Short sleep duration is associated with worse quality of life in Parkinson's disease: A multicenter cross-sectional study.

OBJECTIVE: To characterize sleep duration and investigate its association with quality of life among Parkinson's Disease (PD) patients. METHODS: In this multicenter cross-sectional study, 970 PD patients were divided into five groups based on self-reported sleep duration: <5, ≥5 to <6, ≥6 to <7, ≥7 to ≤8, and >8 h. The quality of life was evaluated using the 39-Item Parkinson's Disease Questionnaire (PDQ-39). Multivariable linear regression analysis, subgroup analysis, and mediation analysis were conducted to examine the association between sleep duration and quality of life. RESULTS: In multivariable linear regression model, patients with sleep duration (<5 h) had significantly higher PDQ-39 scores (ß = 8.132, 95 % CI: 3.99 to 12.266), especially in mobility, activities of daily living, emotional well-being, stigma, social support, cognition, communication, and bodily discomfort (p < 0.05). The association between sleep duration (<5 h) and worse quality of life was more pronounced in patients with higher HY stage, longer disease duration, and sleep disorders. Moreover, a significant indirect effect of sleep duration (<5 h) on quality of life was observed, with UPDRS I, UPDRS II, and UPDRS IV scores acting as mediators. CONCLUSIONS: Short sleep duration (<5 h) is associated with worse quality of life among PD patients. This association was stronger among patients with advanced PD and sleep disorders, while non-motor symptoms and motor complications were identified as significant mediators in this association. These findings highlight the significance of adequate sleep duration and suitable interventions for sleep may help improve quality of life.

Brain Protection Effects of Mild Hypothermia Combined with Distant Ischemic Postconditioning and Thrombolysis in Patients with Acute Ischemic Stroke.

To assess the effectiveness and molecular mechanisms of mild hypothermia and remote ischemic postconditioning (RIPC) in patients with acute ischemic stroke (AIS) who have undergone thrombolysis therapy. A total of 58 AIS patients who received recombinant tissue plasmin activator (rt-PA) intravenous thrombolysis were included in this prospective study. Participants were randomly allocated to the experimental group (rt-PA intravenous thrombolysis plus mild hypothermic ice cap plus remote ischemic brain protection, n = 30) and the control group (rt-PA intravenous thrombolysis plus 0.9% saline, n = 28). The RIPC was performed for 14 consecutive days on both upper limb arteries spaced 2 minutes apart. Five cycles of ischemia-reperfusion were performed sequentially (2-2, 3-3, 4-4, 5-5, 5-0 minutes, respectively). The outcome measures of the National Institute of Health stroke scale (NIHSS) score, volume of cerebral infarction, serum levels of superoxide dismutase (SOD), malondialdehyde (MDA), interleukin-1ß, tumor necrosis factor α, nuclear factors kappa B (NF-κB), and NOD-1ike receptor pyrin 3 (NLRP3) were evaluated at different time points after treatment. Similarly, the 90-day modified Rankin Scale (mRS) scores were compared between the two groups. After treatment, the NIHSS score, MDA, NF-κB, and NLRP3 levels in the experimental group were significantly lower than those in the control group (p < 0.05). While the SOD in the experimental group was significantly higher than in the control group (p < 0.05), the NIHSS scores decreased within groups (all p < 0.05) in both experimental and control groups. The 90-day mRS score (0-2 points) in the experimental group was significantly higher than that in the control group (73.33% vs. 53.57%, p < 0.05) and no significant differences were observed in the safety indices between the two groups (all p > 0.05). Our study shows that combining mild hypothermia and RIPC has a positive effect on brain protection and can significantly reduce the oxidative stress and associated outburst of inflammatory response. The Clinical Trial Registration number is ChiCTR2300073136.

The role of peptidyl-prolyl isomerase Pin1 in neuronal signaling in epilepsy.

