Risk factors of prognosis in older patients with severe brain injury after surgical intervention.

Background: Older patients (aged ≥ 60 years) with severe brain injury have a high mortality and disability rate. The objective of this retrospective study was to assess the clinical risk factors of prognosis in older patients with severe brain injury after surgical intervention and to analyze the prognosis of the surviving group of patients 1 year after discharge.

Methods: Clinical data of older patients with severe brain injury who were admitted to two neurosurgical centers between January 2010 and December 2020 were collected.

The efficacy and safety of several interventions of corticosteroids for CRSwNP patients after endoscope sinus surgery: A protocol for systematic review and network meta-analysis.

Background: Corticosteroid has been a mainstay of chronic rhinosinusitis with nasal polyps (CRSwNP) medical therapy. While endoscopic sinus surgery (ESS) will be performed when patients had failed to respond to maximal medical therapy. Many studies shown that several corticosteroids of interventions (e.

Autophagy Promotes Microglia Activation Through Beclin-1-Atg5 Pathway in Intracerebral Hemorrhage.

Previous study demonstrates that intracerebral hemorrhage (ICH) promotes microglia activation and inflammation. However, the exact mechanism of microglia activation induced by ICH is not clear. In this experiment, microglia autophagy was examined using electron microscopy, conversion of light chain 3(LC3), and monodansylcadaverine (MDC) staining to detect autophagic vacuoles.

Scavenger receptor SRA attenuates TLR4-induced microglia activation in intracerebral hemorrhage.

Scavenger receptor A (SRA) has been shown to participate in the pattern recognition of pathogen infection. However, its role in intracerebral hemorrhage has not been well defined. In this study, we detected SRA and TLR4 expression and inflammatory response of microglia treated with erythrocyte lysate in vitro, and observed the cerebral water content and neurological deficit of ICH mice in vivo.

MicroRNA367 negatively regulates the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage.

Background: Intracerebral hemorrhage (ICH) induces microglial activation and the release of inflammatory cytokines, leading to inflammation in the brain. IRAK4, an essential component of the MyD88-dependent pathway, activates subsets of divergent signaling pathways in inflammation.

Methods: In the experiment, microglia were stimulated with erythrocyte lysates, and then miR-367, IRAK4, NF-ĸB activation and downstream proinflammatory mediator production were analyzed.

Recombinant adenovirus encoding NLRP3 RNAi attenuate inflammation and brain injury after intracerebral hemorrhage.

Numerous evidence have shown that microglia mediated inflammation plays a pivotal role in the development of brain injury after intracerebral hemorrhage (ICH). Therefore anti-inflammation therapy represents a potentially promising approach to ICH. Recently, NLRP3 inflammasome was discovered to facilitate the inflammatory response.

A novel nanoparticle containing neuritin peptide with grp170 induces a CTL response to inhibit tumor growth.

Malignant glioma is among the most challenging of all cancers to treat successfully. Despite recent advances in surgery, radiotherapy and chemotherapy, current treatment regimens have only a marginal impact on patient survival. In this study, we constructed a novel nanoparticle containing neuritin peptide with grp170.

Scavenger receptor SRA attenuates microglia activation and protects neuroinflammatory injury in intracerebral hemorrhage.

Microglia mediated neuroinflammation plays a crucial role in intracerebral hemorrhage (ICH). Therefore, the negative feedback immune mechanism to keep microglia homeostasis and inhibit the related inflammatory injury is important. Scavenger receptor A (SRA), a pattern recognition molecule, is a physiologic negative regulator of immune consequences.

Toll-like receptor-4-mediated autophagy contributes to microglial activation and inflammatory injury in mouse models of intracerebral haemorrhage.

Aims: Much evidence demonstrates that Toll-like receptor-4 (TLR4)-mediated microglial activation is an important contributor to the inflammatory injury in intracerebral haemorrhage (ICH). However, the exact mechanism of TLR4-mediated microglial activation induced by ICH is not clear. In addition, microglial autophagy is involved other forms of nervous system injury.

Regulatory T cells inhibit microglia activation and protect against inflammatory injury in intracerebral hemorrhage.

Numerous evidence demonstrate that microglia mediated inflammatory injury plays a critical role in intracerebral hemorrhage (ICH). Therefore, the way to inhibit the inflammatory response is greatly needed. Treg cells have been shown to play a critical role in immunologic self-tolerance as well as anti-tumor immune responses and transplantation.

Dendritic cells transduced with CPEB4 induced antitumor immune response.

Much evidence leads to the exploration of immunologic approaches for eliminating tumor cells. Cytoplasmic polyadenylation element binding protein 4 (CPEB4) is considered to be a novel therapeutical target for glioblastoma. In this study, we transduced DCs with CPEB4 to explore the immune response in vivo.

