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Liqin Chen,1,* Jiankun Chen,1,2,* Yuwan Wu,1 Jinyao Zhong,1 Fuzhen Zhou,1 Yuntao Liu,1,2 Aiting Xu,3 Jiqiang Li,1,2 Huayang Cai1 1The Second Affiliated Hospital (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People’s Republic of China; 2Guangzhou Key Laboratory of Traditional Chinese Medicine for Prevention and Treatment of Emerging Infectious Diseases, Guangzhou, 510006, Guangdong, People’s Republic of China; 3The People’s Hospital of Yangjiang, Yangjiang, 529500, Guangdong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jiqiang Li; Huayang Cai Email lijiqiangjizhen@163.com ; caihuayang@gzucm.edu.cnBackground: Hypertension has been reported as the most prevalent comorbidity in patients with coronavirus disease 2019 (COVID-19). This retrospective study aims to compare the clinical characteristics and outcomes in COVID-19 patients with or without hypertension.Methods: A total of 944 hospitalized patients with laboratory-confirmed COVID-19 were included from January to March 2020. Information from the medical record, including clinical features, radiographic and laboratory results, complications, treatments, and clinical outcomes, were extracted for the analysis.Results: A total of 311 (32.94%) patients had comorbidity with hypertension. In COVID-19 patients with hypertension, the coexistence of type 2 diabetes (56.06% vs 43.94%), coronary heart disease (65.71% vs 34.29%), poststroke syndrome (68.75% vs 31.25%) and chronic kidney diseases (77.78% vs 22.22%) was significantly higher, while the coexistence of hepatitis B infection (13.04% vs 86.96%) was significantly lower than in COVID-19 patients without hypertension. Computed tomography (CT) chest scans show that COVID-19 patients with hypertension have higher rates of pleural effusion than those without hypertension (56.60% vs 43.40%). In addition, the levels of blood glucose [5.80 (IQR, 5.05– 7.50) vs 5.39 (IQR, 4.81– 6.60)], erythrocyte sedimentation rate (ESR) [28 (IQR, 17.1– 55.6) vs 21.8 (IQR, 11.5– 44.1), P=0.008], C-reactive protein (CRP) [17.92 (IQR, 3.11– 46.6) vs 3.15 (IQR, 3.11– 23.4), P=0.013] and serum amyloid A (SAA) [99.28 (IQR, 8.85– 300) vs 15.97 (IQR, 5.97– 236.1), P=0.005] in COVID-19 patients with hypertension were significantly higher than in patients without hypertension.Conclusion: It is common for patients with COVID-19 to have the coexistence of hypertension, type 2 diabetes, coronary heart disease and so on, which may exacerbate the severity of COVID-19. Therefore, optimal management of hypertension and other comorbidities is essential for better clinical outcomes.Keywords: COVID-19, coronavirus disease, hypertension, clinical characteristics, comorbidities

Intermittent hypoxia is a characteristic pathological change in obstructive sleep apnoea (OSA) that can initiate oxidative stress reaction and pro-inflammatory cytokine release. The purpose of this study was to assess the effect and protective mechanism of Astragaloside IV (AS-IV) in intermittent hypoxia-induced human lung epithelial Beas-2B cells. Human lung epithelial Beas-2B cells were exposed to intermittent hypoxia or normoxia in the absence or presence of AS-IV. MTT assay was performed to determine the cell viability. The levels of reactive oxygen species (ROS), lactate dehydrogenase (LDH), malonaldehyde (MDA), and superoxide dismutase (SOD) were measured to evaluate oxidative stress. The levels of cytokines interleukin (IL)-8, IL-1β, and IL-6 were evaluated by enzyme-linked immunosorbent assay and real-time PCR. The expression of Toll-like receptor 4 (TLR4), mitogen-activated protein kinase (MAPK), and nuclear transcription factor-kappa B (NF-κB) signalling pathways was analysed by western blot. The results showed that AS-IV significantly reduced the levels of ROS, LDH, MDA, IL-8, IL-1β, and IL-6, and increased the level of SOD in intermittent hypoxia-induced Beas-2B cells. It also suppressed the phosphorylation of MAPKs, including P38, c-Jun N-terminal kinase and extracellular signal-regulated kinase, and inhibited the activation of the NF-κB signalling pathway by reducing the phosphorylation of IκBα and p65. AS-IV attenuates inflammation and oxidative stress by inhibiting TLR4-mediated MAPK/NF-κB signalling pathways in intermittent hypoxia-induced Beas-2B cells.

