ObjectiveTo explore the material basis of the "interaction of blood stasis and toxin" mechanism in cerebral ischemia-reperfusion injury， as well as the protective role of Huoxue Huayu Jiedu prescription （HXHYJDF） against ferroptosis. MethodsSixty SPF-grade male SD rats were randomly divided into six groups： sham group， model group， deferoxamine （DFO） group （100 mg·kg^-1）， low-dose HXHYJDF group （4.52 g·kg^-1）， medium-dose HXHYJDF group （9.04 g·kg^-1）， and high-dose HXHYJDF group （18.07 g·kg^-1）， with ten rats in each group. Except for the sham group， the other groups were used to replicate the model of focal cerebral ischemia-reperfusion in the middle cerebral artery of rats by the reforming Longa method. Neurological function was assessed at 1^st， 3^rd， 5^th， and 7^th days post-reperfusion using the modified neurological severity scores （m-NSS）. Brain tissue pathology and the morphology of mitochondria were observed using hematoxylin-eosin （HE） staining and transmission electron microscopy. The contents of malondialdehyde （MDA）， glutathione （GSH）， divalent iron ions （Fe²⁺）， and reactive oxygen species （ROS） in the ischemic cerebral tissue were detected using enzyme-linked immunosorbent assay （ELISA）. Immunohistochemistry and Western blot （WB） were used to detect the expression of iron death marker proteins glutathione peroxidase 4 （GPX4）， ferroportin-1 （FPN1）， transferrin receptor protein 1 （TfR1）， and ferritin mitochondrial （FtMt） in brain tissue. ResultsCompared with the sham group， the mNSS score of the model group was significantly increased （P<0.01）. HE staining showed that the number of neurons in the cortex of brain tissue was seriously reduced， and the intercellular space was widened. The nucleus was fragmented， and the cytoplasm was vacuolated. The results of transmission electron microscopy showed that the mitochondria in the cytoplasm contracted and rounded， and the mitochondrial cristae decreased. The matrix was lost and vacuolated， and the density of the mitochondrial bilayer membrane increased. The results of ELISA showed that the content of GSH decreased significantly （P<0.01）， and the contents of MDA， Fe²⁺， and ROS increased significantly （P<0.01）. The results of immunohistochemistry and WB showed that the expression of GPX4 and FPN1 proteins was significantly decreased （P<0.01）， and the expression of FtMt and TfR1 proteins was significantly increased （P<0.01）. Compared with those of the model group， the m-NSS scores of the high-dose and medium-dose HXHYJDF groups began to decrease on the 3^rd and 5^th days， respectively （P<0.05， P<0.01）. The results of HE and transmission electron microscopy showed that the intervention of HXHYJDF improved the pathological changes of neurons and mitochondria. The results of ELISA showed that the content of GSH in the medium-dose and high-dose HXHYJDF groups increased significantly （P<0.01）， and the contents of MDA， Fe²⁺， and ROS decreased significantly （P<0.05， P<0.01）. The content of GSH in the low-dose HXHYJDF group increased significantly （P<0.01）， and the contents of MDA and ROS decreased significantly （P<0.01）. The results of immunohistochemistry showed that the expression of GPX4 and FPN1 in the high-dose HXHYJDF group increased significantly （P<0.01）， and the expression of FtMt and TfR1 decreased significantly （P<0.01）. The expression of GPX4 and FPN1 in the medium-dose HXHYJDF group increased significantly （P<0.05）， and the expression of TfR1 decreased significantly （P<0.01）. WB results showed that the expression levels of FPN1 and GPX4 proteins in the high-dose， medium-dose， and low-dose HXHYJDF groups were significantly up-regulated （P<0.01）， and the expression levels of FtMt and TfR1 proteins were significantly down-regulated （P<0.01）. ConclusionHXHYJDF can significantly improve neurological dysfunction symptoms in rats with cerebral ischemia-reperfusion injury， improve the pathological morphology of the infarcted brain tissue， and protect the brain tissue of rats with cerebral ischemia-reperfusion injury to a certain extent. Neuronal ferroptosis is involved in cerebral ischemia-reperfusion injury， with increased levels of MDA， Fe²⁺， ROS， and TfR1 and decreased levels of FtMt， FPN1， GPX4， and GSH potentially constituting the material basis of the interaction of blood stasis and toxin mechanism in cerebral ischemia-reperfusion injury. HXHYJDF may exert brain-protective effects by regulating iron metabolism-related proteins， promoting the discharge of free iron， reducing brain iron deposition， alleviating oxidative stress， and inhibiting ferroptosis.

