Clinical features of elderly patients with COVID-19 in Wuhan, China.

BACKGROUND: Elderly patients with coronavirus disease 2019 (COVID-19) who have comorbidities, frailty or profound disabilities experience poor outcomes. We analyzed the clinical characteristics of elderly patients from Wuhan who had COVID-19 during the early stages of the pandemic. AIM: To identify factors affecting the early mortality of elderly patients with COVID-19. METHODS: The records of 234 patients who were 65-years-old or more and were hospitalized in Wuhan Huoshenshan Hospital from February 4 to March 4, 2020 were reviewed. All patients had confirmed COVID-19 and the final date of follow-up was April 4, 2020. RESULTS: There were 163 cases of mild disease (69.66%), 39 cases of severe disease (16.67%) and 32 cases of critical disease (13.68%). Twenty-nine patients died within 1 mo (12.40%), all of whom had critical disease. Surviving patients and deceased patients had no significant differences in age or chronic diseases. Overall, the most common symptoms were fever (65.4%), dry cough (57.3%), fatigue (47.4%) and shortness of breath (41%). The deceased patients had higher levels of multiple disease markers (C-reactive protein, D-dimer, lactate dehydrogenase, alanine amino transferase, aspartate aminotransferase, creatinine kinase and creatinine kinase-MB) and higher incidences of lymphocytopenia and hypoproteinemia. CONCLUSION: This single-center study of elderly patients from Wuhan, China who were hospitalized with COVID-19 indicated that age and chronic diseases were not associated with mortality. Hypertension, diabetes and cardiovascular disease were the most common comorbidities and the most common symptoms were fever, dry cough, fatigue and shortness of breath. Lymphocytopenia, increased levels of D-dimer and other markers indicative of damage to the heart, kidneys or liver were associated with an increased risk of death.

Efficacy of arbidol in COVID-19 patients: A retrospective study.

BACKGROUND: To date, no treatment has proven to be absolutely effective for coronavirus disease 2019 (COVID-19) patients, and further research is necessary. As a traditional antiviral drug, arbidol was widely used in Wuhan at the beginning of the COVID-19 epidemic and is of increasing interest for treating COVID-19 based on in vitro data suggesting activity against severe acute respiratory syndrome (SARS). Although arbidol has been widely used in China to treat COVID-19 patients, clinical trials to date have not clearly substantiated this approach. AIM: To evaluate the efficacy of arbidol for COVID-19. METHODS: A retrospective study was conducted on 132 moderate and severe COVID-19 patients admitted to Jinyintan Hospital and Huoshenshan Hospital (officially designated for COVID-19 treatment) from February to March 2020 in Wuhan, China. This study mainly evaluated the efficacy of arbidol in patients with COVID-19 in the early stage of the SARS coronavirus 2 epidemic. Arbidol was administered at a dose of 200 mg, three times a day, with a 10-d course to adults not receiving any other drugs. Due to the shortage of beds at the time, not every patient could be admitted immediately. We looked for the early stages of the sudden outbreak, places of limited medical resources, limited ward beds, and delayed admission; thus, some patients naturally fit into the control group who did not receive any antiviral drugs. Out of the 132 patients, 72 received arbidol treatment, and 60 did not. We compared the disease course of the two groups and explored the predictors of extended disease duration. RESULTS: Seventy-two patients commenced arbidol, and 60 patients did not receive arbidol treatment. The disease duration in the former group was shorter (23.42 ± 6.92 vs 29.60 ± 6.49, P < 0.001). Multivariate regression analysis showed that the risk of a prolonged course of disease increased by 7.158 times in the non-arbidol treatment group. Ferritin > 483.0 ng/mL and lactate dehydrogenase (LDH) > 237.5 U/L were found to be independent risk factors for protracted cases, with the risk of an extended disease duration increasing to 2.852 times and 5.946 times, respectively. CONCLUSION: The duration course of moderate and severe COVID-19 patients is reduced by 6.183 d when arbidol is administered. Ferritin > 486.5 ng/mL and LDH > 239.5 U/L are independent risk factors for delayed recovery from COVID-19. Early oral administration of arbidol 200 mg t.i.d. with a 10-d course of treatment may be an effective management strategy in COVID-19 patients, particularly those with increased serum ferritin or elevated LDH.

Postoperative Antifungal Treatment of Pulmonary Cryptococcosis in Non-HIV-Infected and Non-Transplant-Recipient Patients: A Report of 110 Cases and Literature Review.

BACKGROUND: To explore the efficacy of postoperative antifungal treatment for preventing the recurrence of pulmonary cryptococcosis (PC) and occurrence of cryptococcal meningitis (CM), a retrospective study was conducted in 112 hospitalized PC patients with or without antifungal treatment following surgery. METHODS: The treatment failure rate, PC recurrence rate, and CM incidence were compared. Additionally, the effectiveness of postoperative antifungal therapy was assessed by gathering and analyzing the published literature. RESULTS: The failure rate (P = .054) and recurrence rate (P = .178) were similar in the 2 groups, but the incidence of CM was lower in the group that received postoperative antifungal treatment (P = .039). CONCLUSIONS: This study did not show any difference in the PC recurrence rate or failure rate in the different treatment duration groups. Thus, a shorter antifungal treatment course of 2 months may be an optional treatment. In addition, upon review of the literature, no case of CM occurrence was reported among the 169 cases given postoperative antifungal treatment.

miR­24 may be a negative regulator of menin in lung cancer.

