Elevated blood pressure is one of the major contributors to cardiovascular disease and premature death. The exposure to ambient fine particulate matter (PM_2.5) is closely associated with changes in blood pressure, and even short-term exposure to PM_2.5 can lead to an increase in blood pressure. PM_2.5 is a complex mixture that exerts different toxicities and triggers increased blood pressure through various mechanisms. Therefore, in this article, we provided a comprehensive review of published studies on the effects of short-term exposure to PM_2.5 and its components on blood pressure, and elaborated potential mechanisms from four aspects, including oxidative stress and inflammatory response, endothelial dysfunction, autonomic nervous system disorders and hypothalamus-pituitary-adrenal axis activation, and epigenome alteration. Given the limitations of existing research, future prospective studies can be conducted on diverse populations, using more precise exposure measurement methods and multi-omics approaches, to further elucidate the mechanisms underlying the effects of PM_2.5 and its various components on blood pressure. The findings would provide a theoretical foundation for effective protection of public health, particularly vulnerable groups.

Objective:To investigate the effect of bilateral globus pallidus internus deep brain stimulation (GPi-DBS) on motor performance, quality of life, sleep quality, neuropsychological status, and mood in patients with Meige syndrome.Methods:The clinical data of 17 patients with Meige syndrome accepted bilateral GPi-DBS in Department of Neurosurgery, People's Hospital of Peking University from May 2019 to March 2021 were retrospectively analyzed. Established and validated rating scales were used to assess the motor performance, quality of life, sleep quality, neuropsychological status, and mood at baseline, and 1 and 2 years after GPi-DBS.Results:Burke-Fahn-Marsden dystonia rating scale (BFMDRS) motor total scores decreased from 14.4±6.2 at baseline to 4.3±2.2 and 3.5±1.9 at 1 and 2 years after GPi-DBS, with significant differences ( P<0.05). BFMDRS disability total scores decreased from 6.2±4.0 at baseline to 2.8±2.0 and 2.2±1.5 at 1 and 2 years after GPi-DBS, with significant differences ( P<0.05). In 36-item Short-Form Health Survey (SF-36), the scores of physical function, role-physical, general health sub-items at 1 and 2 years after GPi-DBS were significantly higher than those at baseline ( P<0.05). No significant differences were noted in scores of sleep quality, neuropsychological function, or mood scales at 1 and 2 years after GPi-DBS compared with those at baseline ( P>0.05). Conclusion:Bilateral GPi-DBS is effective and safe in Meige syndrome, which can improve dystonic symptom and quality of life without adverse effects on sleep quality, neuropsychological function, or emotional status.

Objective:To explore the pathogenesis of glossopharyngeal neuralgia (GPN) in central nervous system from perspective of brain morphology.Methods:A prospective study was performed. Twenty-seven patients with right primary GPN admitted to Department of Neurosurgery, People's Hospital of Peking University from April 2019 to June 2023 and 27 healthy subjects (controls) matched with age, gender, dominant hand, and education level during the same period were recruited. These patients were divided into GPN with neurovascular compression group ( n=18) and GPN without neurovascular compression ( n=9) based on intraoperative presence of neurovascular compression. SPM8 software based on Matlab R2017b programming platform and VBM8 toolbox were used to process the whole-brain high-resolution 3D-T1 brain structural image data of the participants and analyze the differences in the gray matter volume of each brain region between the 2 groups. Pearson correlation was applied to analyze the correlations of gray matter volumes in brain regions enjoying significant difference with baseline data and pain characteristics of these GPN patients. Results:Compared with controls, patients with GPN had significantly reduced gray matter volumes in the left anterior cingulate gyrus, middle temporal gyrus, transverse temporal gyrus, precentral gyrus, postcentral gyrus, right insula, thalamus, inferior parietal lobule, precentral gyrus, middle temporal gyrus, and inferior temporal gyrus ( P<0.05, FDR corrected). Compared with GPN patients with neurovascular compression, GPN patients without neurovascular compression had significantly reduced gray matter volume in the bilateral anterior cingulate gyrus ( P<0.05, FDR corrected). Changes of gray matter volume in the right insula were negatively correlated with disease duration of GPN patients ( r=-0.521, P=0.005). Conclusion:GPN patients have extensive gray matter atrophy in the brain, which may play an essential role in GPN development and maintenance.