With the incidence rate of female tumors rising year by year and its younger trend,the demand for fertility preservation is increasing.The application of fertility preservation technology in young female tumor patients,as well as its ethical,legal,and psychological aspects,posed certain challenges.The effectiveness and safety of the technology,as well as the ethical and legal issues faced in the implementation process,such as the health of offspring after preserving the patient's fertility,patient reproductive autonomy,and the handling of frozen reproductive materials,were all open to discussion.Fertility preservation was not only related to technology and healthcare,but also involved the psychological and emotional needs of patients and their families.In addition,the laws and regulations on fertility preservation need to be further improved,to better protect the reproductive rights of young tumor patients and provide safe legal protection.

Objective To investigate the effects of the rhein on the mitochondria fission and epithelial-mesenchymal transition(EMT)of breast cancer cells MDA-MB-231.Methods Human breast cancer cells were intervened with rhein,and the cells were divided into control group(0 μmol·L-1),low dose rhein group(100 μmol·L-1),and high dose rhein group(200 μmol·L-1).The proliferation activity of the cells was detected by CCK-8,and migrations was detected by Scratch-healing migration assay.The morphology and distribution of mitochondria were detected by transmission electron microscope,and the expression levels of Dynamin-related protein 1(Drp1),mitofusin2(Mfn2),E-cadherin,Vimentin proteins were detected by Western blot.Results Compared with control group,Rhein significantly reduced the protein expression of Drp1、Vimentin(P<0.05),and increased E-cadherin and Mfn2,thus down-regulating mitochondria fission,inhibiting cell proliferation and migration.High dose Rhein was better than low dose.Conclusion Rhein can inhibit the proliferation and migration of breast cancer cells by reducing the expression of Drp1,Vimentin and up-regulating Mfn2,E-cadherin proteins.

ObjectiveTo observe the effects of five Huoxue Huayu prescriptions on blood lipid metabolism， liver tissue and adenosine triphosphate binding cassette transporter A1 （ABCA1） and peroxisome proliferator-activated receptor γ（PPARγ） expression in New Zealand rabbits with blood stasis syndrome， and to compare their differences in order to provide laboratory evidence for clinical selection of prescriptions and drugs. MethodSeventy New Zealand rabbits were randomly divided into normal group （n=10） and model group （n=60）. The blood stasis syndrome was modeled by the method of starvation+high-fat feed+adrenaline. After the models were successfully established， they were randomly divided into Xuefu Zhuyutang（3.55 g·kg^-1·d^-1） group， Danshenyin（1.962 g·kg^-1·d^-1） group， Shixiaosan（0.56 g·kg^-1·d^-1） group， Huoluo Xiaolingdan（2.80 g·kg^-1·d^-1） group， and Taohong Siwutang（2.66 g·kg^-1·d^-1） group， and were given corresponding compound prescriptions by gavage. The normal group and model group were given the same dose of distilled water. After the treatment of 30 consecutive days， blood was taken from the abdominal aorta to detect the content of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein cholesterol （HDL-C）， low-density lipoprotein cholesterol（LDL-C） and apolipoprotein A1 （ApoA1）. Hematoxylin-eosin（HE） staining was used to observe the changes in liver tissue. Real-time polymerase chain reaction （Real-time PCR） and Western blot were used to detect the mRNA and protein expression of ABCA1 and PPARγ in liver tissue， respectively. ResultCompared with the conditions in the normal group， increased mRNA and protein levels of HDL-C， LDL-C， TG， TC， and PPARγ （P<0.01）， decreased ApoA1 level （P<0.05） and decreased mRNA and protein levels of ABCA1 （P<0.01） were found in the model group. Compared with the conditions in the model group， the HDL-C level in the five Huoxue Huayu prescriptions was lowered （P<0.05）， and lowered TG level in Xuefu Zhuyutang group and Shixiaosan group （P<0.05）， decreased LDL-C and TC levels in Shixiaosan group （P<0.05）， and increased ApoA1 level in the Huoluo Xiaolingdan group （P<0.01） and Taohong Siwutang group （P<0.05） were observed. Furthermore， the mRNA and protein levels of ABCA1 in Xuefu Zhuyutang group， Shixiaosan group， Huoluo Xiaolingdan group and Taohong Siwutang group were elevated （P<0.05， P<0.01）， and the elevated levels were higher than that of Danshenyin group （P<0.05）. The mRNA level of PPARγ in the five Huoxue Huayu prescriptions was reduced （P<0.01）， and its protein level was also decreased in Xuefu Zhuyutang group， Shixiaosan group， Huoluo Xiaolingdan group and Taohong Siwutang group （P<0.01）. ConclusionThe five Huoxue Huayu prescriptions had a certain therapeutic effect on dyslipidemia，which might be achieved by up-regulating the expression of ApoA1 and ABCA1 to promote the production of HDL-C and strengthen the excretion of dysfunctional HDL-C. And Xuefu Zhuyutang had the optimal effect in lowering lipid.

