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Article in English | WPRIM | ID: wpr-878305


Objective@#Several COVID-19 patients have overlapping comorbidities. The independent role of each component contributing to the risk of COVID-19 is unknown, and how some non-cardiometabolic comorbidities affect the risk of COVID-19 remains unclear.@*Methods@#A retrospective follow-up design was adopted. A total of 1,160 laboratory-confirmed patients were enrolled from nine provinces in China. Data on comorbidities were obtained from the patients' medical records. Multivariable logistic regression models were used to estimate the odds ratio ( @*Results@#Overall, 158 (13.6%) patients were diagnosed with severe illness and 32 (2.7%) had unfavorable outcomes. Hypertension (2.87, 1.30-6.32), type 2 diabetes (T2DM) (3.57, 2.32-5.49), cardiovascular disease (CVD) (3.78, 1.81-7.89), fatty liver disease (7.53, 1.96-28.96), hyperlipidemia (2.15, 1.26-3.67), other lung diseases (6.00, 3.01-11.96), and electrolyte imbalance (10.40, 3.00-26.10) were independently linked to increased odds of being severely ill. T2DM (6.07, 2.89-12.75), CVD (8.47, 6.03-11.89), and electrolyte imbalance (19.44, 11.47-32.96) were also strong predictors of unfavorable outcomes. Women with comorbidities were more likely to have severe disease on admission (5.46, 3.25-9.19), while men with comorbidities were more likely to have unfavorable treatment outcomes (6.58, 1.46-29.64) within two weeks.@*Conclusion@#Besides hypertension, diabetes, and CVD, fatty liver disease, hyperlipidemia, other lung diseases, and electrolyte imbalance were independent risk factors for COVID-19 severity and poor treatment outcome. Women with comorbidities were more likely to have severe disease, while men with comorbidities were more likely to have unfavorable treatment outcomes.

Adult , Aged , COVID-19/virology , China/epidemiology , Comorbidity , Female , Humans , Male , Middle Aged , Retrospective Studies , Severity of Illness Index , Treatment Outcome
Article in Chinese | WPRIM | ID: wpr-272707


To study the effect of plant protein and animal protein on amino acid metabolism spectrum of Qi and Yin deficiency type 2 diabetic rats. 110 male SD rats were randomly divided into blank group (n=10), diabetic model group (n=20), disease-symptoms group (n=80). The rats of blank group received ordinary feeding, while other groups were fed with high sugar and fat diets. During the whole process of feeding, rats of disease-symptoms group were given with Qingpi-Fuzi (15.75 g•kg⁻¹) once a day through oral administration. Five weeks later, the rats were given with a low dose of STZ (40 mg•kg⁻¹) by intraperitoneal injection to establish experimental diabetic models. Then the models were randomly divided into disease-symptoms group 1 (Qi and Yin deficiency diabetic group, 15.75 g•kg⁻¹), disease-symptoms group 2 (plant protein group, 0.5 g•kg⁻¹), disease-symptoms group 3 (animal protein group, 0.5 g•kg⁻¹), disease-symptoms group 4 (berberine group, 0.1 g•kg⁻¹). The drugs were given for 4 weeks by gavage administration. After 4 weeks of protein intervention, the abdominal aortic blood was collected and serum was isolated to analyze its free amino acid by using AQC pre-column derivatization HPLC and fluorescence detector. Four weeks after the protein intervention, plant protein, animal protein and berberine had no obvious effect on body weight and blood sugar in type 2 diabetic rats. As compared with animal protein group, histidine and proline(P<0.01), serine, glycine, threonine, alanine, tyrosine, valine, methionine, bright+isoleucine, phenylalanine and lysine(P<0.05)changed a lot in rats serum of plant protein group.The results showed that gavage administration of protein would produce effects on amino acid metabolism of Qi and Yin deficiency type 2 diabetic SD rats. Symbolic differential compounds could be found through metabonomics technology, providing experimental basis for early warning of type 2 diabetes and diagnosis of Qi and Yin deficiency syndrome.

