispose of medicine residue on the basis of protecting the environment is an urgent problem to be solved due to the continuous generation of a large amount of waste medicine residue. In this paper, the application of waste medicine residue (large volume produced each year) as a precursor in producing a biochar that could adsorb Pb ion was reported. Biochar is a stable, aromatic, porous substance that is rich in carbon and prepared through pyrolysis of waste biomass under anaerobic conditions. In this study, medicine residue was used as raw material, and high-temperature sintering furnace was used to prepare medicine slag biochar at different temperatures of 200°C, 300°C, 400°C, 500°C, and 600°C. The resulting biochar was characterized by elemental analysis, Fourier transform infrared spectroscopy (FTIR), specific surface area analysis, field emission-scanning electron microscopy (FE-SEM), X-ray diffraction (XRD), and Raman spectroscopy (RS). Experimental results showed that with the increase in pyrolysis temperature, the biochar structure was destroyed. The yield decreased as the temperature gradually decreased from 81.69% to 33.90%. With the increase in temperature, the pH, the ash, and the fixed carbon gradually increased, whereas the number of surface functional groups decreased. The quasi second order kinetic equation can better fit the kinetic characteristics of adsorbing Pb ion by biochar. In general, this study provides a valuable method for recycling medicine residue.
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Plomo , Pirólisis , Adsorción , Carbón Orgánico , TemperaturaRESUMEN
PURPOSE: Epilepsy affects more than 50 million people worldwide and its management can be complicated by comorbidities such as impaired renal function. To optimize epilepsy control in patients with kidney disease, clinicians need to be aware of how antiepileptic drugs (AEDs) are affected by impaired renal function and how the kidneys are affected by epilepsy management strategies. Herein we present a narrative review with systematic literature search to discuss the use of AEDs in patients with renal impairment, including those undergoing dialysis, as well as the nephrotoxic effects of some AEDs. We finally conclude the article by providing practical tips about our approach to using AEDs in the setting of renal disease. METHODS: A literature search targeting epilepsy management in patients with kidney disease was performed in MEDLINE database (1946 to 7th Jan 2019). RESULTS: A total of 1193 articles were found. After duplicate removal, title and abstract screening followed by full text screening, a total of 110 references were included in this review. Additional information was included from drug product monographs. CONCLUSION: The disposition of AEDs can be altered in patients with impaired renal function, leading to a higher risk of AED toxicity or therapy failure. Renal dosage adjustment and close monitoring is recommended. Although AED-induced nephrotoxicity is rare, it is unpredictable and clinicians need to vigilant about this possibility. In addition, AEDs renal adverse reactions and renal drug interactions should be considered when selecting an AED.
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Ellipticine, a natural product from Ochrosia elliptica, has been broadly investigated for its anticancer effects. Although inflammation has been clearly identified as a key factor in the onset and progression of cancer, the relationship between ellipticine and inflammation remains unknown. Hence, the aims of the present study were to assess the effects of ellipticine on the inflammatory responses to lipopolysaccharide (LPS)-induced macrophages and to potentially identify the underlying mechanisms involved. Viability testing showed that ellipticine was not significantly toxic to Raw264.7 cells and actually conveyed protective effects to LPS-stimulated Raw264.7 cells and human peripheral blood monocytes by decreasing the secretion of inflammatory factors (TNF-α and IL-6). The results of western blot analysis and electrophoretic mobility shift assays showed that ellipticine markedly suppressed LPS-induced activation of the JNK/AP-1 (c-Fos and c-Jun) signaling pathway, but not ERK/p38/NF-κB pathway (p65 and p50) activation. Furthermore, ellipticine reduced the inflammatory response and mortality in a mouse model of LPS-induced endotoxic shock. Collectively, these data indicate that ellipticine may be a potential therapeutic agent for the treatment of inflammation-associated diseases.
