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Ischemic cardiovascular disease (ICVD) has high incidence and high mortality worldwide. The studies of its risk factors were mostly concentrated on an individual level, and there are scarce studies on the two levels of risk factors which include individual and regional levels.The data were obtained from a community-based study in 4 cities and 6 counties of Henan, China. Risk factors were initially screened by one-way analysis of variance or chi-square test. Then, they were re-analyzed using a two-level logistic regression model to construct a personal disease risk prediction model.A two-level ICVD risk prediction model comprised 11 variables: age, body mass index (BMI), family history of hypertension, marital status, salt intake, smoking, moderate recreational physical activities, alcohol intake, and education at the individual level. Among the unalterable risk factors, for each additional unit of age and family history of hypertension, the risk of ICVD increased by 1.08 and 1.07 units [β95% confidence interval (95%CI): 0.99-1.16, 0.97-1.17, both p 0.0001], respectively. Among the modifiable risk factors, the ICVD risk increases by 0.67, 0.27, and 0.28 units for each additional unit of BMI, marital status, and education (β95%CI: 0.60-0.74, p 0.0001; β95%CI: 0.14-0.40, p = 0.0012, 0.18-0.37, p = 0.0001).The two-level ICVD risk model can predict that the risk of one person for ICVD will be lower if one is younger, thinner, and well-educated without a family history of hypertension. Overall, the two-level ICVD risk prediction model gets a better fitting effect than the single-level model.

Background: The disease burden of comorbidity is growing steadily in many developing countries, affecting residents' physical and mental health. General Practitioners are considered as the suitable service providers for the prevention and control of comorbidity. However, the current knowledge on the clinical and epidemiological characteristics of comorbidity among inpatients in the general practice departments of hospital is limited, which hinders the precise promotion of the service capacity and quality of GPs. Objective: The current study aimed to analyze the clinical prevalence of comorbidities in central China and to provide evidence-based policy recommendations for quality improvement in general medical services. Methods: The study was conducted at the general practice departments of all 27 tertiary grade-A hospitals of Henan Province, China. 3 registered GPs of each hospital were selected by random, and all direct admissions of the 81 GPs from December 2016 to November 2020 were followed up. The clinical epidemiological characteristics and influencing factors of comorbidity were evaluated using descriptive statistical analysis and logistic regression models. Results: Comorbidity was present in 93.1 percent of the 2385 direct admitted patients, with a male-to-female ratio of 1: 1. Comorbidity was significantly more prevalent in patients aged 45-59 years (OR=3.018, 95% CI=1.945-4.683), 60-74 years (OR=4.349, 95% CI=2.574-7.349), ≥75 years (OR=7.804, 95% CI=3.665-16.616), and those with body mass index (BMI) ≥28 kg/m2 (OR=3.770, 95% CI =1.453-9.785). The circulatory system is the most commonly involved human body system in comorbidity, accounting for 79% of all cases. The endocrine, nutritional, and metabolic systems, as well as the digestive and respiratory systems, were all significantly affected, with prevalence rates of 62 percent, 48 percent, and 37 percent, respectively. Conclusion: Comorbidity is common among the inpatients attending the provincial tertiary grade-A hospitals. Since old age and obesity are independent risk factors for comorbidity, healthy lifestyle interventions should be strengthened, as should the implementation of the patient-centered prevention and control model. Meanwhile, quality improvement priorities should be given to improving GPs' clinical diagnosis and treatment of the circulatory system, endocrine system, metabolic system, digestive system, and respiratory system.

Gout is a multifaceted inflammatory disease involving vascular impairments induced by hyperuricemia. Experiments using human umbilical vein endothelial cells treated with uric acid (UA), monosodium urate (MSU), or serum from gout patients showed increased expression of pro-inflammatory genes (ie, VCAM1, ICAM1, CYR61, CCNA1, and E2F1) with attendant increase in monocyte adhesion. Mechanistically, UA- or MSU-induced SREBP2 expression and its transcriptional activity. RNA sequencing analysis and real-time PCR showed the induction of YAP signaling and pro-inflammatory pathways in HUVECs transfected with adenovirus-SREBP2. The SREBP2 knockdown by siRNA partially abolished UA- or MSU-induced YAP activity, pro-inflammatory gene expression, and monocytes adhesion. Vascular intima from transgenic mice overexpressing SREBP2 in endothelium or mice with hyperuricemia exhibited activated YAP signaling and increased expression of pro-inflammatory genes. Betulin, an SREBP pharmacological inhibitor, attenuated the UA-, MSU-, or gout serum-induced endothelial cell inflammation and dysfunction. In the human study, endothelial cell function, assessed by EndoPAT, was negatively correlated with serum UA level among gouty patients and healthy controls. Collectively, UA or MSU causes endothelial dysfunction via SREBP2 transactivation of YAP. Betulin inhibition of SREBP2 may restrain gout-induced endothelial dysfunction.

