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Formation of the vascular cylinder, a structure critical to water and nutrient transport in higher plants, is highly regulated. Here we identify WRKY15 as an important regulator that suppresses tracheary element (TE) differentiation in Arabidopsis (Arabidopsis thaliana). Overexpression of WRKY15 resulted in discontinuous protoxylem vessel files and TEs with reduced spiral wall thickening/lignification. Expression of a dominant-negative WRKY15 variant, WRKY15-EAR, led to extra protoxylem vessels and ectopic TEs with increased spiral wall thickening/lignification. Ectopic TE formation in the root cortex and hypocotyl/leaf epidermis reveals that the suppression of WRKY15 is sufficient to trigger the transdifferentiation of other types of cells to TEs. Expression profiling, RT-qPCR, and reporter analyses revealed that WRKY15 suppresses the expression of VASCULAR-RELATED NAC DOMAIN7 (VND7), a master transcriptional regulator that promotes TE differentiation. We propose that WRKY15 negatively regulates VND7 expression indirectly based on (1) the absence of a W-box in the promoter of VND7 and (2) the observation that WRKY15 and VND7 are expressed in different cells in the vascular cylinder, with WRKY15 expressed in the procambial cells and VND7 in the protoxylem poles of procambium and differentiating TEs. Future research is needed to reveal the details underlying the interaction of WRKY15 and VND7 in plant vascular development.
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Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Arabidopsis/fisiología , Factores de Transcripción/genética , Factores de Transcripción/metabolismo , Xilema/crecimiento & desarrollo , Arabidopsis/citología , Diferenciación Celular , Pared Celular/genética , Pared Celular/metabolismo , Regulación de la Expresión Génica de las Plantas , Células Vegetales , Raíces de Plantas/citología , Raíces de Plantas/genética , Raíces de Plantas/crecimiento & desarrollo , Plantas Modificadas Genéticamente , Xilema/fisiologíaRESUMEN
We aimed to analyze the efficacy and safety of an inactivated SARS-CoV-2 vaccine in people living with HIV (PLWH). A total of 143 PLWH and 50 healthy individuals were included in this study. A commercially available magnetic chemiluminescence enzyme immunoassay kit was used to detect serum IgG and IgM antibodies against SARS-CoV-2. Serum levels of SARS-CoV-2-specific IgG were significantly higher in the control group than in the PLWH group (p = 0.001). Overall, 76% of individuals in the control group were detected with seropositivity IgG against SARS-CoV-2 compared to 58% in the PLWH group (p = 0.024). In PLWH with IgG seropositivity, CD4+ T-cell counts before antiretroviral therapy (ART) was higher (p = 0.015). Multivariable analysis indicated that CD4+ T cells at IgG detection (odds ratio [OR] = 1.004, p = 0.006) and time after vaccination (OR = 0.977, p = 0.014) were independently associated with seropositivity IgG against SARS-CoV-2 in PLWH. Neutralizing antibody (nAb) titers in PLWH against wild-type SARS-CoV-2 were similar to those in the control group (p = 0.160). The proportion of seropositive nAbs against wild-type SARS-CoV-2 was also similar (95% in the control group vs. 97% in the PLWH group, p = 0.665). Similar results were obtained when nAb was detected against the delta variants with similar titers (p = 0.355) and a similar proportion of seropositive nAbs were observed (p = 0.588). All the side effects observed in our study were mild and self-limiting. The inactivated COVID-19 vaccine appears to be safe with good immunogenicity in Chinese PLWH.
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COVID-19 , Vacunas Virales , Anticuerpos Neutralizantes , Anticuerpos Antivirales , COVID-19/prevención & control , Vacunas contra la COVID-19/efectos adversos , Estudios Transversales , Humanos , Inmunogenicidad Vacunal , Inmunoglobulina G , SARS-CoV-2RESUMEN
Plant growth and development rely on sugar transport between source and sink cells and between different organelles. The plastid-localized sugar transporter GLUCOSE-6-PHOSPHATE TRANSLOCATER1 (GPT1) is an essential gene in Arabidopsis (Arabidopsis thaliana). Using a partially rescued gpt1 mutant and cell-specific RNAi suppression of GPT1, we demonstrated that GPT1 is essential to the function of the embryo suspensor and the development of the embryo. GPT1 showed a dynamic expression/accumulation pattern during embryogenesis. Inhibition of GPT1 accumulation via RNAi using a suspensor-specific promoter resulted in embryos and seedlings with defects similar to auxin mutants. Loss of function of GPT1 in the suspensor also led to abnormal/ectopic cell division in the lower part of the suspensor, which gave rise to an ectopic embryo, resulting in twin embryos in some seeds. Furthermore, loss of function of GPT1 resulted in vacuolar localization of PIN-FORMED1 (PIN1) and altered DR5 auxin activity. Proper localization of PIN1 on the plasma membrane is essential to polar auxin transport and distribution, a key determinant of pattern formation during embryogenesis. Our findings suggest that the function of GPT1 in the embryo suspensor is linked to sugar and/or hormone distribution between the embryo proper and the maternal tissues, and is important for maintenance of suspensor identity and function during embryogenesis.