Epilepsy is a common symptom of many neurological disorders and can lead to neuronal damage that plays a major role in seizure-related disability. The peptidyl-prolyl isomerase Pin1 has wide-ranging influences on the occurrence and development of neurological diseases. It has also been suggested that Pin1 acts on epileptic inhibition, and the molecular mechanism has recently been reported. In this review, we primarily focus on research concerning the mechanisms and functions of Pin1 in neurons. In addition, we highlight the significance and potential applications of Pin1 in neuronal diseases, especially epilepsy. We also discuss the molecular mechanisms by which Pin1 controls synapses, ion channels and neuronal signaling pathways to modulate epileptic susceptibility. Since neurotransmitters and some neuronal signaling pathways, such as Notch1 and PI3K/Akt, are vital to the nervous system, the role of Pin1 in epilepsy is discussed in the context of the CaMKII-AMPA receptor axis, PSD-95-NMDA receptor axis, NL2/gephyrin-GABA receptor signaling, and Notch1 and PI3K/Akt pathways. The effect of Pin1 on the progression of epilepsy in animal models is discussed as well. This information will lead to a better understanding of Pin1 signaling pathways in epilepsy and may facilitate development of new therapeutic strategies.

Characteristics of Cognitive Impairment and Their Relationship With Total Cerebral Small Vascular Disease Score in Parkinson's Disease.

Background: This study aimed to investigate the characteristics of cognitive dysfunctions and their relationship with total cerebral small vascular disease (CSVD) in Parkinson's disease (PD). Methods: A total of 174 idiopathic PD patients who underwent brain magnetic resonance imaging (MRI) were recruited. Demographic information, vascular disease risk factors, motor function (MDS-UPDRS III score), and cognitive level (MoCA, MMSE) were collected for these patients. The total CSVD burden was scored based on lacunes, enlarged perivascular spaces (EPVS), high-grade white matter hyperintensities (WMH), and cerebral microbleeds (CMBs) for each subject. Results: Cognitive scores on MoCA for language, delayed recall, and orientation were significantly reduced in PD patients with CSVD burden ≥ 1 than in those with CSVD burden = 0. Educational level, PDQ 39, and CSVD burden were significantly associated with MoCA scores in individuals with PD. For the whole group, the full model accounted for 33.6% variation in total MoCA scores. In which, CSVD burden explained 2.7% of the results, and the detection of lacunes, WMH, EPVS, and strictly lobar CMBs were significantly correlated with MoCA scores. The stability of the outcomes was confirmed by sensitivity analysis. Conclusion: CSVD can independently contribute to cognitive decline in PD and cause damage in specific cognitive domains. Promoting neurovascular health may help preserve cognitive functions in PD.

Development of Cationic Cellulose-Modified Bentonite-Alginate Nanocomposite Gels for Sustained Release of Alachlor.

The nanocomposite gel prepared from nanoclay and natural polysaccharides showed a good sustained-release property. Herein, a cationic cellulose-modified bentonite-alginate nanocomposite gel was prepared and used to enhance the sustained release of alachlor. The underlying effect and mechanism of the structure of modified bentonite-alginate nanocomposite gels on the release behavior of alachlor were explored by Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), scanning electron microscopy (SEM), and thermogravimetric (TG) analysis. The results showed that the release of alachlor from the nanocomposite gels was dominated by Fickian diffusion and closely related to the adsorption capacity and permeability of the matrix. The cationic cellulose intercalated into the interlayer space of bentonite through an ion exchange reaction, which significantly enhanced the hydrophobicity of bentonite and its interaction with alachlor. The stacking aggregation of bentonite nanoplatelets and permeability of the gel network were decreased through the electrostatic interaction between cationic cellulose and alginate molecular chains, thus remarkably enhancing the sustained-release property of the nanocomposite gel. The release kinetics revealed that the release rate of alachlor from the nanocomposite gel first decreased and then increased as the content of bentonite and modified bentonite gradually increased. Also, the best sustained-release property of the nanocomposite gel was obtained at bentonite and modified bentonite additions of about 10%, under which the release time of 50% alachlor (T 50) from bentonite-alginate and modified bentonite-alginate nanocomposite gels was 4.4 and 5.6 times longer than the release time from pure alginate gels, respectively.

Cationic starch modified bentonite-alginate nanocomposites for highly controlled diffusion release of pesticides.

