Effects of Comorbidities on the Elderly Patients with COVID-19: Clinical Characteristics of Elderly Patients Infected with COVID-19 from Sichuan, China.

OBJECTIVES: The co-occurrence of chronic diseases in the elderly is a common problem. However, the relationship between comorbidities and the prognosis of elderly patients with COVID-19 was not clear. This study was supposed to describe the clinical characteristics of elderly patients with COVID-19 infection from Sichuan province and the effects of comorbidity. DESIGN: A retrospective study. SETTINGS AND PARTICIPANTS: COVID-19 patients from Public Health Clinical Center of Chengdu between December 16, 2019 and February 26, 2020 were included in this study. Patients were divided into elderly group (≥60 years old) and non-elderly group (< 60 years old). RESULTS: Elderly patients with COVID-19 indicated relatively higher proportion of comorbidities, and the most common were atherosclerotic cardiovascular disease (56.5%), hypertension (43.5%) and chronic pulmonary disease (21.7%). The proportion of severe cases was higher in elderly group than that in non-elderly group (73.9% and 42.2%, respectively, P=0.012). During hospitalization, elderly patients indicated relatively higher proportion of complications, such as shock (21.7%), respiratory failure (21.7%). The proportion of patients with a decreased number of CD8+ lymphocytes (82.6%) and B lymphocytes (77.8%) in elderly patients was significantly higher than that in non-elderly group (48.9% and 44.8%, respectively). All 3 deaths were elderly patients with comorbidities and the cell counts of T lymphocyte subsets, B and NK cells of them were significantly decreased at admission. CONCLUSIONS: Elderly patients with COVID-19 had a high proportion of severe cases and comorbidities, more likely to show low immune function, and indicate higher proportion of complications.

BPTF biomarker correlates with poor survival in human NSCLC.

OBJECTIVE: The aim of the present study was to identify the clinical significance of BPTF expression in the development and progression of NSCLC. PATIENTS AND METHODS: The expression of BPTF in 189 pairs of NSCLC and adjacent normal lung tissues were detected by Real-time PCR. The expression of BPTF was investigated in NSCLC and normal control tissues by immunohistochemical staining and immunofluorescence staining. Then, we analyzed the potential relationship between BPTF levels in tumor tissues and existing clinicopathological features of NSCLC, and clinical outcome. RESULTS: It was found that BPTF mRNA was significantly overexpressed in NSCLC tissues in comparison with paired normal control tissues (p < 0.01). Consistent with BPTF mRNA expression, up-expression of BPTF protein was also found in NSCLC tissues. Furthermore, BPTF expression was positively correlated with advanced lymph node metastasis (p = 0.002), clinical stage (p = 0.004), and differentiation (p = 0.014). Moreover, patients with high BPTF expression had significantly poorer survival by Kaplan-Meier method (p < 0.001). Finally, Cox regression analyses showed that high BPTF expression might be an independent prognostic parameter to predict poor prognosis (p < 0.05). CONCLUSIONS: BPTF is important in predicting patient outcomes and is a potential target for the development of therapeutic approaches to NSCLC.

Aspiration thrombectomy and intracoronary tirofiban in ST-segment elevation myocardial infarction : Combination treatment for patients undergoing primary percutaneous coronary intervention.

