Background Although the detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral load in respiratory specimens has been widely used to diagnose coronavirus disease 2019 (COVID-19), it is undeniable that serum SARS-CoV-2 nucleic acid (RNAemia) could be detected in a fraction of COVID-19 patients. However, it is not clear whether testing for RNAemia is correlated with the occurrence of cytokine storms or with the specific class of patients. Methods This study enrolled 48 patients with COVID-19 admitted to the General Hospital of Central Theater Command, People’s Liberation Army, a designated hospital in Wuhan, China. The patients were divided into 3 groups according to the Diagnosis and Treatment of New Coronavirus Pneumonia (sixth edition) guidelines issued by the National Health Commission of China. Clinical and laboratory data were collected, and the serum viral load and interleukin 6 (IL-6) level were determined. Results Analysis of clinical characteristics of 48 cases of COVID-19 showed that RNAemia was diagnosed only in the critically ill group and seemed to reflect the severity of the disease. Furthermore, the level of the inflammatory cytokine IL-6 in critically ill patients increased significantly, almost 10 times that in other patients. More importantly, the extremely high IL-6 level was closely correlated with the detection of RNAemia (R = 0.902). Conclusions Detectable serum SARS-CoV-2 RNA (RNAemia) in patients with COVID-19 was associated with elevated IL-6 concentration and poor prognosis. Because elevated IL-6 may be part of a larger cytokine storm that could worsen outcome, IL-6 could be a potential therapeutic target for critically ill patients with an excessive inflammatory response.

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Tumor budding is a frequent event in tongue squamous cell carcinoma. It independently predicted prognosis of patients with T1/2 stage tongue squamous cell carcinoma and may be used for routing pathological diagnosis and the decision of elective lymph node dissection.

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While post-stroke dementia has been extensively investigated, the large number of patients with mild cognitive impairment (MCI) following stroke has received less attention, and reports on the longitudinal course of such impairment are inconsistent in their findings. We examined patients with MCI (n = 45) or no cognitive impairment (NCI) (n = 59), based on consensus criteria following detailed neuropsychological assessments and magnetic resonance imaging (MRI) scans, and compared them with healthy control subjects (n = 84), all of whom were assessed at two time points, 3 years apart. The MCI at baseline in this group was judged to be vascular in etiology (vaMCI). Incident dementia was diagnosed in 24.4% of vaMCI and 8.5% of NCI subjects and no control subjects over 3 years, giving a rate of conversion of approximately 8% per year in post-stroke vaMCI. The vaMCI group showed greater decline in logical memory than the NCI group. Within the vaMCI group, those who developed dementia had great decline in language and executive function. Compared with NCI patients, those with vaMCI had more vascular risk factors and more white matter hyperintensities on MRI at baseline, but did not differ in their brain or hippocampal volumes. Neither MRI volumetric measures nor interval cerebrovascular events predicted decline in function. The major determinant of decline and categorical transition was impaired performance at baseline, suggesting that those with mild impairment post-stroke are more vulnerable to subsequent decline.

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Neuroleptic malignant syndrome (NMS) is a rare, idiosyncratic reaction that has been reported in association with both firstand second-generation antipsychotic drugs. Although both the incidence of NMS 1 and NMS-related mortality 2 appear to be declining, the accurate and timely recognition of NMS remains a priority because of its potential severity and its association with long-term neuropsychiatric and physical sequelae.3,4 As classically described, NMS presents with abrupt onset of fever, autonomic instability, extrapyramidal signs (EPS) and altered mental state.

Among voltage-gated Ca 21 channels the non-dihydropyridine-sensitive a1E subunit is functionally less well characterized than the structurally related a1A (v-agatoxin-IVA sensitive, P-/Q-type) and a1B (v-conotoxin-GVIA sensitive, N-type) subunits. In the rat insulinoma cell line, INS-1, a tissue-specific splice variant of a1E (a1Ee) has been characterized at the mRNA and protein levels, suggesting that INS-1 cells are a suitable model for investigating the function of a1Ee.In a1E-transfected human embryonic kidney (HEK-293) cells the a1E-selective peptide antagonist SNX-482 (100 nm) reduces a1Ed-and a1Ee-induced Ba 21 inward currents in the absence and presence of the auxiliary subunits b3 and a2d-2 by more than 80%. The inhibition is fast and only partially reversible. No effect of SNX-482 was detected on the recombinant T-type Ca 21 channel subunits a1G, a1H, and a1I showing that the toxin from the venom of Hysterocrates gigas is useful as an a1E-selective antagonist.After blocking known components of Ca 21 channel inward current in INS-1 cells by 2 mm (1/±)-isradipine plus 0.5 mm v-conotoxin-MVIIC, the remaining current is reduced by 100 nm SNX-482 from 212.4^1.2 pA /pF to 27.6^0.5 pA /pF (n 9). Furthermore, in INS-1 cells, glucose-and KCl-induced insulin release are reduced by SNX-482 in a dose-dependent manner leading to the conclusion that a1E, in addition to L-type and non-L-type (a1A-mediated) Ca 21 currents, is involved in Ca 21 dependent insulin secretion of INS-1 cells.