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Antiportadores/metabolismo , Proteínas de Arabidopsis/metabolismo , Arabidopsis/metabolismo , Proteínas de Transporte de Membrana/metabolismo , Proteínas de Transporte de Monosacáridos/metabolismo , Semillas/metabolismo , Antiportadores/genética , Arabidopsis/genética , Proteínas de Arabidopsis/genética , Regulación de la Expresión Génica de las Plantas , Proteínas de Transporte de Membrana/genética , Proteínas de Transporte de Monosacáridos/genética , Semillas/genéticaRESUMEN
BACKGROUND: To investigate the association between hypertension and clinical outcomes, including in-hospital mortality, intensive care unit (ICU) admission, and invasive ventilation in patients with coronavirus disease 2019 (COVID-19) pneumonia. METHODS: We implemented a systematic search of PubMed for articles that assessed clinical outcomes of hypertensive patients infected with SARS-CoV-2. The primary outcomes evaluated included: in-hospital mortality, ICU admission, and the use of invasive ventilation. RESULTS: A total of 18 studies were included, involving 13,293 patients and covering from January 25, 2020, to April 20, 2020. The relationship between hypertension and prognosis in COVID-19 patients was evaluated. Results showed that hypertension was a risk factor for in-hospital mortality in COVID-19 patients (RR: 2.20, 95% CI, 1.83-2.65, P < .001). Moreover, patients with hypertension were more likely to be admitted to ICU (RR: 1.86, 95% CI, 1.13-3.07, P = .001) and to use invasive ventilation (RR: 2.99, 95% CI, 1.73-5.17, P < .001). CONCLUSIONS: Among COVID-19 patients, those combined with hypertension had a significantly higher risk of in-hospital deaths, admission to ICU, and need for invasive ventilation.
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COVID-19 , Hipertensión , COVID-19/complicaciones , Humanos , Hipertensión/complicaciones , Unidades de Cuidados Intensivos , Pronóstico , SARS-CoV-2RESUMEN
BACKGROUND: Acute liver failure (ALF) is a syndrome of severe hepatocyte injury with high rate of mortality. Hepatitis B virus (HBV) infection is the major cause of ALF worldwide, however, the underlying mechanism by which HBV infection leads to ALF has not been fully disclosed. METHODS: D-GalN-induced hepatocyte injury model and LPS/D-GalN-induced ALF mice model were used to investigate the effects of HBV X protein (HBx) in vitro and in vivo, respectively. Cell viability and the levels of Glutathione (GSH), malondialdehyde (MDA) and iron were measured using commercial kits. The expression of ferroptosis-related molecules were detected by qRT-PCR and western blotting. Epigenetic modification and protein interaction were detected by chromatin immunoprecipitation (ChIP) assay and co-immunoprecipitation (co-IP), respectively. Mouse liver function was assessed by measuring aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The histological changes in liver tissues were monitored by hematoxylin and eosin (H&E) staining, and SLC7A11 immunoreactivity was assessed by immunohistochemistry (IHC) analysis. RESULTS: D-GalN triggered ferroptosis in primary hepatocytes. HBx potentiated D-GalN-induced hepatotoxicity and ferroptosis in vitro, and it suppressed SLC7A11 expression through H3K27me3 modification by EZH2. In addition, EZH2 inhibition or SLC7A11 overexpression attenuated the effects of HBx on D-GalN-induced ferroptosis in primary hepatocytes. The ferroptosis inhibitor ferrostatin-1 (Fer-1) protected against ALF and ferroptosis in vivo. By contrast, HBx exacerbates LPS/D-GalN-induced ALF and ferroptosis in HBx transgenic (HBx-Tg) mice. CONCLUSION: HBx facilitates ferroptosis in ALF via EZH2/H3K27me3-mediated SLC7A11 suppression.