Objective: To analyze the hematological characteristics of a patient with Hb Ottawa in conjunction with β-thalassemia. Methods: Peripheral blood samples from the proband and her parents were collected and subjected to red blood cell analysis and hemoglobin electrophoresis. Genotypes of α- and β-globin genes were also analyzed. Results: The proband and her mother were both heterozygotes for Hb Ottawa and β-thalassemia variant IVS II-654, and presented with typical β-thalassemia trait featuring hypochromic microcytic anemia. An abnormal hemoglobin band was detected upon electrophoresis. Conclusion Co-existence of Hb Ottawa and β-thalassemia may not aggravate the phenotype.

Objective To investigate the clinical value of MRI in the diagnosis of oblique vaginal septum syndrome(OVSS),and to improve the diagnostic level for this disease.Methods Clinical and imaging data of 8 patients (7 adolescent females and 1 female in fertility period)with vaginal septum syndrome were analyzed retrospectively.All participants were evaluated by ultrasound examination before MRI scanning,and 1 of them underwent enhanced MRI scan.Results Among the 8 patients with OVSS,the main findings of MRI includes uterine deformity (4 double uterus,3 mediastinal uterus,1 double angle uterus with uterine septum),oblique vaginal septum (7 right oblique septum and 1 left oblique septum).All subjects presented with ipsilateral renal agenesis,and 4 patients with endometriosis,1 patient with ureteral distortion and ectopic opening and 1 patient with double inferior vena cava.6 patients suffered with hemorrhage in the posterior chamber of oblique septum and 2 patients with empyema.Hemorrhage in the contralateral vagina were observed in 3 cases,while no significant abnormality was found in other 5 cases.Conclusion MRI scan has an important clinical value on the diagnosis of OVSS and can provide crucial information for the optimal individual treatment.

Objective To explore the application value of pulse induced contour cardiac output (PiCCO) monitoring in diagnosis and treatment of patients with neurogenic pulmonary edema (NPE).Methods With review of literature, the data of 4 patients of severe neurological disease complicated by NPE admitted into Department of Critical Care Medicine of Huangshan People's Hospital Affiliated to Wannan Medical College from 2011 to 2013 were retrospectively analyzed and discussed in their PiCCO hemodynamic characteristics and processes of treatment.Results The PiCCO of 4 patients with NPE showed that the extravascular lung water index (EVLWI) was increased significantly (EVLWI was 12 - 42 mL/kg on admission and 10 - 22 mL/kg after hospitalization for 24 hours), all revealing a high permeability pulmonary edema type. The capacity balance of the first 24 hours in the 4 cases was all of positive balance (+1 130, +1 200, +1 750, +1 120 mL respectively). In the treatment, the supplementary colloid was strengthened, the vasoactive drugs such as, dopamine, dobutamine, milrinone, etc were applied to improve the circulatory oxygenation, then the EVLWI was declined; finally the disease situation in 3 cases was improved and one died.Conclusions The clinical diagnosis and treatment of NPE is complex, and many contradictions appear in the therapeutic course. PiCCO monitoring is valuable in early diagnosis, identification of pulmonary edema type, guidance in fluid supplement and vascular active drug application, and assessment of disease severity and prognosis.

