[Analysis of serum lipid level in patients with multiple system atrophy].

OBJECTIVE: To explore the serum levels of lipids and lipoproteins in patients with multiple system atrophy (MSA). METHODS: From July 2009 to June 2014, a total of 62 MSA patients from the neurology department of our hospital were enrolled as the case group and 63 healthy individuals were enrolled as control group. The serum levels of lipids and lipoproteins were compared between two groups and also analyzed according to gender, age and disease subtypes. RESULTS: Compared with the healthy controls, abnormal rates of high density lipoprotein cholesterol (HDL-C), apolipoproteins A (ApoA) and apolipoproteins B (ApoB) in MSA patients were decreased significantly (P<0.01), while there is no difference of abnormal rates in TC, TG and LDL-C. Compared with the healthy controls, the serum total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), LDL-C, ApoA and ApoB levels in MSA patients were decreased significantly (P<0.01). There was no significant difference in TG levels. Compared with female MSA patients, the serum TG and LDL-C in male MSA patients were decreased significantly (P<0.05). Compared with male controls, TC, LDL-C, HDL-C, ApoA and ApoB levels of male MSA patients were decreased significantly (P<0.05) whilst there was no significant difference in TG level (P>0.05). Compared with female controls, the serum TC,TG, HDL-C, ApoA and ApoB levels in female MSA patients were decreased significantly (P<0.05) whilst there was no significant difference in LDL-C (P>0.05). There was no significant difference in lipid levels between elder patients (age over 65) and younger patients (age under 65) (P>0.05). Also no significant difference existed between type C and type P of MSA (P>0.05). No significant relationship between course of disease and lipids was found (P>0.05). CONCLUSION: Serum levels of TC, HDL-C, LDL-C, ApoA and ApoB are decreased in MSA patients but all lipid levels are not related to either disease course or subtype, which may indicate that lipids levels are related to the pathogenesis of MSA.

Advances in application of swept-source optical coherence tomography angiography in diagnosis and treatment of diabetic retinopathy.

Diabetic retinopathy (DR) is the most common microvascular complication of diabetes and one of the leading causes of global blinding. More attention should be paid to the diagnosis, treatment and prognosis of DR. Swept-source optical coherence tomography angiography (SS-OCTA) is a novel imaging technique presented in recent years. It can accurately present the various levels of the retina, choriocapillaris, macula, and the optic papillary microcirculation, which is new to the diagnosis and prognosis of DR. However, SS-OCTA is limited by poor fixation or severe media clouding and is susceptible to motion artefacts and segmentation errors. Future limitations need to be addressed and large prospective trials conducted to refine the relevance of SS-OCTA to DR. The present study reviews the advances in clinical application of SS-OCTA in diagnosis, treatment and prognosis of DR.

Deubiquitinase USP29 correlates RORγt expression and its association with thymoma myasthenia gravis.

OBJECTIVE: The objective of this study was to examine the expression of deubiquitylases USP29 in thymomas with myasthenia gravis (MG) and research associated immunological processes. METHODS: 69 MG patients with thymomas, 21 thymoma patients without MG, and 31 healthy controls were classified into three groups (categories): group with MG-associated thymoma (MG-T), group with non-MG-associated thymoma (NMG-T), and group with healthy controls (HC). In thymomas, the mRNA and protein levels of RORγt and USP29 were examined by real-time reverse transcription polymerase chain reaction (real-time RT-PCR) and western blotting. Th17 cell counts in MG patients with thymomas were investigated by flow cytometry. RESULTS: In MG-related thymomas, the mRNA and protein levels of deubiquitylases USP29 were substantially elevated. USP29 post-transcriptionally regulated RORγt. In MG patients with thymomas, the expression of USP29 was positively linked to the RORγt expression and Th17 cell frequency. CONCLUSION: This work exhibited that the elevated USP29 enhanced RORγt expression, which in turn affected the Th17 cell growth in thymomatous MG. Our data suggest that USP29 might take part in the regulation of RORγt expression and Th17 cell generation and constitute an innovative regulatory function for USP29 in autoimmune disease.

Increased cerebrospinal fluid neurofilament light chain in central nervous system inflammatory demyelinating disease.