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Antiinflamatorios/farmacología , Elipticinas/farmacología , Inflamación/prevención & control , Proteínas Quinasas JNK Activadas por Mitógenos/metabolismo , Activación de Macrófagos/efectos de los fármacos , Macrófagos/efectos de los fármacos , Choque Séptico/prevención & control , Factor de Transcripción AP-1/metabolismo , Adulto , Animales , Proliferación Celular/efectos de los fármacos , Modelos Animales de Enfermedad , Humanos , Inflamación/inducido químicamente , Inflamación/enzimología , Inflamación/inmunología , Interleucina-6/metabolismo , Lipopolisacáridos , Macrófagos/enzimología , Macrófagos/inmunología , Masculino , Ratones , Ratones Endogámicos C57BL , Células RAW 264.7 , Choque Séptico/inducido químicamente , Choque Séptico/enzimología , Choque Séptico/inmunología , Transducción de Señal , Factor de Necrosis Tumoral alfa/metabolismoRESUMEN
The gut microbiota is an important contributor to host health and fitness. Given its importance, microbiota composition should not be left to chance. However, what determines this composition is far from clear, with results supporting contributions of both environmental factors and host genetics. To gauge the relative contributions of host genetics and environment, specifically the microbial diversity, we characterized the gut microbiotas of Caenorhabditis species spanning 200-300 million years of evolution, and raised on different composted soil environments. Comparisons were based on 16S rDNA deep sequencing data, as well as on functional evaluation of gut isolates. Worm microbiotas were distinct from those in their respective soil environment, and included bacteria previously identified as part of the C. elegans core microbiota. Microbiotas differed between experiments initiated with different soil communities, but within each experiment, worm microbiotas clustered according to host identity, demonstrating a dominant contribution of environmental diversity, but also a significant contribution of host genetics. The dominance of environmental contributions hindered identification of host-associated microbial taxa from 16S data. Characterization of gut isolates from C. elegans and C. briggsae, focusing on the core family Enterobacteriaceae, were also unable to expose phylogenetic distinctions between microbiotas of the two species. However, functional evaluation of the isolates revealed host-specific contributions, wherein gut commensals protected their own host from infection, but not a non-host. Identification of commensal host-specificity at the functional level, otherwise overlooked in standard sequence-based analyses, suggests that the contribution of host genetics to shaping of gut microbiotas may be greater than previously realized.
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Background Alcohol intake has been suggested to have an impact on the development of many chronic diseases. How alcohol intake may modulate risk of Helicobacter pylori (H. pylori) infection, however, remains a subject open for investigation. A dose-response meta-analysis was performed of epidemiological studies to better quantify this relationship. Materials and methods Twelve observational articles were identified. The summary odds ratio (OR) and confidence intervals (CI) were calculated for alcohol drinkers vs non-drinkers. The summary OR estimates were obtained using the random-effects model and dose-response meta-analysis. Sub-group and sensitivity analysis were also conducted. Results The summary OR was 0.78 (95% CI = 0.69-0.89). The dose-response analysis demonstrated that for drinkers of 10, 15, 30, 60 and 96 g/day alcohol intake, the estimated ORs were 0.80 (95% CI = 0.76-0.85), 0.79 (95% CI = 0.75-0.84), 0.83 (95% CI = 0.78-0.87), 0.85 (95% CI = 0.78-0.93) and 0.87 (95% CI = 0.70-1.06), respectively, compared to non-drinkers. The inverse relationship between alcohol intake and H. pylori infection was consistent, regardless of sex, age, geographic areas, detection methods or beverage types. CONCLUSION: Evidence from these observational studies suggests that moderate alcohol intake is associated with a reduction in H. pylori infection of â¼ 22% and may facilitate elimination of H. pylori.