Article in English | WPRIM | ID: wpr-242825


In this article, the mechanism of inheritance behind inherited hearing loss and genetic susceptibility in noise-induced hearing loss are reviewed. Conventional treatments for sensorineural hearing loss (SNHL), i.e. hearing aid and cochlear implant, are effective for some cases, but not without limitations. For example, they provide little benefit for patients of profound SNHL or neural hearing loss, especially when the hearing loss is in poor dynamic range and with low frequency resolution. We emphasize the most recent evidence-based treatment in this field, which includes gene therapy and allotransplantation of stem cells. Their promising results have shown that they might be options of treatment for profound SNHL and neural hearing loss. Although some treatments are still at the experimental stage, it is helpful to be aware of the novel therapies and endeavour to explore the feasibility of their clinical application.

Animals , Evidence-Based Practice , Genetic Engineering , Genetic Therapy , Hearing Loss, Sensorineural , Genetics , Therapeutics , Humans , Mice , Mice, Inbred C57BL , Stem Cell Transplantation
Chinese Journal of Cardiology ; (12): 406-410, 2013.
Article in Chinese | WPRIM | ID: wpr-261542


<p><b>OBJECTIVE</b>To explore the role and potential mechanism of human α-defensin 1 (HNP-1) on low-density lipoprotein (LDL) oxidation ability of human endothelial cells (EVC304).</p><p><b>METHODS</b>Post incubation with LDL for 3 h, the malondialdehyde (MDA) and protein carbonyl (PCO) were detected in untreated ECV304 (control) and in HNP-1 transfected ECV304 in the presence and absence of siRNA against HNP-1. Flow cytometry and fluorescence microscopy were used to detect the generation of oxygen free radical in the ECV304 which have been pretreated by LDL, LPS and HNP-1, respectively.</p><p><b>RESULT</b>Compared with control group, MDA level was significantly increased in HNP-1 transfected [(4.21 ± 0.03) vs. (3.15 ± 0.02) nmol/mg · pro] or in HNP-1 stimulated ECV304 cells [(14.49 ± 1.10) vs. (9.47 ± 1.18) nmol/mg · pro], which could be significantly downregulated by siRNA [(3.76 ± 0.48) vs. (4.54 ± 0.28) nmol/mg·pro, all P < 0.05]. PCO was also significantly increased in HNP-1 transfected ECV304 cells. The levels of free radical were significantly increased in HNP-1 transfected or HNP-1 stimulated ECV304 cells.</p><p><b>CONCLUSION</b>HNP-1 can enhance the LDL oxidation ability of human endothelial cells via promoting the generation of free radicals.</p>

Cell Line , Endothelial Cells , Metabolism , Humans , Lipoproteins, LDL , Metabolism , RNA, Small Interfering , Transfection , alpha-Defensins , Genetics , Metabolism
Article in Chinese | WPRIM | ID: wpr-305069


<p><b>OBJECTIVE</b>The aim of this study is to investigate the possible associations of chemokines IP-10, Rantes and oxidative stress in chronic hepatits B (CHB).</p><p><b>METHODS</b>70 CHB patients and 10 healthy controls were enrolled in the study. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum levels of IFN-gamma-inducible protein-10 (IP-10) and regulated on activation normal T-cell-expressed and secreted (Rantes) and oxidative stress parameters (glutathione, GSH; glutathione disulfide, GSSG). Correlationship were analyzed by Spearman's rank correlation.</p><p><b>RESULT</b>The levels of IP-10 and Rantes were higher in CHB patients than healthy controls, and strong positive associations were found between IP-10/Rantes and alanine aminotransferase (ALT). The levels of GSH and GSH/GSSG were lower in CHB patients than healthy controls, and GSH and GSH/GSSG were negatively correlated with ALT. The levels of IP-10 and Rantes were negatively correlated with GSH and GSH/GSSG respectively.</p><p><b>CONCLUSION</b>Strong associations were found between chemokines and oxidative stress which participated in the pathogenesis of CHB.</p>

Adult , Alanine Transaminase , Blood , Chemokine CCL5 , Blood , Chemokine CXCL10 , Blood , Female , Glutathione , Blood , Glutathione Disulfide , Blood , Hepatitis B virus , Genetics , Hepatitis B, Chronic , Blood , Metabolism , Virology , Humans , Male , Malondialdehyde , Blood , Middle Aged , Oxidative Stress