To promote the controlled release efficacy of nanocomposites based on alginate and bentonite, (3-chloro-2-hydroxypropyl)trimethyl ammonium grafted starch was prepared and used as modifying agent of the clay. The nanocomposites were characterized by FTIR, XRD, SEM and TG analysis, to reveal the structural effects on the swelling property of the matrix and the release of alachlor, the model compound. Thermodynamics study indicated that the adsorption of alachlor on the bentonite was dominated by hydrophobic interaction with the siloxane surface of the clay and enhanced by the binding of the cationic starch. The electrostatic attraction between alginate and cationic starch bound on the surface also decreased the aggregation of bentonite platelets, leading to a more compact structure of the nanocomposites. The higher adsorption capability and lower permeability of the matrix resulted in a slower release of alachlor, which was dominated by Fickian diffusion mechanism. The release of alachlor first decreased and then increased with increasing content of bentonite and cationic starch modified bentonite in the nanocomposites, reaching a minimum around weight percentage 10%, at which the time taken for 50% of active ingredient to be released were 4.4 and 7.3 times that for the release from pure alginate hydrogel.

A case of ischemic stroke secondary to varicella-zoster virus meningoencephalitis.

Varicella-zoster virus (VZV) lurks in cranial nerves and other brain ganglias after infection. Because middle cerebral artery (MCA) receives the ipsilateral trigeminal ganglia afferent innervations, the reactivated VZV infects the adventitia and intima of cerebral artery wall probably through this way and causes vascular inflammation, finally resulting in artery remodeling, vessel occlusion, and ischemia. In fact, there is a growing clinical recognition that there is an association between VZV reactivation and subsequent stroke. Here, we showed a case of ischemic stroke secondary to varicella-zoster virus meningoencephalitis and reviewed the literature to emphasize the importance of VZV-associated vasculopathy.

Circular RNA circ_0002984 Promotes Cell Proliferation and Migration by Regulating miR-181b-5p/Vascular Endothelial Growth Factor Axis and PI3K-AKT Signaling Pathway in Oxidized Low-Density Lipoprotein-Treated Vascular Smooth Muscle Cells.

ABSTRACT: RNAs (circRNAs) play critical roles in many diseases, including atherosclerosis (AS). However, the role and underlying mechanism of circ_0002984 in AS remain unclear. Vascular smooth muscle cells (VSMCs) treated with oxidized low-density lipoprotein (ox-LDL) were used as a AS cell model. Quantitative real-time polymerase chain reaction was conducted to detect the expression of circ_0002984, miR-181b-5p and vascular endothelial growth factor A (VEGFA). Cell proliferation was evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide assay and 5-ethynyl-2'-deoxyuridine assays. Cell migration was assessed using wound healing assay and transwell assay. All protein levels were analyzed by western blot assay. The interaction between miR-181b-5p and circ_0002984 or VEGFA was confirmed by dual-luciferase reporter, RNA Immunoprecipitation, and RNA pull-down assays. Circ_0002984 and VEGFA were overexpressed, and miR-181b-5p was downregulated in serum of AS patients and ox-LDL-stimulated VSMCs. Circ_0002984 silencing inhibited ox-LDL-induced proliferation and migration in VSMCs. MiR-181b-5p was a target of circ_0002984, and miR-181b-5p inhibition counteracted the suppressing effects of circ_0002984 downregulation on proliferation and migration in ox-LDL-stimulated VSMCs. Additionally, VEGFA was a downstream target of miR-181b-5p and VEGFA upregulation abolished the suppressive influence of miR-181b-5p on proliferation and migration in ox-LDL-exposed VSMCs. Furthermore, circ_0002984 depletion blocked phosphatidylinositol 3 kinase-AKT signaling pathway by regulating miR-181b-5p and VEGFA. Circ_0002984 downregulation suppressed cell proliferation and migration by regulating miR-181b-5p/VEGFA axis and phosphatidylinositol 3 kinase-AKT pathway in ox-LDL-stimulated VEGFA, providing a new mechanism for AS pathogenesis.

HNSC exosome-derived MIAT improves cognitive disorders in rats with vascular dementia via the miR-34b-5p/CALB1 axis.