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Consumo de Bebidas Alcohólicas/epidemiología , Infecciones por Helicobacter/epidemiología , Helicobacter pylori/aislamiento & purificación , Relación Dosis-Respuesta a Droga , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Observacionales como Asunto , Oportunidad Relativa , Factores de RiesgoRESUMEN
CD64 was up-regulated in infection diseases, but there was no report about the change of CD64 in chronic hepatitis B virus (HBV) infection. The purpose of this study was to determine whether there was a dynamic change of CD 64 index and to judge the value to antiviral treatment. 96 CHB patients were enrolled and selected 33 healthy adults as control. We detected the level of CD64, found the level of CD64 were significantly increased in chronic HBV infection patients, especially the lymphocyte CD64 (8.12 ± 0.23 vs. 6.25 ± 0.27; P < 0.001). Further, we proved CD64 index was increased in various stages of chronic HBV infection. ROC curve analysis showed the level of lymphocyte CD64 had higher AUC value than neutrophil or monocyte. Then we monitor longitudinally the impact of the treatment with interferon-α and found that the suppression of viral replication induced by interferon-α resulted in a decrease in CD64 index. In conclusion, this study showed that CD64 index was increased in chronic HBV infection patients and changed with the course of disease, the therapy of interferon-α would correct it, and analysis prompted that the level of lymphocyte CD64 would be more suitable for as a biomarker to judge the condition of chronic HBV infection and the curative effect of interferon-α treatment.
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Chronic hepatitis B (CHB) is a worldwide infectious disease caused by hepatitis B virus (HBV). HBV mainly damages liver cells through immune response. The purpose of this study was to determine whether there were dynamic changes of Treg and Th17 cells and to judge the value of these indicators to antiviral treatment. Twenty-two CHB patients and selected 30 healthy adults were enrolled. Results showed that the expression of Treg (5.72±0.46 vs. 4.42±0.17, p=0.0019) and Th17 (3.94±0.64 vs. 2.66±3.12, p=0.0436) cells was significantly increased in CHB patients, as well as the level of interleukin-17 (IL-17) (16.88±5.37 vs. 8.59±3.31; p=0.004). Then, we monitored longitudinally the impact of the treatment with interferon-α and found that the suppression of viral replication induced by interferon-α resulted in a decrease in Treg, Th17 cells, and IL-17; we also found that the percentage of Treg and Th17 cells went up without clear evidence of clinical autoimmune disease at the end of treatment. Thus, Treg and Th17 cells might play an important role in interferon-α treatment to eliminate HBV. The level of changes may be served to determine the antiviral efficacy of interferon-α therapy.
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Hepatitis B Crónica/inmunología , Hepatitis B Crónica/terapia , Interferón-alfa/uso terapéutico , Linfocitos T Reguladores/inmunología , Células Th17/inmunología , Adulto , ADN Viral/sangre , Monitoreo de Drogas , Femenino , Citometría de Flujo , Humanos , Interleucina-17/análisis , Estudios Longitudinales , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Resultado del Tratamiento , Carga Viral , Adulto JovenRESUMEN
Hepatitis B is a worldwide infectious disease caused by hepatitis B virus (HBV), it leaded to millions of deaths every year, HBV mainly through immune response to damage liver cells. The purpose of this study was to judge the value of Regulatory T cells (Treg) and IL-17(+) T helper cells (Th17) in different chronic HBV infection stages. 96 patients with chronic HBV infection were enrolled and selected 33 healthy adults as control. Detected the expression of Treg and Th17 cells in peripheral blood by flow cytometry and assayed liver function simultaneously. Compared to the control group, the expression of Treg (6.80±1.92 vs. 4.42±0.97; P<0.0001) and Th17 (6.15±4.20 vs. 2.66±1.79; P<0.0001) cells were both increased and the ratio of Treg/Th17 was significantly decreased (1.48±0.89 vs. 2.29±1.31; P=0.0001) in patients with HBV infection. Spearman correlation analysis demonstrated that the level of Treg and Th17 cells were associated with liver function. ROC curve analysis found that Treg and Th17 cells were suitable for as a screening test for early detection of the disease. In conclusion, the expression of Treg and Th17 cells were increased in chronic hepatitis B patients and these indicators were independent risk factors to hepatitis.