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Ferroptosis/fisiología , Fallo Hepático Agudo/virología , Transactivadores/genética , Proteínas Reguladoras y Accesorias Virales/genética , Sistema de Transporte de Aminoácidos y+/metabolismo , Animales , Proteína Potenciadora del Homólogo Zeste 2/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BLRESUMEN
Hepatocellular carcinoma (HCC) is the most prevalent primary liver cancer in adults. Previous studies in our laboratory found that long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was upregulated in HCC cells, which could affect the metastasis and invasion of HCC. However, the underlying mechanism remains unknown. Herein, we studied the interaction between MALAT1 and miR-140 on the regulation of angiogenesis and immunosuppressive properties. We revealed that the expression of MALAT1 and VEGF-A was significantly increased in HCC cells. Knockdown of MALAT1 in HCC cells suppressed the production of VEGF-A, impaired the angiogenesis of HUVECs, and facilitated the polarization of macrophage toward the M1 subset. Mechanistically, the interaction between MALAT1 and miR-140 or between miR-140 and VEGF-A was confirmed by multiple assays. Besides, a negative correlation between MALAT1 and miR-140 was found in HCC tissues. Furthermore, miR-140 inhibition significantly increased VEGF-A expression, promoted angiogenesis of HUVECs, and redirected the polarization of macrophages toward the M2 subset. In addition, in vivo studies also verified the regulatory network of the MALAT1/miR-140 axis on VEGF-A in HCC progression. In summary, this study revealed the mechanism that MALAT1 worked as a putative HCC promotor via inhibiting miR-140. Therefore, targeting MALAT1 or miR-140 might alleviate the progression of HCC in the future.
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Carcinoma Hepatocelular/metabolismo , Tolerancia Inmunológica/fisiología , Neoplasias Hepáticas/metabolismo , MicroARNs/biosíntesis , Neovascularización Patológica/metabolismo , ARN Largo no Codificante/biosíntesis , Animales , Carcinoma Hepatocelular/inmunología , Femenino , Técnicas de Silenciamiento del Gen/métodos , Células Hep G2 , Células Endoteliales de la Vena Umbilical Humana/metabolismo , Humanos , Neoplasias Hepáticas/inmunología , Ratones , Ratones Desnudos , MicroARNs/antagonistas & inhibidores , MicroARNs/inmunología , Neovascularización Patológica/inmunología , ARN Largo no Codificante/inmunología , Ensayos Antitumor por Modelo de Xenoinjerto/métodosRESUMEN
Platelets are critical regulators of liver regeneration, but the mechanisms are still not fully understood. Platelets have been shown to contain a wide variety of microRNAs (miRNAs) and play an important role in many diseases. However, the mechanism that how the platelet microparticles (PMPs)-derived miRNA regulate the hepatocyte proliferation is not very clear. In this study, we have successfully isolated and identified PMPs. We also found that PMPs, which could be well integrated into the HHL-5 cells, could upregulate the level of miR-25-3p in HHL-5 cells. Meanwhile, we found that PMPs-derived miR-25-3p promoted HHL-5 cells proliferation by accelerating cells into the S phase, and enhanced the autophagy by increasing the LC3II expression and reducing the P62 expression. Then, we proved that the miR-25-3p could target the B-cell translocation gene 2 (BTG2) and downregulate the expression levels of the BTG2 gene in HHL-5 cells. In addition, the overexpression of BTG2 significantly inhibited the proliferation and autophagy abilities of HHL-5 cells, while cotransfected miR-25-3p mimics or PMPs could partially rescue HHL-5 cells proliferation and autophagy. Furthermore, we proved that PMPs accelerated hepatocyte proliferation by regulating autophagy pathways. Therefore, PMPs-derived miR-25-3p promoted HHL-5 cell proliferation and autophagy by targeting BTG2, which may be a new therapeutic method for liver regeneration.