BACKGROUND: Central nervous system (CNS) inflammatory demyelinating disease (IDD) is an immune-mediated disease that is pathologically characterized by demyelination and inflammatory infiltration in the CNS and includes clinically isolated syndrome (CIS), multiple sclerosis (MS), and neuromyelitis optica spectrum disorders (NMOSD). IDD is usually characterized by variable symptoms, multivariate imaging, uncertain reactions to treatment, and a variable prognosis, which makes it difficult to diagnose early. In recent years, the role of the neurofilament light chain (NFL), an axonal injury biomarker, in IDD has become increasingly important. We will detect and analyse cerebrospinal fluid (CSF) NFL levels in IDD and normal control patients to determine the significance of NFL in the diagnosis and prognostic prediction of IDD. METHODS: A total of 41 CIS, 34 MS and 73 NMOSD patients and 40 other patients with conditions such as neurosis and migraine with lumbar puncture were enrolled as the patient groups and the normal control (NC) group from the population of in- and outpatients of the Department of Neurology of the Sixth Medical Centre of Chinese People's Liberation Army General Hospital from January 2014 to October 2016. Clinical and neuroimaging features of the patient groups as well as CSF samples from both types of groups were collected, and the NFL levels of CSF were measured by enzyme linked immunosorbent assay. RESULTS: CSF NFL levels in the CIS, MS and NMOSD groups were significantly higher than those in the NC group (P < 0.05, analysis of variance of NFL levels was performed after logarithmic transformation based on 10). There were no statistically significant differences in the CSF NFL levels among the CIS, MS and NMOSD groups (P > 0.05). The NFL levels of CSF in the CIS, MS and NMOSD groups were correlated with the expanded disability status scale score and enhancement in gadolinium-magnetic resonance imaging (all P < 0.05). Gender, oligoclonal band in CSF, aquaporin 4 antibody and 25­hydroxy vitamin D3 [25(OH)D3] in serum were not related to the NFL levels (P > 0.05). CONCLUSION: The NFL level of CSF is conducive to assessing the severity and probable progress of IDD but is not helpful in distinguishing IDD among Chinese.

Vascular endothelial growth factor improves the cognitive decline of Alzheimer's disease via concurrently inducing the expression of ADAM10 and reducing the expression of ß-site APP cleaving enzyme 1 in Tg2576 mice.

Alzheimer's disease (AD) is primarily characterized by the production and deposit of ß-amyloid protein (Aß) in ß-amyloid plaques (APs). On this basis, we investigated whether vascular endothelial growth factor (VEGF), a growth factor with important neuroprotective activity, may provide a therapeutic opportunity for treating AD. We initially found that the expression and production of VEGF was downregulated in the brains of Tg2576 mice during the course of AD development and progression. Restoring VEGF in the brains of Tg2576 mice antagonized the production and deposit of Aß in Tg2576 mice. The addition of VEGF concurrently increased the expression of disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) and decreased the expression of ß-site APP cleaving enzyme 1 (BACE1), which contributes to the enhanced clearance of Aß in vivo. By decreasing the production and deposit of Aß, VEGF improved the cognitive decline of Tg2576 mice. These observations provide a novel implication for VEGF as a therapeutic approach for the treatment of AD.

PGC-1α or FNDC5 Is Involved in Modulating the Effects of Aß1-42 Oligomers on Suppressing the Expression of BDNF, a Beneficial Factor for Inhibiting Neuronal Apoptosis, Aß Deposition and Cognitive Decline of APP/PS1 Tg Mice.

Alzheimer's disease (AD) is generally defined as the aberrant production of ß-amyloid protein (Aß) and hyperphosphorylated tau protein, which are deposited in ß-amyloid plaques (APs) and neurofibrillary tangles (NFTs), respectively. Decreased levels of brain-derived neurotrophic factor (BDNF) have been detected in patients with AD compared to control subjects. However, the underlying molecular mechanisms driving the downregulation of the BDNF remain unknown. Therefore, we explored the mechanisms underlying the regulation of BDNF in the neurons of APP/PS1 transgenic (Tg) mice, an AD experimental model. Using the APP/PS1 Tg mice, we found that BDNF expression was markedly downregualted at the age of 3- and 9-month-old. After cerebroventricular injection (i.c.v) of Aß1-42 oligomers into the mice, BDNF was also found to be decreased, which demonstrated the critical roles of the Aß1-42 oligomers in regulating the expression of BDNF. In neuronal culture, peroxisome proliferators-activated receptor γ coactivator 1α (PGC-1α) and fibronectin type III domain-containing 5 (FNDC5) were found to be downregulated by treatment with the Aß1-42 oligomers. In addition, overexpression of either PGC-1α or FNDC5 reversed the suppressive effects of the Aß1-42 oligomers on the expression of BDNF in neuroblastoma 2a (n2a) cells. More importantly, elevating the levels of PGC-1α, FNDC5 or BDNF in the n2a cells counteracted the effects of the Aß1-42 oligomers on neuronal apoptosis. Additionally, intranasal administration BDNF in the APP/PS1 Tg mice decreased the Aß deposition and reduced the cognitive decline of the mice.