OBJECTIVE: To explore the molecular mechanism by which hippocampal neural stem cell (HNSC) exosome (exo)-derived MIAT improves cognitive disorders in rats with vascular dementia (VD). METHODS: Rat hippocampal tissues were collected, and HNSCs and hippocampal neuronal cells (HNCs) were isolated, purified, and identified. Then the exosomes (exo) of the HNSCs were extracted and identified. A VD rat model was constructed. HE staining was used to evaluate the hippocampal pathology in each group. The expressions of the RNAs in the HNSCs were intervened, and the cells were then grouped. ELISA was used to measure the of TNF-α, IL-1, and Aß1-42 expression levels. The kits were used to determine the oxidative stress factor levels. The targeting relationships among MIAT, miR-34b-5p, and CALB1 were measured using dual-luciferase assays. The MIAT expressions in exo were measured using qRT-PCR. The proliferation and apoptosis of the HNCs were determined using CCK-8 and Annexin V-FITC/PI staining, respectively. The CALB1, TH, and Bcl-2 protein expressions were determined using Western blot. The Morris water maze test was used for the spatial learning and memory testing. RESULTS: The hippocampal tissues in the model group were clearly damaged, but the pathological characteristics were significantly improved in the exo group. The exo group also showed an increased SOD level, decreased MDA and ROS levels, and down-regulated TNF-α, IL-1, and Aß1-42 expressions (all P<0.05). MiR-34b-5p had a targeting relationship with both MIAT and CALB1, and MIAT was found to be expressed in exo. The oe-MIAT-exo group and the miR-34b-5p inhibitor group showed significantly up-regulated CALB1, TH, and Bcl-2 protein expressions in the HNCs, increased cell viability, as well as reduced apoptosis, but the si-MIAT-exo group showed the opposite results (all P<0.05). The MiR-34b-5p inhibitor partially reversed the effect on the si-MIAT-exo group. The miR-34b-5p mimic group showed significantly down-regulated CALB1, TH, and Bcl-2 protein expressions in the HNCs, inhibited cell viability, as well as increased apoptosis, but the oe-CALB1 group showed the opposite results (all P<0.05). Oe-CALB1 partially reversed the effect on the miR-34b-5p mimic group. The memory and learning abilities of the rats in the oe-MIAT-exo group and the model + exo group were significantly improved but not as much as they were in the normal rats. CONCLUSION: MIAT-containing exo from HNSCs can improve cognitive disorders in VD rats via the miR-34b-5p/CALB1 axis.

Stigma and Associated Correlates of Elderly Patients With Parkinson's Disease.

Background: Stigmatizing experiences is common in Parkinson's disease (PD) and appears to provide a negative contribution to the quality of life. Our aim of this study was to investigate the extent of stigma and its predictive factors in patients with PD from our hospital in Shanghai, China. Methods: In 276 individuals with PD (135 women and 141 men), stigma was measured by the 24-item Stigma Scale for Chronic Illness (SSCI). Multivariate linear regression model was used to assess predictors of stigma including demographics (age and gender), disease duration, stage (Hoehn and Yahr Scale), motor function (Unified Parkinson's Disease Rating Scale Part 3, UPDRS-III), non-motor symptoms (Non-Motor Symptoms Scale, NMSS), cognitive level (Mini-Mental State Examination, MMSE), as well as anxiety (Hamilton Anxiety Rating Scale, HAM-A) and depressive disorders (Hamilton Depression Rating Scale, HAM-D-24). Results: The total score of SSCI was 49.9 ± 14.3, and 48.5% of the patients checked "rarely" to "sometimes." For the total sample, the full model accounted for 47.8% of the variance in stigma (P < 0.05). Higher UPDRS-III scores, longer course of disease, younger age, tremor-dominant subtype, and higher depression scores were significantly associated with stigma among individuals with PD. Conclusion: Our finding suggested a mild-to-moderate level of stigma in patients with PD. Tremor-dominant subtype, longer course of disease, younger age, severe motor symptoms, and depression are the predictors of stigma in PD.