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Gamma-aminobutyric acid (GABA) is an important metabolite which functions in plant growth, development, and stress responses. However, its role in plant defense and how it is regulated are largely unknown. Here, we report a detailed analysis of GABA induction during the resistance response to Pseudomonas syringae in Arabidopsis thaliana. While searching for the mechanism underlying the pathogen-responsive mitogen-activated protein kinase (MPK)3/MPK6 signaling cascade in plant immunity, we found that activation of MPK3/MPK6 greatly induced GABA biosynthesis, which is dependent on the glutamate decarboxylase genes GAD1 and GAD4. Inoculation with Pseudomonas syringae pv tomato DC3000 (Pst) and Pst-avrRpt2 expressing the avrRpt2 effector gene induced GAD1 and GAD4 gene expression and increased the levels of GABA. Genetic evidence revealed that GAD1, GAD2, and GAD4 play important roles in both GABA biosynthesis and plant resistance in response to Pst-avrRpt2 infection. The gad1/2/4 triple and gad1/2/4/5 quadruple mutants, in which the GABA levels were extremely low, were more susceptible to both Pst and Pst-avrRpt2. Functional loss of MPK3/MPK6, or their upstream MKK4/MKK5, or their downstream substrate WRKY33 suppressed the induction of GAD1 and GAD4 expression after Pst-avrRpt2 treatment. Our findings shed light on both the regulation and role of GABA in the plant immunity to a bacterial pathogen.
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Proteínas de Arabidopsis/metabolismo , Arabidopsis/metabolismo , Arabidopsis/microbiología , Pseudomonas syringae/patogenicidad , Ácido gamma-Aminobutírico/metabolismo , Arabidopsis/inmunología , Proteínas de Arabidopsis/genética , Regulación de la Expresión Génica de las Plantas/genética , Regulación de la Expresión Génica de las Plantas/fisiología , Enfermedades de las Plantas/microbiología , Inmunidad de la Planta/genética , Inmunidad de la Planta/fisiología , Plantas Modificadas Genéticamente/inmunología , Plantas Modificadas Genéticamente/metabolismo , Plantas Modificadas Genéticamente/microbiología , Transducción de Señal/genética , Transducción de Señal/fisiologíaRESUMEN
Secondary plant metabolites, represented by indole glucosinolates (IGS) and camalexin, play important roles in Arabidopsis immunity. Previously, we demonstrated the importance of MPK3 and MPK6, two closely related MAPKs, in regulating Botrytis cinerea (Bc)-induced IGS and camalexin biosynthesis. Here we report that CPK5 and CPK6, two redundant calcium-dependent protein kinases (CPKs), are also involved in regulating the biosynthesis of these secondary metabolites. The loss-of-function of both CPK5 and CPK6 compromises plant resistance to Bc. Expression profiling of CPK5-VK transgenic plants, in which a truncated constitutively active CPK5 is driven by a steroid-inducible promoter, revealed that biosynthetic genes of both IGS and camalexin pathways are coordinately upregulated after the induction of CPK5-VK, leading to high-level accumulation of camalexin and 4-methoxyindole-3-yl-methylglucosinolate (4MI3G). Induction of camalexin and 4MI3G, as well as the genes in their biosynthesis pathways, is greatly compromised in cpk5 cpk6 mutant in response to Bc. In a conditional cpk5 cpk6 mpk3 mpk6 quadruple mutant, Bc resistance and induction of IGS and camalexin are further reduced in comparison to either cpk5 cpk6 or conditional mpk3 mpk6 double mutant, suggesting that both CPK5/CPK6 and MPK3/MPK6 signaling pathways contribute to promote the biosynthesis of 4MI3G and camalexin in defense against Bc.
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Glucosinolatos/metabolismo , Indoles/metabolismo , Tiazoles/metabolismo , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Botrytis/patogenicidad , Regulación de la Expresión Génica de las Plantas/fisiología , Quinasas de Proteína Quinasa Activadas por Mitógenos/genética , Quinasas de Proteína Quinasa Activadas por Mitógenos/metabolismo , Proteínas Quinasas Activadas por Mitógenos/genética , Proteínas Quinasas Activadas por Mitógenos/metabolismo , Inmunidad de la Planta/fisiología , Transducción de Señal/fisiologíaRESUMEN
Increasing evidence supports the significance of long non-coding RNA in cancer development. Several recent studies suggest the oncogenic activity of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in hepatocellular carcinoma. In this study, we explored the molecular mechanisms by which MALAT1 modulates hepatocellular carcinoma biological behaviors. We found that microRNA-204 was significantly downregulated in sh-MALAT1 HepG2 cell and 15 hepatocellular carcinoma tissues by quantitative real-time polymerase chain reaction analysis. Through bioinformatic screening, luciferase reporter assay, RNA-binding protein immunoprecipitation, and RNA pull-down assay, we identified microRNA-204 as a potential interacting partner for MALAT1. Functionally, wound-healing and transwell assays revealed that microRNA-204 significantly inhibited the migration and invasion of hepatocellular carcinoma cells. Notably, sirtuin 1 was recognized as a direct downstream target of microRNA-204 in HepG2 cells. Moreover, si-SIRT1 significantly inhibited cell invasion and migration process. These data elucidated, by sponging and competitive binding to microRNA-204, MALAT1 releases the suppression on sirtuin 1, which in turn promotes hepatocellular carcinoma migration and invasion. This study reveals a novel mechanism by which MALAT1 stimulates hepatocellular carcinoma progression and justifies targeting metastasis-associated lung adenocarcinoma transcript 1 as a potential therapy for hepatocellular carcinoma.
