Objective To explore the effect of heat shock protein 70(HSP70)expression in the role of Curcumin inhibited staurosporine(STS)-mediated neurons toxic injury.Methods The primary cultured hippocampal neurons was cultured in vitro and the stress damage model of STS-induced nerve cell toxicity was established.The experiment were divided into six groups according to the added drugs:normal control group,the STS model group (final concentration was 20μmol/L),Quercetin+STS model group(final concentration were 10 μmol/L and 20 μmol/L,respectively),Curcumin+STS pretreatment group(for 20μmol/L final concentration),Curcumin+Quercetin+STS treatment group(final concentration were 20μmol/L,10μmol/L and 20μmol/L,respectively)and Curcumin treatment group(final concentration was 20μmol/L).The cell viability were determined by thiazole blue (MTT)method,cell toxicity were measured by lactate dehydrogenase(LDH)release rate and HPS70 expression were detected by Western Blot. Results MTT results showed that the cell viability of Curcumin+STS pretreatment group was significantly higher than STS model group(P<0.001).Compared with Quercetin+STS model group,the cell viability of Curcumin+Quercetin+STS treatment group had little change.LDH results show that the nerve cell toxicity of Curcumin+STS pretreatment group was obviously less than that of STS model group(P<0.001).Western Blot results show that compared with STS model group,HSP70 protein expression in Curcumin+STS pretreatment group was significantly increased(P<0.001).Conclusion Curcumin can inhibit STS-mediated neurons toxicity stress damage though increasing HSP70 expression,when added Quercetin to block HSP70 expression in nerve cells,the inhibiting effect of Curcumin on STS-mediated neuron toxic stress injury is counteract.

Objective: To investigate the feasibility and reliability of the Brockport physical fitness test in visually impaired adolescents in China to determine its applicability in clinical practice and research. Methods: A total of 41 visually impaired adolescents 10-17 years of age were included. Body mass index (BMI), dominant grip strength, modified curl up, trunk lift, shoulder stretch, back saver sit and reach and PACER were tested twice with a 1 week interval by the same tester using the same instrument. Results: Each item in the Brockport physical fitness test was completed. The intraclass correlation coefficients for height, weight, BMI, dominant grip strength, modified curl up, trunk lift, back saver sit and reach (left/right leg straight), and PACER in all subjects were 1.00, 1.00, 1.00, 0.94, 0.75, 0.78, 0.90, 0.87, 0.89, respectively. In blind subjects, the corresponding values were 1.00, 1.00, 1.00, 0.97, 0.80, 0.92, 0.89, 0.87, 0.87, respectively. In low vision subjects, the corresponding values were 1.00 , 1.00, 1.00, 0.90, 0.71, 0.40, 0.89, 0.85, 0.85, respectively. The Cohen kappa values for shoulder stretch (left/right hand on top) were 0.79 and 0.78 in all subjects, 0.72 and 0.64 in blind subjects, and 0.87 and 1.00 in low vision subjects. Conclusion The Brockport physical fitness test is a feasible and reliable physical fitness test for visually impaired adolescents in China, however, trunk lift is not recommended for adolescents with low vision.

Astrocytes are an abundant subgroup of cells in the central nervous system (CNS) that play a critical role in controlling neuronal circuits involved in emotion, learning, and memory. In clinical cases, multiple chronic brain diseases may cause psychosocial and cognitive impairment, such as depression and Alzheimer's disease (AD). For years, complex pathological conditions driven by depression and AD have been widely perceived to contribute to a high risk of disability, resulting in gradual loss of self-care ability, lower life qualities, and vast burden on human society. Interestingly, correlational research on depression and AD has shown that depression might be a prodrome of progressive degenerative neurological disease. As a kind of multifunctional glial cell in the CNS, astrocytes maintain physiological function via supporting neuronal cells, modulating pathologic niche, and regulating energy metabolism. Mounting evidence has shown that astrocytic dysfunction is involved in the progression of depression and AD. We herein review the current findings on the roles and mechanisms of astrocytes in the development of depression and AD, with an implication of potential therapeutic avenue for these diseases by targeting astrocytes.
Alzheimer Disease ; Astrocytes ; Depression ; Humans ; Neurons

OBJECTIVETo identify the MPL L391-V392ins12 spliceosome and analyze its frequencies in patients with myeloproliferative neoplasms (MPN).

METHODSMPL aberrant spliceosome was identified through reverse transcription polymerase chain reaction (RT-PCR)combined with cloning sequencing. The mutation of this spliceosome in 248 MPN patients and 200 normal people was determined by allele-specific polymerase chain reaction (AS-PCR).

RESULTSA novel aberrant spliceosome of MPL gene (MPL L391-V392ins12)was identified, i.e. 36 bp intron was retained between exon7 and exon8, and there were 12 amino acids (EGLKLLPADIPV)inserted. MPL L391-V392ins12 mutation was detected in 19 (7.66%)of the 248 patients with MPN, including 1 (1.92%) of 52 patients with PV, 14 (9.66%) of 145 with ET, and 4 (7.84%) of 51 with PMF. And the mutation was not detected in the group of 200 normal people.

CONCLUSIONMPL L391-V392ins12 spliceosome is an aberrant spliceosome present in the MPN. It can be detected in PV, ET and PMF, and more frequently in ET and PMF. This mutation may play an important role in the process of MPN.

Humans ; Mutation ; Myeloproliferative Disorders ; genetics ; Neoplasms ; genetics ; Polymerase Chain Reaction ; Receptors, Thrombopoietin ; genetics ; Spliceosomes