Microglial activation with reduction in autophagy limits white matter lesions and improves cognitive defects during cerebral hypoperfusion.

Microglial activation plays a vital role in the pathogenesis of white matter lesions (WMLs) during chronic cerebral hypo perfusion. Autophagy has been associated with both microglia survival and cell death. Yet, the role of autophagy during microglial activation in chronic cerebral ischemia is still unknown.

Sinomenine inhibits microglia activation and attenuates brain injury in intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) causes morbidity and mortality and commonly follows the reperfusion after an ischemic event. Microglial activation mediated cytokine and protease secretion contributes to brain injury in ICH. Previous studies have shown that sinomenine possesses potent immunoregulatory properties.

A novel nanoparticle containing MOG peptide with BTLA induces T cell tolerance and prevents multiple sclerosis.

Accumulative evidence demonstrates that multiple sclerosis (MS) is caused by activation of myelin Ag-reactive CD4+ T cells. Therefore, the CD4+ T cells specific for myelin Ag may be the important therapeutical target of MS. The novel coinhibitory receptor B and T lymphocyte attenuator (BTLA) may have a regulatory role in maintaining peripheral tolerance, however, its role in MS is still unknown.

[Effects of simvastatin on expression of CTGF and α-SMA in renal tubulointerstitium of rats with diabetic nephropathy].

Objective: To investigate the effects of low-dose simvastatin on the expression of connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA) in the renal tubulointerstitium of rats with diabetic nephropathy.

Methods: Sixty male SD rats were randomly divided into three groups: Group C (control group), Group D, in which diabetes was induced by stroptozotocin (STZ) and Group DS, in which STZ-induced diabetic rats were treated with low-dose (no cholesterol-lowering effect) simvastatin. The following parameters were measured after 6 weeks and 12 weeks in each groups, respectively: body weight and kidney weight, 24-h urinary albumin excretion (UAE), biochemical indexes including blood glucose (GLU), low density lipoprotein (LDL), high density lipoprotein (HDL), triglycerides (TG) and serum creatinine (SCr).

Clinical study of plasma thrombomodulin detection.

The purpose of this study was to investigate the clinical value of plasma thrombomodulin (PTM) in different diseases or in different severity or complications of diseases, PTM in 979 patients and 60 healthy controls was determined by ELISA method. The results showed that the PTM level in the control group was 20.40 +/- 7.

Association of uteroglobin G38A polymorphism with IgA nephropathy: a meta-analysis.

Both uteroglobin knockout and antisense transgenic mice develop pathological and clinical features similar to immunoglobulin A (IgA) nephropathy. However, several association studies of uteroglobin G38A polymorphism and IgA nephropathy showed controversial findings. We used meta-analysis to assess the impact of the uteroglobin G38A polymorphism on susceptibility to and progression of IgA nephropathy.

Effects of simvastatin on oxidative stress in streptozotocin-induced diabetic rats: a role for glomeruli protection.

Aims: To study the effects of simvastatin on oxidative stress in rats with early stage diabetic nephropathy.

Methods: 60 male Sprague-Dawley rats were divided into three groups: control group (CN), streptozotocin (STZ)-induced diabetic rats group (DM) and STZ-induced diabetic rats group treated with simvastatin (DM+S). The following parameters were measured at weeks 6 and 12 in similar rats chosen randomly from each group: body and kidney weight, 24-hour urinary albumin excretion (UAE), biochemical indexes including blood glucose (GLU), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides (TG), serum creatinine (SCr), antioxidant enzymes including superoxide dismutase (SOD), glutathione S-transferase (GST), catalase (CAT) in plasma, lipid peroxidation production as malondialdehyde in plasma (MDAp) and erythrocytes (MDAe), morphology parameters such as glomerular volume (GV) and mesangial area/total glomerular area (M/T).

Oxidative stress and damage induced by abnormal free radical reactions and IgA nephropathy.

Objective: To estimate the oxidative stress and oxidative damage induced by abnormal free radical reactions in IgA nephropathy (IgAN) patients' bodies.

Methods: Seventy-two IgA N patients (IgANP) and 72 healthy adult volunteers (HAV) were enrolled in a random control study design, in which the levels of nitric oxide (NO) in plasma, lipoperoxide (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric methods.

Results: Compared with the HAV group, the averages of NO in plasma, and LPO in plasma and in erythrocytes in the IgANP group were significantly increased (P<0.

Abnormal reactions of free radicals and oxidative damages in the bodies of patients with chronic glomerulonephritis.

Objective: To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis.

Methods: Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays.

Results: Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.