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Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , MicroARNs/genética , ARN Largo no Codificante/genética , Sirtuina 1/genética , Apoptosis/genética , Carcinoma Hepatocelular/patología , Movimiento Celular/genética , Proliferación Celular/genética , Progresión de la Enfermedad , Femenino , Regulación Neoplásica de la Expresión Génica , Células Hep G2 , Humanos , Neoplasias Hepáticas/patología , Masculino , Invasividad Neoplásica/genética , Sirtuina 1/biosíntesisRESUMEN
Stand diversification is considered a promising management approach to increasing the multifunctionality and ecological stability of forests. However, how tree diversity affects higher trophic levels and their role in regulating forest functioning is not well explored particularly for (sub)tropical regions. We analyzed the effects of tree species richness, community composition, and functional diversity on the abundance, species richness, and beta diversity of important functional groups of herbivores and predators in a large-scale forest biodiversity experiment in south-east China. Tree species richness promoted the abundance, but not the species richness, of the dominant, generalist herbivores (especially, adult leaf chewers), probably through diet mixing effects. In contrast, tree richness did not affect the abundance of more specialized herbivores (larval leaf chewers, sap suckers) or predators (web and hunting spiders), and only increased the species richness of larval chewers. Leaf chemical diversity was unrelated to the arthropod data, and leaf morphological diversity only positively affected oligophagous herbivore and hunting spider abundance. However, richness and abundance of all arthropods showed relationships with community-weighted leaf trait means (CWM). The effects of trait diversity and CWMs probably reflect specific nutritional or habitat requirements. This is supported by the strong effects of tree species composition and CWMs on herbivore and spider beta diversity. Although specialized herbivores are generally assumed to determine herbivore effects in species-rich forests, our study suggests that generalist herbivores can be crucial for trophic interactions. Our results indicate that promoting pest control through stand diversification might require a stronger focus on identifying the best-performing tree species mixtures.
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Herbivoria , Árboles , Animales , Biodiversidad , Ecosistema , BosquesRESUMEN
Patients with acute-on-chronic hepatitis B liver failure (HBV-ACLF) show high morbidity and mortality. Independent prognostic predictors of short-term HBV-ACLF mortality include the Child-Turcotte-Pugh (CTP) score, the model for end-stage liver disease (MELD) score, other MELD-based indices and the dynamic changes in these indices. The aims of this study were to evaluate the existing prognostic scores in a large cohort of HBV-ACLF patients and create a new predictive model. We retrospectively reviewed 392 HBV-ACLF patients from December 2008 to November 2011 and evaluated their 3-month survival. The predictive accuracy of CTP, MELD and MELD-based indices and the dynamic changes in the MELD-related scores (Δ scoring systems) upon admission and after two weeks of treatment were compared using the area under the receiver operating characteristic (ROC) curve method. Life-threatening factors and a series of bio-clinical parameters were studied by univariate and multivariate analyses. Among the existing scores, MELD had the best predictive ability. However, our new regression model provided an area under the curve of 0.930 ± 0.0161 (95% CI: 0.869 to 0.943), which was significantly larger than that obtained with the MELD score at admission and after two weeks of treatment as well as with the dynamic changes of the MELD score (0.819, 0.921, and 0.826, respectively) (Z=3.542, P=0.0004). In a large cohort of patients retrospectively reviewed for this study, our prognostic model was superior to the MELD score and is, therefore, a promising predictor of short-term survival in patients with HBV-ACLF.