Objective To investigate the distribution characteristics and risk factors of infectious pathogens after open limb fracture surgery.Methods From January 2016 to December 2018,180 patients with open limb fracture admitted to Hangzhou Hospital of Zhejiang Medical and Health Group were selected to observe the infection after operation.Pathogens were isolated and identified by automatic biological analyzer and bacterial identification system,and drug resistance test was carried out by K-B method.Multivariate logistic regression analysis was used to analyze the risk factors of infection after open limb fracture surgery.Results Among 180 cases of open limb fracture,29 cases had postoperative infection,the infection rate was 16.11％.Among 29 cases of post-operative infection,34 strains of pathogenic bacteria were isolated,including 19 strains of Gram-positive bacteria,13 strains of Gram-negative bacteria and 2 strains of fungi.The resistance rate of Staphylococcus aureus to penicillin G was high,and the resistance rate was 80.00％.Univariate analysis showed that there were no statistically significant differences in gender,BMI,injury site,smoking history,hypertension and intraoperative bleeding between the two groups (x2 =0.252,0.416,0.734,0.856,0.572,all P ＞ 0.05).There were statistically significant differences in age,diabetes mellitus,operation time,hospitalization time,wound contamination and drainage tube placement time between the two groups (x2 =21.537,9.664,17.244,15.459,24.327,19.804,all P ＜ 0.05).The single factor analysis showed that age ＞ 60 years old,diabetes mellitus,operation time ＞ 3h,hospitalization time ＞ 14d,wound contamination and drainage tube placement time ＞ 4d were independent risk factors for infection after open limb fracture surgery.Conclusion Postoperative infection rate of open limb fracture is high.Gram-positive bacteria are the main pathogenic bacteria.Postoperative infection is affected by many factors.In order to prevent postoperative infection,specific measures should be taken and antibiotics should be used reasonably in strict accordance with drug sensitivity test.

Objective To investigate the clinical characteristics,early diagnosis,and rational treatments of traumatic renal artery thrombosis or other traumatic emboli.Methods We summarized the clinical data of 10 patients with traumatic renal artery thrombosis or other traumatic emboli.Results Six of ten patients had left renal artery thrombosis,while four of the ten patients had right renal artery thrombosis.Ultrasonography reported a reduced blood flow signal in one patient,and then renal artery embolism was confirmed by enhanced CT.The other nine patients were directly definitely diagnosed as renal artery embolism by enhanced CT.Four patients were treated with low molecular weight heparin calcium,in whom the CT follow-up showed no obvious blood reperfusion in injured kidneys,but the renal function was in normal range.Renal hypertension occurred in two patients,and one of them received nephrectomy because of poorly controlled hypertension with medication.Conclusions Clinical symptoms,signs and laboratory examinations show no specific findings for diagnosis of traumatic renal artery thrombosis.The color Doppler ultrasound is a preliminary screening method for,and an enhanced CT scan is an effective method for,diagnosis of renal artery thrombosis.The early recovery of renal blood circulation is an evidence of effective treatment.Major concerns are supposed to focus on renal function and blood pressure during followup.

Objective To investigate the effect of extremely low frequency-electromagnetic field (ELF-EMF) on bone mesenchymal stem cells (BMSCs) differentiating into neuron like cells in vitro and research its mechanism.Methods BMSCs were collected from rats by means of whole bone marrow adherent.Flow cytometry was used to assay cell surface marker at passage 3.And then,BMSCs were assigned into four groups:ELF-EMF group,ELF-EMF+U0126 (inhibitor) group,U0126 group and control group;cells were induced by medium (2％ DMSO and 200 μmol/L BHA) for 5 h.In the process of neural induction,ELF-EMF group and ELF-EMF+U0126 group were received 10 Hz,500 GS ELF-EMF stimulation.Besides,ELF-EMF+U0126 group and U0126 group were pretreated with 50 μmol/L extracellular signal-regulated kinase (ERK)1/2 inhibitor U0126.The morphology of BMSCs was observed under inverted microscope.The expression of nestin was detected by immunofluorescent staining and Western blotting to identify and determine the differentiation.Western blotting was applied to detect the preotein level of phosphorylase-ERK1/2 after ELF-EMF exposure.Results BMSCs presented a single long spindle morphology,growing with close whirlpoor-like arrangement;CD90 expression rate was up to 97.9％,while that of CD45 only 4.7％.After induction,each group of cells showed similar shape with neuron-like cells gradually.As compared with the other three groups,ELF-EMF group had significantly higher expression levels of nestin and phosphorylatd ERK1/2 detected by immunofluorescent staining and Westem blotting,respectively (P＜0.05).Meanwhile,the expression levels of nestin among the ELF-EMF+U0126 group,U0126 group and control group were not statistically significant (P＞0.05).Conclusion ELF-EMF could promote neuronal differentiation of mesenchymal stem cells via activation of ERK1/2 signaling pathways.

OBJECTIVETo investigate the protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury in rats.

METHODSFocal transient cerebral ischemia-reperfusion injury was induced in male SD rats using modified suture occlusion technique. The rats were randomly divided into 5 groups: Sham group, Model group, Apelin-low dose (A) group, Apelin-middle dose (B) group and Apelin-high dose (C) group. Apelin-13 was injected into lateral cerebral ventricle, and the neurological function score, brain edema, infarct volume, apoptosis, malondialdehyde (MDA), superoxide dismutase (SOD) and extracellular regulated kinase1/2 (ERK1/2) protein were measured.