Effects of argatroban therapy for stroke patients: A meta-analysis.

BACKGROUND: The therapeutic efficacy and safety of argatroban for stroke patients remain controversial. The purpose of this study was to collect all evidence and perform a meta-analysis to comprehensively evaluate the effects of argatroban for stroke patients compared with no-argatroban regimens. METHODS: The databases of PubMed, EMBASE and the Cochrane library were searched from their inception up to December 2020. Categorical outcomes were summarized as odds ratio (OR) and 95% confidence interval (CI); while continuous data were pooled as standardized mean difference (SMD) and 95%CI. RESULTS: A total of 11 studies were enrolled. Overall meta-analysis showed infusion of argatroban significantly improved neurological functions of stroke patients compared with control treatment, showing increased National Institutes of Health Stroke Scale (NIHSS) score change (SMD = 1.02; 95% CI, 0.58-1.46, p < 0.001), modified Barthel Index (SMD = 3.81; 95% CI, 2.72-4.89, p < 0.001) as well as a decreased incidence of early neurological deterioration (OR = 0.48; 95% CI: 0.28-0.84, p = 0.01). Argatroban treatment did not increase the risk of symptomatic intracerebral hemorrhage (p = 0.733), asymptomatic intracranial hemorrhage (p = 0.608), gastrointestinal bleeding (p = 0.601), major systemic hemorrhage (p = 0.582) and mortality (p = 0.797), except minor systemic hemorrhage (OR = 2.40; 95% CI: 1.15-5.02, p = 0.020). Subgroup analyses for NIHSS score change and complications obtained the similar conclusions. CONCLUSION: Argatroban infusion may be an effective and safe therapeutic option to improve functional outcomes of stroke patients.

The Pin1-CaMKII-AMPA Receptor Axis Regulates Epileptic Susceptibility.

Pin1 is a unique isomerase that regulates protein conformation and function after phosphorylation. Pin1 aberration contributes to some neurological diseases, notably Alzheimer's disease, but its role in epilepsy is not fully understood. We found that Pin1-deficient mice had significantly increased seizure susceptibility in multiple chemical inducing models and developed age-dependent spontaneous epilepsy. Electrophysiologically, Pin1 ablation enhanced excitatory synaptic transmission to prefrontal cortex (PFC) pyramidal neurons without affecting their intrinsic excitability. Biochemically, Pin1 ablation upregulated AMPA receptors and GluA1 phosphorylation by acting on phosphorylated CaMKII. Clinically, Pin1 was decreased significantly, whereas phosphorylated CaMKII and GluA1 were increased in the neocortex of patients with epilepsy. Moreover, Pin1 expression restoration in the PFC of Pin1-deficient mice using viral gene transfer significantly reduced phosphorylated CaMKII and GluA1 and effectively suppressed their seizure susceptibility. Thus, Pin1-CaMKII-AMPA receptors are a novel axis controlling epileptic susceptibility, highlighting attractive new therapeutic strategies.

Wearing-off Identification in Parkinson's Disease: The shapd-woq Study.

Objectives: To clarify the frequency of wearing-off phenomenon (WO) and the validity of the Chinese version of the 9-item wearing-off questionnaire (CWOQ-9) in WO identification in this large population. Methods: Parkinson's patients treated with antiparkinsonian medications were consecutively recruited into this observational, cross-sectional investigation. Patients completed the CWOQ-9 prior to the independent clinician assessment. Results: A total of 1,385 patients were included in the analysis. The mean age was 69.7 ± 9.5 years and the mean disease duration was 5.8 ± 4.7 years. Clinicians identified WO in 763 patients, with an overall prevalence of 55.1%. In patients within 1 year of disease duration, clinicians diagnosed WO in eight patients, with a percentage of 12.9%. With the disease progression, the WO frequency gradually increased to 76.2% in patients with 10-15 years of disease duration. Then, it slowly decreased at a longer disease duration. The occurrence of WO was closely associated with the disease duration, H&Y staging, and levodopa daily dose. CWOQ-9 identified 1,071 patients (1071/1398, 77.33%) that had WO-related symptoms. The mean CWOQ-9 score was 3.4 ± 1.6. CWOQ-9 corresponded with clinician assessments of WO in 734 of 763 cases; clinicians disagreed with the CWOQ-9 considering the presence of WO in 337 of 1,071 cases. The sensitivity and specificity of CWOQ-9 were 96.2 and 45.8%, respectively. Conclusions: WO occurred frequently at the early and middle stage of PD. CWOQ-9 was qualified as a pre-visiting screening tool for clinicians to better identify WO.

