The Long-Term Effect of COVID-19 Disease Severity on Risk of Diabetes Incidence and the Near 1-Year Follow-Up Outcomes among Postdischarge Patients in Wuhan.

We assessed the nearly 1-year health consequences following discharge and related risk factors of COVID-19 infection and further explored the long-term effect of COVID-19 disease severity on the risk of diabetes incidence. This prospective study included 248 COVID-19 patients discharged from Wuhan Hospital of Traditional Chinese Medicine who were followed up between 1 March and 10 June 2021. Logistic regression models were used to evaluate risk factors. The top ten symptoms were shortness of breath (30.3%), sore or dry throat (25.7%), cough (23.2%), expectoration (23.2%), body pain (22.3%), chest tightness (20.8%), palpitations (17.8%), sleep difficulties (17.0%), fatigue (16.6%), and anxiety (15.3%). Hypertension was associated with fatigue (OR = 2.51, 95% CI: 1.08, 5.80), shortness of breath (OR = 2.34, 95% CI: 1.16, 4.69), palpitations (OR = 2.82, 95% CI: 1.26, 6.31), expectoration (OR = 2.08, 95% CI: 1.01, 4.30), and sore or dry throat (OR = 2.71, 95% CI: 1.30, 5.65). Diabetes was associated with palpitations (OR = 3.22, 95% CI: 1.18, 8.81). Critical illness was associated with an increased risk of diabetes incidence after discharge (OR = 2.90, 95% CI: 1.07, 7.88), which seemed more evident in males. Long COVID-19 symptoms were common at 1-year postdischarge; hypertension and diabetes could be projected as potential risk factors. We are among the first researchers to find that critical illness is associated with incident diabetes after discharge.

ADAMTS-13-regulated nuclear factor E2-related factor 2 signaling inhibits ferroptosis to ameliorate cisplatin-induced acute kidney injuy.

ADAMTS-13 plays an important role in acute kidney injury (AKI), but the mechanism of cisplatin (CP) induced AKI remains unclear. Ferroptosis is increased in CP-induced AKI, and ADAMTS13 levels are associated with ferritin expression. In this article, we will explore the relationship between the three. After CP induction, mice were given 0.1 and 0.3 nmol/kg ADAMTS-13, and then serum creatinine (Scr) and blood urea nitrogen (BUN) were detected by the kits. The pathological changes of renal tissue were observed by staining with HE and PAS staining, and Western blot detected the expressions of KIM1 and NGAL in renal tissu. Perl's staining detected iron deposition in renal tissues, the kits detected iron levels, and western blot detected the expression of ferroptosis related proteins. Then the mechanism was further explored by adding ferroptosis inhibitors Ferrostatin 1 (Fer-1) and iron supplements Fe. The expression of Nrf2 pathway related proteins were detected by Western blot. We found that ADAMTS13 alleviated CP-induced ferroptosis in AKI mice with renal function impairment and tubular damage. Fer-1partially reversed CP-induced AKI, and Fe exacerbated this effect. ADAMTS13 alleviated CP-induced inflammatory response and oxidative stress in AKI mice, during which the Nrf2 signaling pathway was abnormal. Overall, ADAMTS-13-regulated Nrf2 signaling inhibits ferroptosis to ameliorate CP-induced AKI.

Xuezhikang improves the outcomes of cardiopulmonary resuscitation in rats by suppressing the inflammation response through TLR4/NF-κB pathway.

BACKGROUND/AIMS: Xuezhikang (XZK), a red yeast rice extract with lipid-lowering effect, contains a family of naturally statins, such as lovastatin. In recent years, its effect beyond the regulation of lipids has also been received increasing attention. Therefore, the purpose of this study was to explore the protective effects and possible molecular mechanisms of XZK on brain injury after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR), and to investigate whether it has a dose-dependent effect and the difference with lovastatin. METHODS: Rats were treated with low-dose XZK (XZK-L, 20 mg/kg/d), high-dose XZK (XZK-H, 200 mg/kg/d) and lovastatin by gavage once daily for 2 weeks before CA. The levels of TNF-α, IL-6 and IL-1ß were evaluated at 1, 4, and 72 h post-CA/CPR. The survival rate, neurological deficit score (NDS), and expression of TLR4, phosphorylated NF-κB and TNF-α in hippocampal tissues were evaluated at 72 h post-CA/CPR. RESULTS: CA/CPR induced a significant increase in serum TNF-α, IL-6 and IL-1ß, as well as increased expressions of TLR4, phosphorylated NF-κB and TNF-α in the hippocampus. Both low-dose and high-dose XZK treatment inhibited the expression of these inflammatory cytokines. In addition, it reduced the number of defibrillations and shortened the duration of CPR required for return of spontaneous circulation (ROSC). XZK treatment also improved neurological function and 72-hour survival rate in rats. However, high-dose XZK was superior to lovastatin in the suppression of IL-1ß mRNA level and TNF-α protein level in hippocampal tissue after CPR. There were no significant differences observed among high-dose XZK, low-dose XZK and lovastatin groups in other respects. CONCLUSION: These results indicated that XZK had a protective effect against brain injury post-CA/CPR. The mechanisms underlying the protective effects of XZK may be related to the suppressing of CA/CPR-induced inflammatory response through the inhibiting TLR4/NF-κB signaling pathway.