Background Recent studies have suggested that vitamin D deficiency in children is widespread. But the vitamin D status of Chinese children is seldom investigated. The objective of the present study was to survey the serum levels of 25-hydroxyvitamin D [25(OH)D] in more than 6,000 children aged 1 month to 16 years in Hangzhou (latitude: 30°N), the capital of Zhejiang Province, southeast China. Methods The children aged 1 month to 16 years who came to the child health care department of our hospital, the children's hospital affiliated to Zhejiang university school of medicine, for health examination were taken blood for 25(OH) D measurement. Serum 25(OH) D levels were determined by direct enzyme-linked immunosorbent assay and categorized as < 25, < 50, and < 75 nmol/L. Results A total of 6,008 children aged 1 month to 16 years participated in this cross-sectional study. All the subjects were divided into subgroups according to their age: 0-1y, 2-5y, 6-11y and 12-16y representing infancy, preschool, school age and adolescence stages respectively. The highest mean level of serum 25(OH)D was found in the 0-1y stage (99 nmol/L) and the lowest one was found in 12-16y stage (52 nmol/L). Accordingly, the prevalence of serum 25(OH)D levels of < 75 nmol/L and < 50 nmol/L were at the lowest among infants (33.6% and 5.4% respectively) and rose to the highest among adolescents (89.6% and 46.4% respectively). The mean levels of serum 25(OH)D and the prevalence of vitamin D deficiency changed according to seasons. In winter and spring, more than 50% of school age children and adolescents had a 25(OH)D level at < 50 nmol/L. If the threshold is changed to < 75 nmol/L, all of the adolescents (100%) had low 25(OH)D levels in winter and 93.7% school age children as well. Conclusions The prevalence of vitamin D deficiency and insufficiency among children in Hangzhou Zhejiang province is high, especially among children aged 6-16 years. We suggest that the recommendation for vitamin D supplementation in Chinese children should be extended to adolescence.

Abnormal hyperphosphorylation of the cytoskeletal protein tau is a characteristic feature of neurodegeneration in Alzheimer's disease (AD) brain. Okadaic acid (OA), a protein phosphatase inhibitor, induces neuronal death and hyperphosphorylation of tau. In the present study using a model of microinjection of OA into rat frontal cortex, we aimed to investigate if OA-induced hyperphosphorylation of tau and neuronal death are related to the expression of Bcl-2, an apoptosis inhibitor, or Bax, an apoptosis inducer. Immunohistochemistry and Western blot analysis showed that OA injection dose- and time-dependently induced the expression of Bcl-2 and Bax protein in the surrounding of OA injection areas, which were similar with that of AT8 immunostaining, a marker of hyperphosphorylated tau. However, the ratios of Bcl-2 over Bax had a negative relationship to the expression of AT8. Furthermore, double fluorescent staining showed that AT8-positive neurons mainly costained with terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick-end labeling, a marker of DNA damage, indicating that tau hyperphosphorylation may be associated with DNA damage in the neurons of rat brain. In the areas more adjacent to the OA injection site, most neurons with AT8-positive staining showed vulnerability to OA toxicity and could be triple-stained with Bcl-2 and Bax or double-stained with Bcl-2. However, in the areas further from the OA injection site, neurons with few AT8-positive staining showed resistance to OA toxicity and only stained with Bcl-2, but not Bax. The results suggest that the ratios of Bcl-2 over Bax expression may have an effect on tau hyperphosphorylation and neuronal death following OA injection. © 2005 Wiley-Liss, Inc.