One- and two-photon responsive injectable nano-bundle biomaterials from co-assembled lipopeptides for controlling molecular diffusion.

An injectable biomaterial has been prepared through co-assembly of lipopeptides C4-Bhc-Glu-Glu-NH2 and C14-Phe-Lys-Lys-NH2. This biomaterial contained a large number of nanofibre bundles (nano-bundles, NBs) of lipopeptide co-assemblies and performed like hydrogels. The morphologies of the NBs were observed by transmission electron microscopy (TEM) and atomic force microscopy (AFM). The rheological properties were investigated with a rheometer. Excitingly, the NB biomaterials exhibited shear thinning and self-healing properties, and could be used as injectable biomaterials. The coumarin group in the lipopeptides endowed the NB biomaterials with both ultraviolet (UV, a one photon process) and near-infrared (NIR) light (a two photon process) responsiveness. A small molecule (Doxorubicin, DOX) and a large molecule (bovine serum albumin, BSA) were used as model drugs, and both of them could be encapsulated in the NB biomaterials and could also be released sustainably or explosively under different conditions (with or without one- and two-photon irradiation). DOX and BSA have different release behaviors because of the NBs. Cell assays showed that the co-assembled NB biomaterials exhibited low cytotoxicity to normal cells. However, when DOX was loaded, the NB biomaterials could kill HeLa cells sustainably. Under UV and NIR irradiation, HeLa cells could be killed rapidly because of the burst release of DOX. The co-assembled supramolecular NB biomaterials with dual-responsiveness, tunable rheological properties and multi-drug encapsulating ability might have potential in biomedical engineering.

Light- and pH-Controlled Hierarchical Coassembly of Peptide Amphiphiles.

The coassembly behavior of peptide amphiphiles (PAs) C4-Bhc-EE-NH2 and C14-FKK-NH2 has been investigated by transmission electron microscopy, atomic force microscopy, fluorescence microscopy, circular dichroism, Fourier transform infrared spectroscopy, and 1H nuclear magnetic resonance. These two PAs coassembled into nanofibers by electrostatic and π-π stacking interactions at a low concentration and further aggregated into nanofiber bundles via charge complementation on the surface of nanofibers. As the charge number varied with pH, the bundles could be disassembled/assembled with pH regulation. More interestingly, as C4-Bhc-EE-NH2 was a photodegradable molecule, the bundles could also be responsive to both ultraviolet (UV) and near-infrared (NIR) light. In contrast to the reversible pH-dependent response, the light responses were irreversible as C4-Bhc-EE-NH2 broke under UV or NIR radiation. The highlight of this article is that structural changes were realized for control at the aggregate level, not only at the molecular level. With this inspiration, we hope that we can support the novel biomaterial construction and exploitation of new functions of biomaterials.

[Changes in T helper lymphocytes and their subsets in children with tic disorders].

OBJECTIVE: To explore the changes in T helper lymphocytes and their subsets in children with tic disorders (TD) and their clinical significance. METHODS: Flow cytometry was used to measure the percentages of T helper lymphocytes and their subsets in the peripheral blood of children with TD and healthy children (controls). RESULTS: The percentage of T helper lymphocytes was significantly lower in the TD group than in the control group (P<0.001). The abnormal rate of T helper lymphocytes in the TD group was significantly higher than that in the control group (68.7% vs 18.8%; P<0.001). The percentage of T helper lymphocytes was negatively correlated with Yale Global Tic Severity Scale score (r=-0.3945, P<0.001). As for the subsets of T helper lymphocytes, the TD group had a significantly higher percentage of Th1 cells and a significantly lower percentage of Th2 cells compared with the control group (P<0.001). CONCLUSIONS: The abnormality of T helper lymphocytes and the imbalance of their subsets may be associated with the pathogenesis of TD in children. The percentage of T helper lymphocytes can be used as an indicator for assessing the severity of TD.