RESULTSNeurological function scores, percentage of brain water content, infarct volumes and TUNEL-positive cells in B and C groups were lower than those in Model group (P<0.05). The level of MDA in the tissue bomogenate of brain tissue in the surrounding area of ischemia of B and C groups was lower than that of Model group, while the activity of SOD was higher (P<0.05). There was no significant difference in ERK1/2 protein expression among the groups (P>0.05). P-ERK1/2 increased in Model group and A, B, and C groups compared with Sham group (P<0.05), and that of A, B, and C group was higher than that of Model group (P<0.05).

CONCLUSIONApelin-13 may play an important role by inhibiting oxidative stress to protect against focal cerebral ischemia-reperfusion injury; ERK1/2 signaling pathway may be involved in the protective mechanism of Apelin-13.

Animals ; Apoptosis ; Brain Edema ; Brain Ischemia ; drug therapy ; Intercellular Signaling Peptides and Proteins ; pharmacology ; Male ; Malondialdehyde ; metabolism ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; drug therapy ; Signal Transduction ; Superoxide Dismutase ; metabolism

Objective To investigate the protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury in rats. Methods Focal transient cerebral ischemia-reperfusion injury was induced in male SD rats using modified suture occlusion technique. The rats were randomly divided into 5 groups: Sham group, Model group, Apelin-low dose (A) group, Apelin-middle dose (B) group and Apelin-high dose (C) group. Apelin-13 was injected into lateral cerebral ventricle, and the neurological function score, brain edema, infarct volume, apoptosis, malondialdehyde (MDA), superoxide dismutase (SOD) and extracellular regulated kinase1/2 (ERK1/2) protein were measured. Results Neurological function scores, percentage of brain water content, infarct volumes and TUNEL-positive cells in B and C groups were lower than those in Model group (P<0.05). The level of MDA in the tissue bomogenate of brain tissue in the surrounding area of ischemia of B and C groups was lower than that of Model group, while the activity of SOD was higher (P<0.05). There was no significant difference in ERK1/2 protein expression among the groups (P>0.05). P-ERK1/2 increased in Model group and A, B, and C groups compared with Sham group (P<0.05), and that of A, B, and C group was higher than that of Model group (P<0.05). Conclusion Apelin-13 may play an important role by inhibiting oxidative stress to protect against focal cerebral ischemia-reperfusion injury; ERK1/2 signaling pathway may be involved in the protective mechanism of Apelin-13.

Objective To investigate the protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury in rats. Methods Focal transient cerebral ischemia-reperfusion injury was induced in male SD rats using modified suture occlusion technique. The rats were randomly divided into 5 groups: Sham group, Model group, Apelin-low dose (A) group, Apelin-middle dose (B) group and Apelin-high dose (C) group. Apelin-13 was injected into lateral cerebral ventricle, and the neurological function score, brain edema, infarct volume, apoptosis, malondialdehyde (MDA), superoxide dismutase (SOD) and extracellular regulated kinase1/2 (ERK1/2) protein were measured. Results Neurological function scores, percentage of brain water content, infarct volumes and TUNEL-positive cells in B and C groups were lower than those in Model group (P<0.05). The level of MDA in the tissue bomogenate of brain tissue in the surrounding area of ischemia of B and C groups was lower than that of Model group, while the activity of SOD was higher (P<0.05). There was no significant difference in ERK1/2 protein expression among the groups (P>0.05). P-ERK1/2 increased in Model group and A, B, and C groups compared with Sham group (P<0.05), and that of A, B, and C group was higher than that of Model group (P<0.05). Conclusion Apelin-13 may play an important role by inhibiting oxidative stress to protect against focal cerebral ischemia-reperfusion injury; ERK1/2 signaling pathway may be involved in the protective mechanism of Apelin-13.

Objective To investigate the pathological changes and mechanism in the urethra by parturition-induced stress urinary incontinence.Methods Sprague Dawley female rats underwent vaginal balloon dilation for 4 hours immediately after delivery.One week later,the rats were anesthetized and both ovaries were excised.Then a rat model of stress urinary incontinence (SUI) was successfully established.One month after ovariectomy,conscious cystometry and Leak-Point Pressure (LPP) were measured by MP150.Histological examination and Western blotting were performed after functional assays.Results (1) 85％ of rats presented astress urinary incontinence in the model group.(2) The urethras in SUI rats had decreased muscles,and striated muscles showed fragmentized and disorganized.(3) Elastic fibers were long,well organized and tightly connected to the muscle bundles in sham group,while elastic fibers showed fragmentation and disorganization in the model group.(4) The protein expression of vascular endothelial growth factor (VEGF) and blood vessels were reduced in SUI rats as compared with the sham rats.Conclusions Muscle and elastic fibers in the urethra are disrupted in SUI rat.VEGF may play an important role in regulation of pathological changes in urethra.