Goldsteinjain9355

This study was to investigate the clinical characteristics and laboratory parameters of severe fever with thrombocytopenia syndrome (SFTS).

A detailed retrospective analysis of clinical records for SFTS patients was conducted. Fifty-one cases confirmed SFTS virus infected were enrolled. The clinical characteristics and laboratory parameters between survivors and non-survivors were analyzed.

All patients aged between 30 and 80 years were farmers or residing in wooded and hilly areas. All patients occurred between April and October. The major clinical manifestations were fever, fatigue, diarrhea, myalgia, nausea and vomiting. Conscious disturbance, lymph node enlargement and hemorrhage were common. Fatal outcome occurred in 31.4% (16/51) of patients. Compared with survivors group, in non-survivors group, the proportion of consciousness disturbance, age, the levels of AST, LDH, Bun, Cr, PT and APTT were significantly increased, and PLT was significantly decreased. The age, PLT, AST, LDH, Cr, PT and APTT were the risk factors for fatal outcomes. read more Moreover, the age (OR, 1.245; 95% CI, 1.052-1.474) and APTT (OR, 1.095; 95% CI, 1.005-1.192) were the independent risk factors for fatal outcomes. Heteromorphic lymphocyte and hemophagocytosis could be found in SFTS patients, especially the proportion of finding hemophagocytosis was significantly higher in non-survivors group compared with survivors group.

These results suggest SFTS is a systemic infection, the age and APTT can be used as potential predictors referring to severe SFTS cases.

These results suggest SFTS is a systemic infection, the age and APTT can be used as potential predictors referring to severe SFTS cases.

Intracranial angiomatous meningioma (AM) is a rare subtype of meningioma. Here, we investigated the clinical and pathological features of AMs.

We performed a retrospective study of 23 intracranial AMs verified by postoperative pathology at Huashan Hospital North between 2013 and 2018. Clinical data, radiological and pathological findings, and information on treatment and outcomes were collected and analyzed. Additionally, the literature on intracranial AMs was reviewed.

The sample comprised 13 men and 10 women with AMs. The mean age was 54.2 years, and the mean duration of symptoms was 14.9 months. Headache and epilepsy were the most common symptoms. The most common AMs locations were the cerebral convexity and parasagittal/falx region. The rates of vascular signs, homogeneous enhancement, and peritumoral brain edema (PTBE) on magnetic resonance images were high. Histologically, besides typical meningioma cells, AMs had an abundant vascular component and low Ki-67 index. The extent of PTBE was related ted benign biological characteristics despite frequent and severe PTBE, and the extent of PTBE was related to MVD of tumors. Simpson I resection is the best treatment, and the prognosis is usually good after total tumor removal, while gamma knife is recommended for small residual tumor.

It remains unclear why the optimal haemoglobin target is lower in patients with chronic kidney disease (CKD) than in non-CKD persons. Arteriosclerosis and consequent impaired arterial function comprise a central cardiovascular risk mechanism in CKD. We hypothesized that the optimal haemoglobin target depends on its opposing effects on arterial stiffness and pressure pulsatility in CKD.

Arterial stiffness (aortic pulse wave velocity), wave reflection (augmentation index, reflected wave pressure and reflection magnitude), and pressure pulsatility (central systolic and pulse pressure, peripheral pulse pressure, pressure amplification and forward wave pressure) were assessed in 48 dialysis patients.

In established confounder and diabetes adjusted linear regression models, haemoglobin levels were directly associated with arterial stiffness (partial R=0.366, p=0.03) and inversely with central systolic pressure (partial R=-0.344, p=0.04), central pulse pressure (partial R=-0.403, p=0.01), peripheral pulse presoptimal haemoglobin target in dialysis patients is ~11g/dl and determined by its differential and contrasting effects on arterial stiffness and pressure pulsatility.

This study suggests that the optimal haemoglobin target in dialysis patients is ~11g/dl and determined by its differential and contrasting effects on arterial stiffness and pressure pulsatility.

Evidences indicate that the balance between macrophage M1 and M2 polarization is essential for the regulation of pulmonary inflammation during mechanical ventilation (MV). Yes-associated protein (YAP) is a key component of the Hippo pathway and was suggested to regulate macrophage polarization. This study was designed to investigate whether YAP contributes to pulmonary inflammation during MV.

Wild-type and macrophage YAP knockout mice were mechanically ventilated for 12 hours to induce pulmonary injuries. At the end of MV, animals were sacrificed for pulmonary tissue collection and macrophage isolation. In addition, the induction of macrophage polarization was performed in isolated macrophages with or without YAP overexpression in vitro. Pulmonary injuries, YAP expression, macrophage polarization and cytokines were measured.

Here, we show that MV induces lung injury together with pulmonary inflammation as well as upregulated YAP expressions in pulmonary macrophages. In addition, our results indicate that YAP deficiency in macrophages attenuates pulmonary injury, accompanied with decreased production of pro-inflammatory cytokines including IL (interleukin)-1β, IL-6 and tumor necrosis factor-alpha (TNF-α). Moreover, both in vivo and in vitro studies indicate that YAP deficiency enhances M2 polarization while inhibits M1 polarization. In contrast, YAP overexpression inhibits the induction of M2 polarization but improves M1 polarization.

Our results report for the first time that the induction of YAP in macrophages contributes to pulmonary inflammation during MV through the regulation of M1/M2 polarization.

Our results report for the first time that the induction of YAP in macrophages contributes to pulmonary inflammation during MV through the regulation of M1/M2 polarization.