AIM: Primary percutaneous coronary intervention is the most effective treatment for patients with ST-segment elevation myocardial infarction (STEMI). This study aimed to investigate whether the combination of aspiration thrombectomy with intracoronary tirofiban treatment can result in smaller infarcts and better patient prognosis compared with aspiration thrombectomy alone. PATIENTS AND METHODS: In all, 150 patients with STEMI underwent primary percutaneous coronary intervention. Group A received aspiration thrombectomy and group B received a combination treatment of aspiration thrombectomy with intracoronary tirofiban. The endpoint was major adverse cardiovascular events, including myocardial (re)infarction, cardiovascular death, and target vessel revascularization. RESULTS: The clinical characteristics of the groups were not significantly different (p > 0.05). The percentage of patients whose thrombolysis in myocardial infarction (TIMI) myocardial perfusion grades were less than 3 was significantly higher for group B than for group A (13.9 vs. 3.8 %, p = 0.029). The infarct size on cardiac magnetic resonance imaging was significantly different between groups (p = 0.036). At 6 months after the operation, the echocardiography results were better for patients in group B than for those in group A (p = 0.024 and p = 0.016, respectively). The frequency of bleeding complications and major adverse cardiac events of the groups were not significantly different (p > 0.05). CONCLUSION: Aspiration thrombectomy with intracoronary tirofiban in patients with STEMI is safe and effective. For cases with a large angiographic thrombus burden, tirofiban did not increase the rate of bleeding complications or major adverse cardiovascular events.

Effects of 7-bromoethoxybenzene-tetrahydropalmatine on voltage-dependent currents in guinea pig ventricular myocytes.

AIM: To study the anti-arrhythmic mechanism of 7-bromoethoxybenzene-tetrahydropalmatine (EBP). METHODS: Whole-cell current and voltage clamp on isolated guinea pig ventricular cells. RESULTS: EBP 30 mumol.L-1 prolonged APD90 from 430 +/- 47 ms to 514 +/- 61 ms (n = 5, P < 0.05) without effects on the action potential amplitude and resting potential. Delayed outward K+ current and its tail current were blocked by EBP in a concentration-dependent fashion, while EBP did not change the amplitudes of the sodium current, the L type calcium current, and the inwardly rectifying potassium current. CONCLUSION: The mechanism of anti-arrhythmic action of EBP was to prolong the APD through inhibiting the delayed rectified potassium current.

Autoantibodies against ADP/ATP carrier from patients with dilated cardiomyopathy increase activity of voltage-dependent Ca channels in isolated cardiac myocytes.

The effects of autoantibodies against the ADP/ATP carrier, from sera of patients with dilated cardiomyopathy, on calcium channel current (ICa) were studied in enzymatically-isolated guinea pig ventricular myocytes by using a whole cell patch-clamp method. The results showed that the autoantibodies enhanced ICa in a concentration-dependent manner. Verapamil inhibited enhancement of ICa induced by the autoantibodies. Control sera (without the autoantibodies) did not affect ICa. This study suggests that anti-ADP/ATP carrier autoantibodies from sera of patients with dilated cardiomyopathy may enhance ICa and cause calcium overload. Disturbing Ca-channel gating by autoantibodies may contribute to the pathogenesis of dilated cardiomyopathy.

[Modulation of 3,4-diaminopyridine-evoked norepinephrine release from rat hippocampal slices by activation of alpha 2-adrenoceptor].

The effects of the alpha 2-adrenoceptor agonist clonidine and antagonist yohimbine were investigated on 3,4-diaminopyridine(DAP)-evoked [3H]norepinephrine ([3H]NE) release from rat hippocampal slices in the presence and absence of extracellular Ca2+. The slices were preincubated with [3H]NE and superfused in the presence of desipramine 1 mumol.L-1.[3H]overflow was evoked by addition of DAP 100 mumol.L-1 for 10 min to the superfusion medium. Clonidine and yohimbine inhibited and enhanced the 3,4-DAP-evoked [3H]NE release in a concentration-dependent manner both in the presence and absence of extracellular Ca2+. The effect of yohimbine was abolished by clonidine and was additive with the effect of ruthenium red. In the presence of extracellular Ca2+ the clonidine effect was not altered by addition of omega-conotoxin GVIA 0.1 mumol.L-1 or by removal of extracellular Ca2+, suggesting that the Ca2+ entry was not involved in the modulatory mechanisms of DAP-evoked [3H]NE release by activation of alpha 2-receptor. In the absence of extracellular Ca2+ the clonidine effect was reduced by the presence of ruthenium red 10 mumol.L-1, supporting the hypothesis that alpha 2-adrenoceptor activation might affect the intracellular mechanism of Ca2+ homeostasis.