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Hepatitis B/complicaciones , Fallo Hepático/etiología , Enfermedad Aguda , Adulto , Enfermedad Crónica , Femenino , Humanos , Masculino , Persona de Mediana Edad , PronósticoRESUMEN
Purpose: This study aims to investigate the relationship between estimated pulse wave velocity (ePWV) and metabolic syndrome (MetS) in people living with HIV (PLWH), proposing a novel and convenient predictor for early detection of MetS in PLWH. Patients and Methods: A total of 485 PLWH were enrolled. These participants were categorized into two groups based on the estimated pulse wave velocity (ePWV) level. Demographic and clinical data were collected to investigate the correlation between ePWV and MetS. Results: The cohort of 485 PLWH was categorized into high-ePWV and low-ePWV groups based on ePWV cutoff value of 10 m/s. We observed significant differences in components of MetS including triglycerides (TG, P < 0.05), HDL cholesterol (HDL-C, P < 0.01), systolic blood pressure (SBP, P < 0.001), diastolic blood pressure (DBP, P < 0.05), and fasting plasma glucose (FPG, P < 0.001) between the two groups. Furthermore, we employed receiver operating characteristic (ROC) curves to demonstrate the effectiveness of ePWV as a predictive indicator for MetS in PLWH (AUC = 0.739, P < 0.001). According to the ROC curve, the optimal cut-off value of ePWV was 7.4 m/s, and its sensitivity and specificity in diagnosing MetS in PLWH were 79.03% and 64.07%, respectively. Although the 7.4 m/s cutoff increased the false positive rate compared to the traditional cutoff, it significantly reduced the rate of missed diagnoses, effectively identifying 79.03% of PLWH with MetS. Conclusion: ePWV is a non-invasive and convenient novel biomarker with predictive capabilities for MetS in PLWH.
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BACKGROUND AND AIM: The long-term outcomes of patients with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) remain not well known. This study aimed to investigate whether aMAP score can predict re-hospitalization, hepatocellular carcinoma (HCC) occurrence and long-term mortality in patients with HBV-ACLF. METHODS: A total of 82 patients diagnosed with HBV-ACLF and survived over 6 months were enrolled. The median follow-up period was 105 (75.9, 134.1) months. The Cox proportional hazards or logistic regression analysis was used to determine independent risk factors. Cumulative incidence of HCC and survival rate were evaluated using Kaplan-Meier analysis. RESULTS: Multivariate analysis identified that the aMAP risk score was an independent predictor of re-hospitalization (odds ratio [OR] = 1.112, 95% confidence interval [CI]: 1.021-1.211, p = 0.015), hepatocellular carcinoma occurrence (hazards ratio [HR] = 2.277, 95% CI: 1.014-5.114, p = 0.046) and mortality (HR = 1.366, 95% CI: 1.040-1.794, p = 0.025). High-risk aMAP scores were associated with higher risk of HCC occurrence and mortality. CONCLUSION: A higher aMAP score was an independent risk predictor of re-hospitalization, HCC occurrence and mortality, respectively, in HBV-ACLF patients who survived over 6 months, which can be applicable for early risk stratification and clinical decision.
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Objective: The objective of this study was to evaluate the characteristics of high body mass index (BMI) and normal weight people living with HIV after antiretroviral therapy (ART) and establish a model. Methods: A total of 290 people living with HIV after 1 year of ART treatment were enrolled and divided into two groups based on whether their BMI index was <24 or ⩾24 at week 48. The demographic, clinical data were collected and analyzed. Multivariable logistic regression analysis was performed. A model was established and use to predict the occurrence of certain diseases. Results: A total of 290 people living with HIV were included in this study; 200 had a normal BMI (BMI < 24) and 90 were high BMI (BMI ⩾ 24) after 1-year ART. Their baseline characteristics were significantly different in relation to age (p = 0.007), sex distribution (p = 0.040), ART regimen (p = 0.040), alanine aminotransferase levels (p < 0.001), and three major serum lipid levels: triglycerides (p < 0.001), cholesterol (p = 0.011), and low-density lipoprotein (p = 0.005). A multivariate logistic regression analysis resulted in the development of a model for the diagnosis of high BMI and hyperlipidemia. The model score is an independent risk factor for hyperlipidemia (odds ratio = 2.674, p = 0.001) and high BMI (p < 0.001). The model score is significantly correlated with the controlled attenuation parameter (CAP) value (r = 0.230, p < 0.001) and can be used to divide the severity of liver steatosis based on CAP value. Conclusions: This study demonstrated a easy-to-use model to detect high BMI, hyperlipidemia, and liver steatosis in people living with HIV without risk factors for BMI changing at baseline after 1 year of ART treatment.