The incidence of lung cancer in China increases annually, and effective targets for the diagnosis and treatment of lung cancer are urgently needed. miRNAs are currently considered to be involved in the regulation of tumor development and growth. miR­24 has been found to contribute to the development of several tumors. Menin is a key tumor suppressor gene, and its expression is generally low in lung cancer. The effects of miR­24 on the biological behavior of lung cancer cells were detected by MTT and Transwell assays. In the present study, miR­24 was found to be associated with menin, affecting the activity of the SMAD3 pathway in lung cancer by inhibiting menin expression. miR­24 may promote the growth and metastasis and inhibit the apoptosis of lung cancer cells by targeting menin. Therefore, the aim of the present study was to provide a new theoretical basis for the targeted therapy of lung cancer.

miR-646 is a key negative regulator of EGFR pathway in lung cancer.

BACKGROUND: As one of the leading cause of cancer-related deaths in the worldwide, lung cancer needs to be understood better. Nowadays, increasing point mutations of specific oncogenes are biomarkers used to predict the therapeutic effect of targeted therapy and lung cancer has entered the age of individual treatment. At present, many relevant researchers have suggested that EGFR is a biomarker used to predict the therapeutic effect of targeted therapy. A large number of evidence indicates that EGFR/Akt pathway plays important role in cancer growth and metastasis. AIM OF THE STUDY: In this paper, we found EGFR was a target of miR-646. RESULTS: Overexpression of miR-646 not only downregulated EGFR/Akt pathway, but also inhibited lung cancer cell proliferation and metastasis. At the same time, miR-646 was a prognosis factor for overall survival. CONCLUSION: Our finding could provide new insights into the molecular therapeutic of lung cancer.

HDAC1 inhibition by melatonin leads to suppression of lung adenocarcinoma cells via induction of oxidative stress and activation of apoptotic pathways.

Melatonin is an indoleamine synthesized in the pineal gland that shows a wide range of physiological and pharmacological functions, including anticancer effects. In this study, we investigated the effect of melatonin on drug-induced cellular apoptosis against the cultured human lung adenocarcinoma cells and explored the role of histone deacetylase (HDAC) signaling in this process. The results showed that melatonin treatment led to a dose- and time-dependent decrease in the viability of human A549 and PC9 lung adenocarcinoma cells. Additionally, melatonin exhibited potent anticancer activity in vitro, as evidenced by reductions of the cell adhesion, migration, and the intracellular glutathione (GSH) level and increases in the apoptotic index, caspase 3 activity, and reactive oxygen species (ROS) in A549 and PC9 cells. Melatonin treatment also influenced the expression of HDAC-related molecules (HDAC1 and Ac-histone H3), upregulated the apoptosis-related molecules (PUMA and Bax), and downregulated the proliferation-related molecule (PCNA) and the anti-apoptosis-related molecule (Bcl2). Furthermore, the inhibition of HDAC signaling using HDAC1 siRNA or SAHA (a potent pan-inhibitor of HDACs) sensitized A549 and PC9 cells to the melatonin treatment. In summary, these data indicate that in vitro-administered melatonin is a potential suppressor of lung adenocarcinoma cells by the targeting of HDAC signaling and suggest that melatonin in combination with HDAC inhibitors may be a novel therapeutic intervention for human lung adenocarcinoma.

Effects of PEMF on microcirculation and angiogenesis in a model of acute hindlimb ischemia in diabetic rats.

Hindlimb ischemia is a major complication of diabetic patients due to poor neovascularization. Therapy with pulsed electromagnetic fields (PEMF) can promote angiogenesis in ischemic lesions. However, the efficacy and therapeutic mechanisms of PEMF in diabetes-related hindlimb ischemia are unclear. Sprague-Dawley rats were injected with streptozocin to induce diabetes, and 10 weeks later diabetic rats were subjected to surgical induction of acute hindlimb ischemia. The rats were randomized and treated with PEMF, and the blood perfusion of individual rats was determined longitudinally by laser Doppler perfusion imaging (LDPI). The neovascular density was examined using immunofluorescent analysis of CD31 expression and alkaline phosphatase (AP) staining. The levels of VEGF, VEGFR, FGF-2, and FGFR1 expression, and ERK 1/2 and P38 phosphorylation in the muscles were characterized using enzyme-linked immunosorbent assay (ELISA) and Western blot assays. The values of LDPI in the PEMF-treated rats at 14 and 28 days post surgery were significantly greater than those in the controls, accompanied by significantly elevated levels of anti-CD31 and AP staining. The relative levels of FGF-2 and FGFR1, but not VEGF and VEGFR expression, and ERK1/2, but not P38 phosphorylation, in the muscles of the PEMF-treated rats were significantly higher than those in the controls. Our data indicated that PEMF enhanced acute hindlimb ischemia-related perfusion and angiogenesis, associated with up-regulating FGF-2 expression and activating the ERK1/2 pathway in diabetic rats. Therefore, PEMF may be valuable for the treatment of diabetic patients with ischemic injury.