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Objective To analyze the distribution of ApoE and SLCO1B1 genetic polymorphisms of patients with cardiovascular and cerebrovascular diseases in Han nationality of Hebei region. Methods Patients with cardiovascular and cerebrovascular diseases admitted to our hospital corresponding department from June 2019 to October 2020 were selected. The polymorphisms of ApoE and SLCO1B1 genes in 4193 patients with cardiovascular and cerebrovascular diseases were detected qualitatively by polymerase chain reaction (PCR)⁃fluorescence probe technique, to analyze the distribution characteristics of polymorphism and compare the genotype distribution difference between male and female. Results The observed mutation frequencies of ApoE and SLCO1B1 gene polymorphism of Han nationality in Hebei region were consistent with the Hardy⁃Weinberg genetic balance. Moreover, there was no significant difference in the distribution of ApoE gene polymorphism at 388T > C and 526C > T and SLCO1B1 gene polymorphism at 388A > G and 521T > C between men and women (P > 0.05). Among the six genotypes of ApoE in Han nationality people, genotype ɛ3/ɛ3 accounted for 68.57% (2875/4193), followed by ɛ3/ɛ4 (15.48%, 649/4193), ɛ2/ɛ3 (12.81%, 537/4193), ɛ2/ɛ4 (1.69%, 71/4193), ɛ4/ɛ4 (0.98%, 41/4193), and ɛ2/ɛ2 (0.48%, 20/4193). There was no significant difference in the distribution of ApoE gene phenotypes between male and female (P=0.223). Among the seven genotypes of SLCO1B1 gene, *1b/*1b and *1a/*1b accounted for the largest proportion 39.57% (1659/4193) and 31.05% (1302/4193), while other genotypes *1b/*15, *1a/*1a, *1a/*15, *15/*15 and *1a/*5 accounted for 14.31% (600/4193), 7.20% (302/4193), 6.42% (269/4193), 1.43% (60/4193) and 0.02% (1/4193) respectively. There was no significant difference in the distribution of SLCO1B1 gene phenotypes between male and female (P=0.078). Conclusions The distribution of ApoE and SLCO1B1 gene polymorphisms is different in patients with cardiovascular and cerebrovascular diseases in Han nationality of Hebei region, and the distribution of ApoE and SLCO1B1 genetic polymorphisms is independent of gender.

Abnormal cholesterol metabolism is an established feature of Alzheimer's disease (AD). Cerebrospinal fluid (CSF) is the fluid surrounding the central nervous system, and the protein and lipid content alterations in the CSF could be biomarkers for degenerative changes in the brain. The laboratory diagnosis of AD is limited to the analysis of three biomarkers in CSF: Aβ42, total tau, and phospho-tau. The purpose of this analysis is to systematically analyze the available data describing the biomarkers of cholesterol and its metabolites in the CSF of subjects with AD. MEDLINE, EMBASE, and the Cochrane Central database were systematically queried to collect studies that have evaluated the markers of cholesterol and its metabolites in the CSF of subjects with mild cognitive impairment (MCI) or AD and age-matched controls. Analysis of the published data shows that the levels of cholesterol are increased in MCI subjects; 24-hydroxycholesterol and 27-hydroxycholesterol are elevated in AD and MCI subjects compared to controls. There is a significant dysfunction of cholesterol metabolism in the CSF of AD subjects. This analysis indicates that in addition to the available biomarkers in the CSF, such as Aβ42, total tau, and phospho-tau, 24-hydroxycholesterol, 27-hydroxycholesterol, and cholesterol appear to be sensitive biomarkers for the evaluation of MCI and AD. [ABSTRACT FROM AUTHOR]

A high-power continuous-wave (CW) laser-diode (LD) pumped acousto-optic Q-switched Nd:YVO4 laser is presented. A short pulse at 1064 nm is obtained. With a repetition rate of 50 kHz, a maximum average output power of 5.72 W is achieved. The optical-conversion efficiency and the slope efficiency are 28% and 32.4%, respectively. At the repetition rate of 10 kHz and the pulse width of 16.3 ns, the maximum single-pulse energy of 286 μJ and the peak power of 13 kW are acquired. The laser can be used as a signal source for free-space optical communication. The output signal agrees well with the modulate signal. © 2004 Wiley Periodicals, Inc. Microwave Opt Technol Lett 42: 281–283, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.20278 [ABSTRACT FROM AUTHOR]

