Objective To investigate the effects of dienogest on pain relief and inflammation in endometriosis(EMs),as well as its impact on the brain-derived neurotrophic factor(BDNF)/tropo-myosin receptor kinase B(TrkB)and nuclear factor kappa-B(NF-κB)/NOD-like receptor protein 3(NLRP3)inflammatory pathways.Methods An allograft method was used to establish an EMs rat model.The rats were randomly divided into sham-operated group(n=16),model group(n=16),low-dose dienogest group(n=16),medium-dose dienogest group(n=16)and high-dose dienogest group(n=16).After 7 days of treatment,the implantation volume and writhing response frequency were recorded.Enzyme-linked immunosorbent assay(ELISA),reverse transcription-polymerase chain reaction and Western blotting were employed to measure the expression levels of vascular endothelial growth factor(VEGF),inducible nitric oxide synthase(iNOS),interleukin(IL)-6,IL-1β and tumor necrosis factor(TNF)-α in the EMs rat models.Serum levels of BDNF,TrkB,NF-κB and NLRP3 were detected.Results Compared with model group,dinorgestrel significantly reduced ectopic endo-metrial volume and torsion response of EMs(P＜0.05).Compared with model group,dinorgestrel significantly decreased the expression of VEGF,iNOS,IL6,IL-1 β and TNF-α in EMs model(P＜0.05).In addition,compared with model group,dienogest significantly decreased the expressions of BDNF,TrkB,NF-κB and NLRP3 in ectopic endometrium(P＜0.05).Conclusion Dinorgestrel can relieve EMS-related dysmenorrhea and inflammation,and its mechanism of action may be partly mediated by BDNF/TrkB pathway and NF-κB/NLRP3 pathway.

Background::The association and its population heterogeneities between low-density lipoprotein cholesterol (LDL-C) and all-cause and cardiovascular mortality remain unknown. We aimed to examine the dose-dependent associations of LDL-C levels with specific types of cardiovascular disease (CVD) mortality and heterogeneities in the associations among different population subgroups.Methods::A total of 2,968,462 participants aged 35-75 years from China Health Evaluation And risk Reduction through nationwide Teamwork (ChinaHEART) (2014-2019) were included. Cox proportional hazard models and Fine-Gray subdistribution hazard models were used to estimate associations between LDL-C categories (<70.0, 70.0-99.9, 100.0-129.9 [reference group], 130.0-159.9, 160.0-189.9, and ≥190.0 mg/dL) and all-cause and cause-specific mortality.Results::During a median follow-up of 3.7 years, 57,391 and 23,241 deaths from all-cause and overall CVD were documented. We observed J-shaped associations between LDL-C and death from all-cause, overall CVD, coronary heart disease (CHD), and ischemic stroke, and an L-shaped association between LDL-C and hemorrhagic stroke (HS) mortality ( P for non-linearity <0.001). Compared with the reference group (100.0-129.9 mg/dL), very low LDL-C levels (<70.0 mg/dL) were significantly associated with increased risk of overall CVD (hazard ratio [HR]: 1.10, 95% confidence interval [CI]: 1.06-1.14) and HS mortality (HR: 1.37, 95% CI: 1.29-1.45). Very high LDL-C levels (≥190.0 mg/dL) were associated with increased risk of overall CVD (HR: 1.51, 95% CI: 1.40-1.62) and CHD mortality (HR: 2.08, 95% CI: 1.92-2.24). The stronger associations of very low LDL-C with risk of CVD mortality were observed in individuals with older age, low or normal body mass index, low or moderate 10-year atherosclerotic CVD risk, and those without diagnosed CVD or taking statins. Stronger associations between very high LDL-C levels and all-cause and CVD mortality were observed in younger people. Conclusions::People with very low LDL-C had a higher risk of all-cause, CVD, and HS mortality; those with very high LDL-C had a higher risk of all-cause, CVD, and CHD mortality. On the basis of our findings, comprehensive health assessment is needed to evaluate cardiovascular risk and implement appropriate lipid-lowering therapy for people with very low LDL-C.

Objective Intracerebral hemorrhage(ICH),the second most common type of stroke,can cause long-lasting disability in the afflicted patients.The study was conducted to examine the patterns of change in endogenous neural stem cells(eNSCs)and in the regenerative microenvironment after ICH,to observe the relationship between the migration of eNSCs and the pattern of change in the polarization state of immune cells in the microenvironment,and provide a research basis for research on clinical nerve repair.Methods The collagenase injection method was used for modeling.The ICH model was induced in adult female Sprague-Dawley(SD)rats by injecting type Ⅶ collagenase(2 U)into the brain tissue of rats.All the experimental rats weighed 280-300 g.In order to simulate the ICU at different time points,including the acute phase(within 1 week),subacute phase(1-3 weeks),and the chronic phase(over 3 weeks),brain tissues were harvested at 3 day post injection(3 DPI),10 DPI,20 DPI,and 30 DPI to evaluate the modeling effect.Immunofluorescence staining of the brain tissue sections was performed with DCX antibody to observe the pattern of change in the migration of eNSCs in the brain tissue at different time points.Immunofluorescence staining of brain tissue sections was performed with CD206 antibody and CD86 antibody for respective observation of the pattern of change in pro-inflammatory(M1-type)and anti-inflammatory(M2-type)immune cells in the regenerative microenvironment of the brain tissue after ICM.Results Spontaneous ICH was successfully induced by injecting type Ⅶ collagenase into the brain tissue of SD rats.The volume of the hematoma formed started to gradually increase at 3 DPI and reached its maximum at 10 DPI.After that,the hematoma was gradually absorbed and was completely absorbed by 30 DPI.Analysis of the pattern of changes in eNSCs in the brain tissue showed that a small number of eNSCs were activated at 3 DPI,but very soon their number started to decrease.By 10 DPI,eNSCs gradually began to increase.A large number of eNSCs migrated to the hemorrhage site at 20 DPI.Then the number of eNSCs decreased significantly at 30 DPI(P<0.01).Analysis of the immune microenvironment of the brain tissue showed that pro-inflammatory(M1 type)immune cells increased significantly at 10 and 20 DPI(P<0.01)and decreased at 30 DPI.Anti-inflammatory(M2 type)immune cells began to increase gradually at 3 DPI,decreased significantly at 20 DPI(P<0.05),and then showed an increase at 30 DPI.Conclusion After ICH in rats,eNSCs migrating toward the site of ICH first increase and then decrease.The immune microenvironment demonstrates a pattern of change in which inflammation is suppressed at first,then promoted,and finally suppressed again.Inflammation may have a stimulatory effect on the migration of eNSCs,but excessive inflammatory activation has an inhibitory effect on the differentiation and further activation of eNSCs.After ICH,the early stage of repair and protection(10 d)and the subacute phase(20 d)may provide the best opportunities for intervention.