BACKGROUND:Tougu Xiaotong Capsule (TGXTC) is a clinical prescription for the treatment of osteoarthritis;however, its mechanism has not been ful y elucidated. Urokinase-type plasminogen activator (uPA) system participating in the degradation of the extracel ular matrix of articular cartilage and hyperplasia of joint synovium plays an important role in the pathological process of osteoarthritis. OBJECTIVE:To investigate the effects of TGXTC medicated serum on the expression of uPA, uPA receptor (uPAR), plasminogen activator inhibitors (PAIs), matrix metal oproteinase-3 (MMP-3), interleukin-1 beta (IL-1β) and tumor necrosis factor-α(TNF-α) in osteoarthritis synovial cel s of rats and to discuss the mechanism by TGXTC medicated serum prevents and cures osteoarthritis. METHODS:Rat models with knee osteoarthritis were established by injecting 4%papain into the knee joint cavity. Primary synoviocytes and osteoarthritis synoviocytes were cultured with col agenase digestion method. The cultured synoviocytes were divided into normal group, model group and TGXTC group. The western blot method was adopted to detect uPA, uPAR, PAI, MMP-3, IL-1βand TNF-αprotein expression of synoviocytes after acting by TGXTC medicated serum for 72 hours. RESULTS AND CONCLUSION:The expression of uPA, uPAR, MMP-3, IL-1βand TNF-αwere decreased, while PAI was increased in the TGXTC group, and there were significant differences when compared with model group. In a word, TGXTC can significantly inhibit the expression of uPA, uPAR, MMP-3, IL-1β, TNF-α, and improve PAI expression in synoviocytes, which may partly explain the mechanism of the treatment of Tougu Xiaotong Capsule on osteoarthritis.

Objective Cerebral ischemic tolerance induced by cerebral ischemic preconditioning has become a hotspot in the researches of ischemic cerebrovascular disease, and its specific mechanism remains to be clarified.This study was to explore the brain protection mechanisms of cerebral ischemic preconditioning by observing the expressions of HIF-1αand VEGF in the cortex area sur-rounding the infarct locus in rats with focal cerebral ischemia /reperfusion ( I/R) after cerebral ischemic preconditioning. Methods A total of 130 male SD rats were randomly divided into three groups:sham operation, middle cerebral artery occlusion, and cerebral is-chemic preconditioning, the animals in the latter two groups subjected to 2, 6, 12, 24, 48 and 72 h of I/R.The expressions of HIF-1α and VEGF at different time points were detected by immunohistochemistry and Western blot. Results In the middle cerebral artery occlusion group, the expressions of HIF-1αand VEGF positive cells and proteins increased at 2 h after I/R, reached the peak at 24 h, and then gradually decreased to and at 72 h, but still higher than in the sham operation group (P<0.05).The expressions of HIF-1αand VEGF positive cells were significantly higher in the cerebral ischemic preconditioning than in the middle cerebral artery occlusion group (all P<0.05), so were the expressions of HIF-1αand VEGF positive proteins in the former group than in the latter (all P<0.05).The sham operation group showed only a little in-crease in the expressions of HIF-1αand VEGF positive cells and proteins. Conclusion Cerebral ischemia reperfusion injury induces the expressions of HIF-1αand VEGF, which can be further upregulated by brain ischemic preconditioning.

Objective To observe the changes of ischemic preconditioning on the expression of hypoxia inducible fac?tor (HIF)-1αand vascular endothelial growth factor (VEGF) in ischemia hippocampus CA1 region after focal cerebral isch?emia/reperfusion (I/R) in rats, and the mechanisms of brain protection from brain ischemia preconditioning (BIP) thereof. Methods The male SD rats were randomly divided into three groups:sham operation (SO) group,middle cerebral artery oc?clusion (MCAO) group and brain ischemia preconditioning (BIP) group. The MCAO group and BIP group were further divid?ed into six subgroups according to perfusion time after I/R including 2 h, 6 h, 12 h, 24 h, 48 h and 72 h. The ischemia pre?conditioning model rats were established. Immunohistochemistry and Western blot assay were used to observe the expres?sions of HIF-1αand VEGF in ischemia hippocampal CA1 region. Results Neurological function deficit was not observed in SO group. Compared with MCAO group, there was a lower neurological function deficit score in BIP group. In MCAO group and BIP group, the expressions of HIF-1αand VEGF positive cells and protein increased at 2 h after I/R, then gradu?ally increased from 6 h to12 h and reached the maximum level at 24 h, then gradually decreased. The levels were still higher at 72 h than those of SO group. The number of HIF-1αand VEGF positive cells and protein were significantly increased in MCAO group and BIP group than that of SO group (P<0.05). The number of HIF-1αpositive cells was higher in BIP group than that in MCAO group except 2 h and 6 h reperfusion groups. The expression of VEGF positive cells, HIF-1αand VEGF protein were significantly higher in BIP group than those in MCAO group at different time points (P < 0.05). Conclusion Ischemic preconditioning plays a protective role in brain, which may be related to up-regulation of HIF-1αand VEGF.