Background: Generalized anxiety disorder (GAD) is a relatively common mental disorder. Recently, inflammation, an important factor for the development of depression, has attracted increasing attention. Several studies have shown that inflammatory cytokines can affect the pathophysiological processes of several nervous system diseases. We hypothesized that there is a correlation between the levels of lipopolysaccharide (LPS)-stimulated inflammatory cytokines and the clinical symptoms of GAD., Aim: To investigate the predictive effect of LPS-stimulated inflammatory cytokines on symptoms of GAD., Methods: This was a cross-sectional study in which 89 patients with GAD diagnosed at The First Hospital of Hebei Medical University from January 2022 to December 2022 and 70 individuals without anxiety and depression (controls) during the same period were included. Fasting venous blood was collected from all the subjects in heparin tubes, and another 3 ml of blood was supplemented with LPS (10 ng/ml). The plasma levels of 12 cytokines [Interleukin (IL)-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, IL-17A, IL-12p70, and IFN-α] were detected., Results: Post-LPS stimulation, the levels of IL-1β, IL-6, IL-8, IL-10, and TNF-α in both the control and GAD groups were significantly elevated above those in the nonstimulated groups, with IL-6 and IL-8 showing marked increases. Increases in IL-8 and TNF-α were statistically significant in the GAD group ( P < 0.05). IL-1β, IL-6, IL-8, IL-10, and TNF-α were found to be significantly correlated with Hamilton Anxiety Rating Scale (HAMA) scores ( P < 0.05). A negative correlation was observed between IL-10 levels and HAMA scores. Further analysis revealed that TNF-α was associated with mental anxiety, whereas IL-1β, IL-8, and IL-10 were associated with physical anxiety symptoms, with IL-10 showing a negative correlation with physical anxiety. IL-6 was associated with both mental and physical aspects of anxiety., Conclusion: The physical symptoms of GAD are related to inflammatory factors. IL-1β, IL-8, IL-10, and TNF-a can be used as predictors of physical or mental anxiety in patients with GAD., Competing Interests: Conflict-of-interest statement: The authors declared that they have no conflicts of interest regarding this work., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

In the aging brain, cognitive function gradually declines and causes a progressive reduction in the structural and functional plasticity of the hippocampus. Transcranial magnetic stimulation is an emerging and novel neurological and psychiatric tool used to investigate the neurobiology of cognitive function. Recent studies have demonstrated that low-frequency transcranial magnetic stimulation (≤1 Hz) ameliorates synaptic plasticity and spatial cognitive deficits in learning-impaired mice. However, the mechanisms by which this treatment improves these deficits during normal aging are still unknown. Therefore, the current study investigated the effects of transcranial magnetic stimulation on the brain-derived neurotrophic factor signal pathway, synaptic protein markers, and spatial memory behavior in the hippocampus of normal aged mice. The study also investigated the downstream regulator, Fyn kinase, and the downstream effectors, synaptophysin and growth-associated protein 43 (both synaptic markers), to determine the possible mechanisms by which transcranial magnetic stimulation regulates cognitive capacity. Transcranial magnetic stimulation with low intensity (110% average resting motor threshold intensity, 1 Hz) increased mRNA and protein levels of brain-derived neurotrophic factor, tropomyosin receptor kinase B, and Fyn in the hippocampus of aged mice. The treatment also upregulated the mRNA and protein expression of synaptophysin and growth-associated protein 43 in the hippocampus of these mice. In conclusion, brain-derived neurotrophic factor signaling may play an important role in sustaining and regulating structural synaptic plasticity induced by transcranial magnetic stimulation in the hippocampus of aging mice, and Fyn may be critical during this regulation. These responses may change the structural plasticity of the aging hippocampus, thereby improving cognitive function.