UV and NIR dual-responsive self-assembly systems based on a novel coumarin derivative surfactant.

Controllable self-assembly systems have attracted increasing attention in both the academic and industrial fields recently. Herein, we designed and synthesized a new photo-degradable anionic surfactant (PAS) with a coumarin group which could be degraded by both UV and NIR light. Thus, the micelles that are formed by sodium salts of PAS (PAS-Na) could be broken controllably under UV or NIR irradiation. Surface tension measurements, DLS, and Cryo-TEM were adopted to investigate the formation and disruption of PAS-Na micelles. PAS could also form wormlike micelles and vesicles when they co-assembled with common surfactant tetradecyldimethylamine oxide (C14DMAO). These wormlike micelles and vesicles could be degraded by UV and NIR irradiation due to the participation of PAS. Accordingly, the rheology properties of the wormlike micelles and vesicles were also changed significantly. Finally, the stimulus-responsive system was used to control the diffusion of hydrophobic and hydrophilic molecules. And it has shown controllable release effects on both the hydrophobic and hydrophilic molecules.

Selectively driving cholinergic fibers optically in the thalamic reticular nucleus promotes sleep.

Cholinergic projections from the basal forebrain and brainstem are thought to play important roles in rapid eye movement (REM) sleep and arousal. Using transgenic mice in which channelrhdopsin-2 is selectively expressed in cholinergic neurons, we show that optical stimulation of cholinergic inputs to the thalamic reticular nucleus (TRN) activates local GABAergic neurons to promote sleep and protect non-rapid eye movement (NREM) sleep. It does not affect REM sleep. Instead, direct activation of cholinergic input to the TRN shortens the time to sleep onset and generates spindle oscillations that correlate with NREM sleep. It does so by evoking excitatory postsynaptic currents via α7-containing nicotinic acetylcholine receptors and inducing bursts of action potentials in local GABAergic neurons. These findings stand in sharp contrast to previous reports of cholinergic activity driving arousal. Our results provide new insight into the mechanisms controlling sleep.

Transplantation of Schwann cells co-cultured with brain-derived neurotrophic factor for the treatment of experimental autoimmune neuritis.

The aim of this study was to investigate the effects of transplantation of Schwann cells (SCs) co-cultured with brain-derived neurotrophic factor (BDNF) for the treatment of experimental autoimmune neuritis (EAN). Primary SCs were co-cultured with various BDNF concentrations, and the optimum concentration was determined by cell proliferation, and NGF and FGF levels. A rat model of EAN was established by immunization with 400µg of P2 peptide dissolved in Freund's complete adjuvant. SCs were labeled with CFSE and injected into the cisterna magna 14days after immunization. We found proliferation of SCs, and NGF and FGF levels were highest at a BDNF concentration of 50ng/mL. Compared with EAN group, SCs+BDNF group showed the lower paralysis scores from day 34 to day 45, and in sciatic nerves showed a significant decrease in inflammatory cell infiltration (involved CD4-, CD8- and CD68-positive cells) at days 25 and 35, an alleviated demyelination at days 35 and 45, and an increase in S-100-positive cells and a decrease in NGF-positive cells at each time point (P<0.05). Compared with the EAN group, the SCs+BDNF group showed, in sciatic nerves, the mRNA level of NGF was significantly decreased but that of S-100 was increased at day 25, the mRNA level of CCL3 was also remarkably reduced at day 35, and the mRNA level of CD11a, CCL3 and NGF was reduced but that of S-100 was elevated at day 45 (P<0.05). There were no differences in results between the SCs group and EAN group. In the end, we draw the conclusions that the exogenous SCs injected through cisterna magna can migrate to the injured peripheral nerves, BDNF promotes the proliferation and secretory function of SCs in vitro, and BDNF-treated SCs in vivo can reduce paralysis, inflammation, and demyelination and improve the self-repair capability of body in EAN.