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This study focused on the mental health of people living with HIV(PLWHIV) and explored their relationship between loneliness and perceived social support, health related quality of life (HRQoL) with a method of structural equation model. We collected clinical and psychological data from consecutively enrolled PLWHIV. A total of 201 PLWHIVs were enrolled and measured with self-reporting survey instruments of UCLA Loneliness Scale, Self-Rating Depression Scale, Self-Rating Anxiety Scale, Social Support Ratio Scale and Short Form Health Survey-36. The levels of loneliness, depression, anxiety, perceived social support and HRQoL were assessed. PLWHIV enrolled were divided into two groups of loneliness and non-loneliness based on their UCLA Loneliness Scale scores. Multivariable analysis indicated that being married is a protective factor associated with loneliness (OR = 0.226; P = 0.032). We further found the loneliness group had a higher level of depression (P < 0.001) and anxiety (P < 0.001), but lower level of HRQoL (P < 0.001) than the non-loneliness group. We found there was a positive linear correlation between social support and HRQoL among the enrolled PLWHIVs (r2 = 0.0592; P = 0.0005). A structural equation model (SEM) was established to evaluate whether the loneliness played as a mediation role between social support and HRQoL. The model showed loneliness as a mediation from social support leading to a decrease of HRQoL. Our findings showed a potential psychological pathway from social support to HRQoL, suggesting the need for interventions focusing on social support may improve poor HRQoL lead by loneliness.
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Depresión , Calidad de Vida , Humanos , Calidad de Vida/psicología , Depresión/psicología , Soledad/psicología , Salud Mental , Apoyo SocialRESUMEN
INTRODUCTION: Long noncoding RNA Mirt2 has been proven to be a suppressor of lipopolysaccharide (LPS) (a key player in sepsis)-induced inflammation responses. Therefore, Mirt2 may also participate in sepsis. This study was carried out to analyze the interactions between Mirt2 and microRNA-1246 (miR-1246) in sepsis, with a specific focus on sepsis-induced acute lung injury (sepsis-ALI). METHODS: Forty sepsis patients (sepsis group; 23 males and 17 females; 40-65 years, 48.6 ± 6.3 years), 40 sepsis patients with acute lung injury (sepsis-ALI group, 23 males and 17 females; 40-65 years, 48.7 ± 6.4 years), and 40 healthy controls (control group, 23 males and 17 females; 40-65 years, 48.6 ± 6.1 years) were included. Mirt2 and miR-1246 expression in plasma samples from these patients were determined by a reverse transcription-quantitative polymerase chain reaction (PCR). Overexpression of Mirt2 and miR-1246 was achieved in human bronchial epithelial cells (HBEpCs) to explore the interaction between them. The effects of Mirt2 overexpression on miR-1246 methylation were analyzed by methylation-specific PCR. Cell apoptosis analysis was performed to analyze the role of Mirt2 and miR-1246 in the apoptosis of HBEpCs. RESULTS: Mirt2 expression was downregulated in sepsis and was further downregulated in patients with sepsis-ALI. Mirt2 and miR-1246 found to be positively correlated. Downregulation of Mirt2 and miR-1246 was observed in HBEpCs with LPS treatment. In HBEpCs, Mirt2 overexpression increased miR-1246 expression but decreased its gene methylation. Cell apoptosis analysis showed that Mirt2 and miR-1246 negatively regulated the apoptosis of HBEpCs induced by LPS. In addition, miR-1246 inhibition reduced the inhibitory effects of Mirt2 overexpression on cell apoptosis. CONCLUSIONS: Mirt2 may upregulate miR-1246 through methylation to suppress lung cell apoptosis.
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Pulmón , MicroARNs , ARN Largo no Codificante , Apoptosis , Humanos , Lipopolisacáridos , Masculino , Metilación , MicroARNs/genética , ARN Largo no Codificante/metabolismoRESUMEN
BACKGROUND: The prognosis of hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is extremely poor due to multiple organ dysfunction. OBJECTIVES: To investigate the prognostic risk factors and create a 90-day prognostic predictive model for the patients with HBV-ACLF. METHODS: Demographic information, clinical examination, and laboratory test results of the enrolled patients were collected to study the prognostic risk factors. Univariate and multivariate analysis and stepwise Logistic regression were performed to develop the predictive model. External validation was performed to verify the model. RESULTS: A total of 333 HBV-ACLF patients and 86 HBV-non-ACLF patients were included in this study. Age, alpha-fetoprotein (AFP), total bilirubin (TBIL), platelet (PLT), and international normalized ratio (INR) were found to be independent risk factors for poor outcomes of HBV-ACLF patients. The formula identified for the linear predictor (LP) of the prognosis of HBV-ACLF patients is thus: LPACLF=-5.04-0.056×age-0.002×AFP-0.010×PLT+0.002×TBIL+0.877×INR. The area under curve (AUC) of the receiver operating characteristic curve (ROC) was 0.7835 (95% CI 0.7248-0.8423). CONCLUSIONS: A predictive model with good calibration and discrimination for 90-day survival of HBV-ACLF patients, including 5 variables, namely age, AFP, PLT, TBIL, and INR was established. Platelet count was a sensitive and dynamic variable for the prognosis of HBV-ACLF.