Neural stem cells (NSCs) are valuable self-renewing cells that can maintain the capacity to differentiate into specific brain cell types. NSCs may repair and even replace the brain tissue, and ultimatley promoting the central nervous system regeneration. Therefore, it is important, for scientists and pjysicians, to study the method for efficient culture and differentiation of NSCs. Our previous study demonstrated that Bone Marrow Stromal Cells (BMSCs) can directly regulate the differentiation of NSCs into neurons, and soluble molecules excreted by BMSCs played a key role in this process. Hereby, we further identified the BMSCs-induced neurons could form the synapses, convey dopamine and express voltage-depend and receptor-depend calcium channels. Moreover, the extracellular signal-regulated protein kinase ERK1/2 pathway was founded to be involved in the process of neuron differentiation and proliferation by the in vitro experiments. Finally, by using protein array, we, for the first time, found that the cytokine-induced neutrophil chemoattractant-3 (CINC-3, a small molecule cytokine) can promote the leukocytes invasion into the inflammation site, and have the ability to induce mesencephal NSCs into neurons. Consequently, these positive findings suggested that our BMSCs-induced culture system could provide a useful tool to investigate the molecular mechanisms of neural differentiation of NSCs, which may be benifical for neurodegenerative diseases in the near future.

Aim: To explore the relationship between the expression of hemeoxygenase-1 (HO-1) and the dopaminergic system impairment in MPTP-treated SAMP8 mice., Methods: 6-month-old male SAMP8 mice received MPTP (20 mg/kg) subcutaneous injection at 2-h intervals for 4 times, and the control group was treated with an equal volume of normal saline. Mice were sacrificed at 6 h, 24 h, 3 d and 8 d after the first injection for the detection of the changes of tyrosine hydroxylase (TH) and HO-1 in the nigrostriatal system by immunohistochemistry and Western blotting., Results: TH-positive neuronal loss was visible at 6 h (14.23%, P<0.05), 24 h (23.85%, P<0.01), 3 d (36.77%, P<0.001), and 8 d (45.90%, P<0.001), and the significant progression of dopaminergic neuronal loss occurred most prominently in the MPTP group from 24 h to 3 d (24 h vs 3 d, P<0.05). There was a significant decrease of striatal TH immunoreactive cells in the MPTP group (P<0.05). Additionally, HO-1 positive cells were detected in striatum just only at 3 d, with the increase of HO-1 protein expression in MPTP groups. Western blot analysis showed no change of HO-1 protein levels in the midbrain after MPTP treatment compared to those of the normal saline group., Conclusion: MPTP caused the loss of dopaminergic neuron number and the decrease of TH protein levels in SAMP8 mice. The up-regulation of HO-1 was ephemeral, and its effects related with Parkinson's disease was limited in this study.

Aim: To investigate the effect of MPP+ on the midbrain neurons of SAMP8 mouse in vitro, which provide the cell model for PD study., Methods: SAMP8 mouse primary midbrain cell cultures were obtained from mice within 1 day after birth. On the sixth day after culturing, the cultures were treated with 100 micromol/L of MPP+ for 6 hours, 9 hours, 12 hours and 24 hours, then the cells were fixed and followed by immunofluorescence or Western blot analysis for the expressed location and the level of TH respectively., Results: MPP+ led to the morphological changes of primary cultured midbrain neurons of SAMP8 mouse. The neurons had intact morphous with strong immunoreactivity, many and long dendrites in control group. Compared with the control group, the neurons had fewer and thinness dendrites with weak immunoreactivity in MPP+ group. MPP+ significantly decreased midbrain neurons numbers with marked decrease of TH protein levels after its treatment for 9 h., Conclusion: MPP+ had neurotoxicity effect on primary cultured midbrain neurons of SAMP8 mouse. Since MPP+ led to marked decrease of neuronal numbers and TH protein levels, it is suggested that MPP+ can cause the DA neuronal degeneration in primary midbrain cell cultures.