[3,4-Diaminopyridine-evoked norepinephrine release from hippocampal in the absence of extracellular calcium].

Slices of rat hippocampus, preincubated with [3H]norepinephrine ([3H]NE), were superfused and stimulated by addition of 3,4-diaminopyridine (3,4-DAP) for 10 min to the superfusion medium. 3,4-DAP-evoked [3H]NE release both in the absence and presence of extracellular Ca2+. 3,4-DAP-evoked Ca(2+)-independent release of [3H]NE was highly sensitive to sodium channel blocker, tetrodotoxin (TTX, 100% inhibition), suggesting that Na+ per se entered into nerve terminals but not depolarization of membrane followed by Ca2+ channel opening is necessary for 3,4-DAP-evoked Ca(2+)-independent release of [3H]NE. Phorbol ester PDB increased by 480% of control and polymyxin B (PMB) decreased 3,4-DAP-evoked [3H]NE release by 94% of control in the absence of extracellular Ca2+ indicating that the alterations of voltage-dependent Ca(2+)-currents into the cells are not involved in the mechanism of the modulation of 3,4-DAP-evoked [3H]NE release by protein kinase C.

[Enhancing effect of protein kinase C activation on high K(+)-induced norepinephrine release].

Raising the concentration of K+ in the superfusion medium increased the release of [3H]norepinephrine ([3H]NE) from rabbit hippocampus slices preincubated with [3H]NE. This evoked [3H]NE release was modulated by presynaptic alpha 2-adrenergic, presynaptic opioid kappa- and A1-adenosine receptors and augmented with increasing K+ concentration (20-120 mmol.L-1). The enhancement or inhibition of this release by activator (phorbol ester) or inhibitor (polymyxin B) of protein kinase C was blocked by tetrodotoxin and reduced with increasing K+ concentration. It was suggested that the Na(+)-influx was involved in the protein kinase C effect on the K(+)-evoked [3H]NE release.

[3,4-Diaminopyridine and 4-aminopyridine evoked neurotransmitter release].

We used 3,4-diaminopyridine (3,4-DAP) and 4-aminopyridine (4-AP) as stimuli for evoking [3H]norepinephrine ([3H]NE) release in rabbit hippocampal slices to investigate the mechanism underlying the aminopyridines evoked [3H]NE release and the effect of protein kinase C activator phorbol ester PDB. 3,4-DAP and 4-AP evoked [3H]NE release were concentration dependent and enhanced by phorbol ester PDB. 4-AP (300 mumol.L-1) evoked [3H]NE release and enhancement of this evoked release by PDB were antagonized by protein kinase C inhibitor polymyxin B and almost abolished by tetrodotoxin. N-ethylmaleimide inhibited the facilitatory effect of PDB on 3,4-DAP evoked [3H]NE release implicating that G-protein is involved in the modulation of evoked [3H]NE release. 3,4-DAP evoked also dopamine release in caudate nucleus, and acetylcholine release in hippocampus suggesting that the mechanism by which 3,4-DAP evoked transmitters release is similar to that of electrical stimulation.

[Effect of extracellular calcium on enhancement of norepinephrine release in hippocampus by phorbol ester].

Rabbit hippocampal slices were preloaded with [3H]norepinephrine ([3H]NE) and superfused with medium. Tetrodotoxin(TTX) inhibited [3H]NE release evoked by high K+, but did not affect on that evoked by Ca(2+)-pulse. The facilitatory effect of phorbol ester (PDB) on high K(+)-evoked [3H]NE release was elevated with increasing extracellular Ca2+ concentration. In the case of Ca(2+)-pulse-evoked [3H]NE release, the enhancement by PDB was decreased with increasing Ca2+ concentration in the extracellular space. It was suggested that the facilitation of Ca(2+)-influx was not involved in the mechanism of action of protein kinase C.