Background: COVID-19 epidemic has become a significant public health crisis affecting global health. We aimed further to clarify the clinical and medical expense characteristics of COVID-19. Methods: In this retrospective, single-center study, we included all cured cases with confirmed COVID-19 in Henan Provincial People's Hospital from Jan 23 to Mar 10, 2020. Cases were analyzed for demographic, epidemiological, clinical, and radiological features and medical expense data. Findings: The average age of the 54 successfully treated patients with COVID-19 was 53.2 years old (SD 19.0), including 27 men and 27 women. Off this, 31 (57.4%) patients had chronic diseases. Patients commonly had clinical manifestations of fever (45 [83.3%] patients), cough (29[54.7%] patients), expectoration (28 [51.9%] patients), fatigue (24[44.4%] patients) and diarrhea (8[14.8%] patients) on admission. There was a 10-day interval from the onset of signs and symptoms to hospital admission. About 80% of them got recovery after a two-week treatment. During the treatment, 43(78.2%) patients had at least one comorbid illness, and 11(20.4%) had more than five comorbid illnesses. The mean interval from the onset of signs and symptoms to hospital discharge was 20.5 (IQR 16-29) days. The median total medical expense of the treated patient, in general, was 2579.6 (IQR 1366.1-4837.6) U.S. dollars. Still, the median medical expense was 8904.1 (IQR 6660.1- 27143.8) U.S. dollars in patients with more than five comorbid conditions during the treatment. Interpretation: There is a 3-week interval from the onset of signs and symptoms to cure, and most hospitalized patients get recovery within two weeks. Although COVID-19 can result in fatal respiratory diseases and even death. The total medical expense of cases with more than five comorbid conditions during the treatment is higher. Quite a few COVID cases with other serious diseases are likely to account for most of the total medical expenses. Funding Statement: This study was funded by National Natural Science Foundation of China (number 71603132), and the Central Government Guides the Development of Local Science and Technology Special Fund of China (number Z135050009017). Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: The study was approved by the Henan Provincial People's Hospital Ethics Committee

The aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) in the vascular wall are crucial pathological events involved in cardiovascular impairments including hypertension, heart failure, and atherosclerosis. At the molecular level, the mammalian target of rapamycin (mTOR)-ribosomal protein S6 kinase beta-1 (p70S6K) signaling pathway is essential to potentiate VSMC proliferation and migration. Although angiotensin II receptor type 1 ­(AT1-R) antagonists such as valsartan and telmisartan have a significant cardiovascular protective effect, the molecular basis of this class of drugs in VSMC proliferation and migration remains elusive. By using cultured VSMCs, adenosine monophosphate-activated protein kinase (AMPK) α2 knockout mice, and hypertensive rat models, this study investigated whether AT1-R antagonists can inhibit the mTOR-p70S6K signaling pathway in VSMCs and the vascular wall. Valsartan activated AMPK, which in turn suppressed reactive oxygen species production and consequently attenuated VSMC proliferation and migration. In vivo, a clinical dose of telmisartan significantly inhibited the mTOR-p70S6K signaling pathway in the vascular wall of wild-type but not AMPKα2–/– mice. Furthermore, spontaneously hypertensive rats had significantly elevated phosphorylation of mTOR and p70S6K in the aorta compared to Wistar-Kyoto rats, which were reduced by telmisartan administration. These data suggest that AT1-R antagonists inhibit VSMC proliferation and migration via their regulation of AMPK, mTOR, and p70S6K, which contribute to the cardioprotective effects of these drugs.