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How to maintain the genetic integrity of cultured human embryonic stem (hES) cells is raising crucial concerns for future clinical use in regenerative medicine. Mitomycin C(MMC), a DNA damage agent, is widely used for preparation of feeder cells in many laboratories. However, to what extent MMC affects the karyotypic stability of hES cells is not clear. Here, we measured residual MMC using High Performance Liquid Chromatography-Mass Spectrometry/Mass Spectrometry following each step of feeder preparation and found that 2.26 ± 0.77 and 3.50 ± 0.92 ng/ml remained in mouse feeder cells and human feeder cells, respectively. In addition, different amounts of MMC caused different chromosomal aberrations in hES cells. In particular, one abnormality, dup(1)(p32p36), was the same identical to one we previously reported in another hES cell line. Using Affymetrix SNP 6.0 arrays, the copy number variation changes of the hES cells maintained on MMC-inactivated feeders (MMC-feeder) were significantly more than those cultured on γ-inactivated feeder (IR-feeder) cells. Furthermore, DNA damage response (DDR) genes were down-regulated during long-term culture in the MMC-containing system, leading to DDR defect and shortened telomeres of hES cells, a sign of genomic instability. Therefore, MMC-feeder and MMC-induced genomic variation present an important safety problem that would limit such hES from being applied for future clinic use and drug screening.
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Técnicas de Cultivo de Célula/métodos , Daño del ADN , Células Madre Embrionarias/efectos de los fármacos , Inestabilidad Genómica , Mitomicina/toxicidad , Apoptosis/efectos de los fármacos , Ciclo Celular/efectos de los fármacos , Células Cultivadas , Cromatografía Líquida de Alta Presión , Células Madre Embrionarias/patología , Humanos , Cariotipificación , Mitomicina/análisis , Reacción en Cadena de la Polimerasa , Espectrometría de Masas en TándemRESUMEN
AIM: To quantify the association between Helicobacter pylori (H. pylori) infection and migraine. METHODS: A systematic literature search of PubMed and EMBASE was conducted from inception to December 2013. Studies that provided data dealing with H. pylori infection in patients with migraine, as well as healthy controls, were selected. Meta-analysis was carried out using the odds ratio (OR) with a fixed or random effects model, and a 95%CI for the OR was calculated. An unconditional logistic regression model was used to analyze potential parameters related to H. pylori prevalence. Subgroup analyses were conducted as methods of detection and evidence grade. RESULTS: Five case-control studies published between 2000 and 2013 were finally identified, involving 903 patients, with a total H. pylori infection rate of 39.31%. The prevalence of H. pylori infection was significantly greater in migraineurs than in controls (44.97% vs 33.26%, OR = 1.92, 95%CI: 1.05-3.51, P = 0.001). A sensitivity test indicated that no single study dominated the combined results. Univariate regression analysis found that publication year, geographical distribution and evidence grade were relevant to the results and were the main reason for the heterogeneity. Subgroup analysis found a significantly greater infection rate of H. pylori in Asian patients with migraine, but no statistically significant infection rate in European patients. The ORs were 3.48 (95%CI: 2.09-5.81, P = 0.000) and 1.19 (95%CI: 0.86-1.65, P = 0.288), respectively. CONCLUSION: The pooled data suggest a trend of more frequent H. pylori infections in patients with migraine.
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Infecciones por Helicobacter/epidemiología , Helicobacter pylori/aislamiento & purificación , Trastornos Migrañosos/epidemiología , Pueblo Asiatico , Infecciones por Helicobacter/diagnóstico , Infecciones por Helicobacter/microbiología , Humanos , Modelos Logísticos , Trastornos Migrañosos/diagnóstico , Trastornos Migrañosos/microbiología , Oportunidad Relativa , Prevalencia , Medición de Riesgo , Factores de Riesgo , Población BlancaRESUMEN
BACKGROUND: Helicobacter pylori infection is reportedly associated with extradigestive diseases such as immune thrombocytopenic purpura and coronary heart disease. The risk factors for autoimmune thyroid diseases (ATDs) remain largely unknown, and whether H. pylori infection is associated with ATDs is still controversial. The aim of this meta-analysis was to determine the association between H. pylori infection and ATDs. METHODS: Studies comparing the prevalence rate of H. pylori infection in patients with ATDs and healthy controls, published in English, were identified through a systematic search in MEDLINE and EMBAS up to June 2012. Serological or nonserological tests were used to confirm H. pylori infection and the presence of cytotoxin-associated gene A (CagA) antigens. The odds ratios (OR) and associated 95% confidence intervals [CI] were obtained. RESULTS: Seven studies involving a total of 862 patients met the inclusion criteria and thus were included in our meta-analysis. Overall, H. pylori infection was associated with ATDs (OR 1.92 [CI 1.41-2.61]); the association was significant for Graves' disease (OR 4.35 [CI 2.48-7.64]) but not for Hashimoto's thyroiditis (OR 1.45 [CI 0.92-2.26], p=0.11). No association was observed in the subanalysis of studies using only enzyme-linked immunosorbent assay to detect H. pylori infection (OR 1.38 [CI 0.86-2.19], p=0.18). Five of the seven articles reported the association of CagA seroprevalence and ATDs. CagA seropositivity significantly increased the risk for ATDs by 2.24-fold [CI 1.06-4.75]. CONCLUSIONS: Both the prevalence of H. pylori infection and the seroprevalence of CagA-positive strains are associated with ATDs. These findings suggest that H. pylori infection potentially plays a part in the development of ATDs.