Objective To explore the endovascular treatment of Budd-Chiari syndrome (BCS) in young child. Methods The clinical data of one young child diagnosed with BCS and treated with endovascular therapy were retrospectively analyzed. Results The 23-month-old female suffered from repeated abdominal distension for 3 months and was diagnosed with BCS by vascular ultrasound Doppler and magnetic resonance examination. After confirmation of the diagnosis, endovascular treatment was performed. Then the occluded blood vessels resumed blood stream, urine output increased, and abdominal distension was significant relieved. Conclusions In young children, BCS is rare, the condition is complex, and endovascular therapy is effective.

Objective To explore the neuroprotective mechanism of propofol by comparing the influence of propofol and isoflurane on inflammatory cytokines ( TNF-α、IL-1、ICAM-1 ) in patients with intracranial tumors. Methods One hundred and sixty-eight patients with intracranial neoplasm were randomly divided into two groups:the propofol ( Group P) and isoflurane (Group I),84 cases in each. Patients were given with propofol (3-6 μg·mL-1) by plasma target-controlled infusion or with continuously inhaled isoflurane ( 1%-2%) , respectively. The serum levels of TNF-α, IL-1 and ICAM-1 were detected before anesthesia and at 0,24,and 48 h after operation. Results The serum levels of TNF-α,IL-1 and ICAM-1 were significantly increased after operation as compared to baseline in both groups. The serum level of TNF-α was(69. 11±8. 95) and (76. 26±11.28) μg·mL-1,IL-1 was(21.57±3.19) and (29.58±4.38) ng·L-1,and ICAM-1 was (1.63±0.24)and (1.94±0.29) g·L-1 at 24 h post operation in Group P and Group I,respectively. These inflammatory cytokine levels were significantly higher in group I compared to group P at 24 and 48 h after operation (P<0. 05 or P<0. 01). Conclusion The target-controlled infusion of propofol brings about lower level of inflammatory reaction than isoflurane inhalation in patients with intracranial neoplasm,which may attribute to the mechanism of brain protection against injury.

Objective To evaluate the effect of surgical trauma on the cognitive function and expression of hepcidin and ferroportin 1 (FP1) in hippocampus in aged rats.Methods One hundred male Sprague-Dawley rats,aged 18 months,weighing 400-500 g,were randomly divided into 2 groups with 50 rats in each group:control group (group C) and surgical trauma group (group ST).The rats were anesthetized with chloral hydrate,but underwent no operation in group C.The rats Were anesthetized with chloral hydrate and underwent 30 min of modified exploratory laparotomy in group ST.Ten rats were chosen from each group at 24 h after operation and the cognitive function was assessed using Morris water-maze test for 6 consecutive days.Ten rats were sacrificed on 1st,3rd,5th and 7th days after beginning of Morris water-maze test and brains were removed for determination of hepcidin and FP1 expression in hippocampus by PCR and Western blot.Results Compared with group C,the escape latency was significantly prolonged,the time of staying at the original platform quadrant and frequency of crossing the original platform were decreased on 3rd,4th and 5th days after beginning of Morris water-maze test,and the expression of hepcidin was up-regulated and the expression of FP1 was down-regulated at each time point in group ST (P ＜ 0.05).Conclusion Surgical trauma can decrease the cognitive function in aged rats and the mechanism may be related to up-regulation of hepcidin expression and down-regulation of FP1 expression in hippocampus.

Objective:To compare etomidate in propylene glycol(Eto-PG) with a new galenic preparation of etomidate solved in a lipid emulsion of soya-bean oil(Eto-Lip).Method:Sixty patients were randomly divided into 2 groups:Eto-PG group and Eto-Lip group.The dosage of etomidate was 0.3mg/kg.Hemodynamic change and side effects(pain on iv-injection,involuntary movement, phlebitis, thrombophlebitis etc.) were observed.Result:There were no difference between the two groups in the incidence of involuntary movement.Side effects at the site of injection,both immediate and after operation,were encountered with Eto-PG but were not encountered in the lipid emulsion. Conclusion:Eto-Lip can reduce some undesired side effects without changing its pharmacodynamics.