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Insuficiencia Hepática Crónica Agudizada , Virus de la Hepatitis B , Insuficiencia Hepática Crónica Agudizada/diagnóstico , Bilirrubina , Humanos , Recuento de Plaquetas , Valor Predictivo de las Pruebas , alfa-FetoproteínasRESUMEN
BACKGROUND: Actinomycosis is a rare indolent infectious disease with nonspecific clinical presentations that delay diagnosis. Although actinomycosis is thought to be more prevalent in developing countries, data from developing countries are scarce. This study aimed to profile actinomycosis in developing countries and identify how it differed from profiles of developed countries. METHODS: Patients fulfilling the inclusion criteria for actinomycosis from Nanfang Hospital in southern China between January 1999 and December 2018 were retrospectively analyzed. We described clinical characteristics, diagnostic procedures, differential diagnosis, and management of actinomycosis of clinical significance. RESULTS: Thirtyone patients were included in this study. The disease was diagnosed predominately in the orocervicofacial (n = 14), cardiothoracic (n = 11), abdominopelvic (n = 5), and soft tissue (n = 1) regions. Diagnosis was obtained by either histopathology (n = 29, 94%) or microbiology (n = 2, 6%). Only one-third of patients presented with general symptoms, such as fever and weight loss. Ten were lost during follow-up, and the median duration of antibiotic use was 93.5 days (interquartile range 28-300), whereas the median follow-up time was 34 months (interquartile range 9-132). Ten patients receiving complete resection of the lesion were cured without postoperative use of antibiotics. Only one patient relapsed during the follow-up period. CONCLUSIONS: Actinomycosis is a rare disease even in developing countries, and both misdiagnosis and missed diagnosis are common. Diagnosis was often delayed and was obtained postoperatively from histopathology in developing countries. Hence, clinicians should be aware of this disease in patients with high risk factors. In the future, specific molecular methods may help to improve early diagnosis and treatment.
Asunto(s)
Actinomicosis , Actinomicosis/diagnóstico , Actinomicosis/tratamiento farmacológico , Actinomicosis/epidemiología , Antibacterianos/uso terapéutico , Diagnóstico Diferencial , Errores Diagnósticos , Humanos , Estudios RetrospectivosRESUMEN
Aim: To evaluate health-related quality of life (HRQoL) of chronic hepatitis B (CHB) and hepatitis B virus (HBV) related cirrhosis patients and analyzed specific differences in all dimensions of HRQoL. Methods: A total of 349 patients met selection criteria were enrolled. The 36-Item Short-Form Health Survey was adopted. Results: Results showed that the physiological HRQoL of the cirrhotic group was significantly lower than that of the non-cirrhotic group (P = 0.003), the psychological HRQoL was also lower (P = 0.006). HRQoL was significantly negatively correlated with liver stiffness (P = 0.001). We further evaluated the risk factors associated with poor HRQoL in HBV-related cirrhosis patients. Results showed that positive HBV DNA viral load (OR = 6.296, P = 0.041) and HCC family history (OR = 36.211, P = 0.001) were independent factors associated with HRQoL in HBV-related cirrhosis. For better risk stratification of patients, multivariable analyses were conducted to explore the independent factors that affected specific physiological and psychological HRQoL. In specific physiological HRQoL, results show that marital status (OR = 9.971, P = 0.034), positive HBV DNA viral load (OR = 6.202, P = 0.042) and antiviral drugs (OR = 0.45, P = 0.031) were independent factors associated with physiological HRQoL in cirrhosis patients. In psychological HRQoL, only HCC family history was independent risk factors associated with psychological HRQoL (OR = 42.684, P = 0.002). Conclusion: We found that the impaired HRQoL dimensions of HBV related cirrhosis patients differ between the various subpopulations. According to our results, risk stratification, medical decision making and personalizing interventions could be made.