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Antígenos Bacterianos/sangre , Autoinmunidad , Proteínas Bacterianas/sangre , Medicina Basada en la Evidencia , Enfermedad de Graves/etiología , Infecciones por Helicobacter/fisiopatología , Helicobacter pylori/inmunología , Tiroiditis Autoinmune/etiología , Antígenos Bacterianos/genética , Antígenos Bacterianos/metabolismo , Proteínas Bacterianas/genética , Proteínas Bacterianas/metabolismo , Biomarcadores/sangre , Comorbilidad , Enfermedad de Graves/epidemiología , Enfermedad de Graves/inmunología , Enfermedad de Graves/microbiología , Enfermedad de Hashimoto/epidemiología , Enfermedad de Hashimoto/etiología , Enfermedad de Hashimoto/inmunología , Enfermedad de Hashimoto/microbiología , Infecciones por Helicobacter/epidemiología , Infecciones por Helicobacter/inmunología , Infecciones por Helicobacter/microbiología , Helicobacter pylori/aislamiento & purificación , Helicobacter pylori/metabolismo , Humanos , Prevalencia , Factores de Riesgo , Tiroiditis Autoinmune/sangre , Tiroiditis Autoinmune/epidemiología , Tiroiditis Autoinmune/inmunologíaRESUMEN
Melanized appressoria are highly specialized infection structures formed by germ tubes of the rice blast fungus Magnaporthe oryzae for plant infection. M. oryzae also forms appressorium-like structures on hyphal tips. Whereas appressorium formation by conidial germ tubes has been well characterized, formation of appressorium-like structures by hyphal tips is under-investigated. In a previous study, we found that the chs7 deletion mutant failed to form appressoria on germ tubes but were normal in the development of appressorium-like structures on artificial hydrophobic surfaces. In this study, we compared the differences between the formation of appressoria by germ tubes and appressorium-like structures by hyphal tips in M. oryzae. Structurally, both appressoria and appressorium-like structures had a melanin layer that was absent in the pore region. In general, the latters were 1.4-fold larger in size but had lower turgor pressure than appressoria, which is consistent with its lower efficiency in plant penetration. Treatments with cAMP, IBMX, or a cutin monomer efficiently induced appressorium formation but not the development of appressorium-like structures. In contrast, coating surfaces with waxes stimulated the formation of both infection structures. Studies with various signaling mutants indicate that Osm1 and Mps1 are dispensable but Pmk1 is essential for both appressorium formation and development of appressorium-like structures on hyphal tips. Interestingly, the cpkA mutant was reduced in the differentiation of appressorium-like structures but not appressorium formation. We also observed that the con7 mutant generated in our lab failed to form appressorium-like structures on hyphal tips but still produced appressoria by germ tubes on hydrophobic surfaces. Con7 is a transcription factor regulating the expression of CHS7. Overall, these results indicate that the development of appressorium-like structures by hyphal tips and formation of appressoria by germ tubes are not identical differentiation processes in M. oryzae and may involve different molecular mechanisms.