Japan has accumulated much experience in medical education through a long time exploration.Through some reform measures,such as training talent physicians,reforming education systems,choosing core teaching courses,and establishing comprehensive education system,Japanese medical education has been well promoted,which will be helpful to our country's medical education reforms.

The authors analyzed current situation of teachers and students' law consciousness and proposed that we should well know the rights and obligations of the doctor and patient and improve the quality of case history.

We conducted Chinese-English bilingual education on clinical study of medical students and also discussed related problems.Chinese-English bilingual education has very good results in improving professional English study of medical students.

Objective To evaluate the clinical effect of breast implant on congenital mammary dysplasia with mild pigeon chest deformity. Methods From January 2003 to July 2009,10 cases of female mammary dysplasia (between 20 to 31 years of age) underwent breast implant surgery. Subpectoral placement and transaxillary incision were selected. The surgeon marked the range of the operation on the skin, made a 3-4 cm incision in the armpit, separated the tissue until the pectoral lateral margin, cut the pecto-ralis fascia and bluntly created a suitable pocket under the pectoralis major for the implant. After the implant was placed in the pocket, the incision was closed. Results Ten cases of breast implant surgery did not pose the complications of local skin necrosis, infection, implant shift, heart and lungs dysfunction after one year follow-up. The appearance of anterior chest wall deformity was markedly improved. Conclusions The application of breast implant surgery in the treatment of congenital mammary dysplasia with mild pigeon chest deformity should be promoted, because of the double surgical effect of easy performing, minimal surgical damage, perfect breast shape and concealed deformity.

BACKGROUND:There is no effective treatment for muscle atrophy caused by peripheral nerve damage. Skeletal muscle cel s, a structural unit of muscle contraction, can be used for studies on muscle atrophy when cultured in vitro.
OBJECTIVE:To investigate the promotion effect of neuron-secreted factors on the growth of skeletal muscle cel s in vitro.
METHODS:Skeletal muscle cel s primary cultured in vitro were divided into two groups:experimental group with neuron-secreted factors, and control group with common culture medium, respectively. Afterwards, the number of skeletal muscle cel s and expression level of alpha actin were detected by hematoxylin-eosin staining and immunohistochemical staining, respectively.
RESULTS AND CONCLUSION:The number of skeletal muscle cel s and expression level of alpha actin in the experimental group were significantly higher than those in the control group (P<0.05). In conclusion, neuron-secreted factors have the ability of promoting the growth of skeletal muscle cel s and may be helpful for denervated muscle atrophy.

OBJECTIVETo study the clinical features and diagnosis of 7 patients with atypical mantle cell lymphoma (MCL).

METHODSThe 7 MCL patients were misdiagnosed as chronic lymphocytic leukemia (CLL) due to a score of 4 for their immunophenotypes. The clinical features and diagnosis of such patients were retrospectively analyzed.

RESULTSSix patients had superficial lymphadenectasis but their lymph nodes could not be palpated. All 7 patients were as stage IV considering bone marrow infiltration. Scores of immunophenotype of CLL were 4, and interphase fluorescence in situ hybridization (FISH) for t(11;14) were positive in all patients.

CONCLUSIONSome MCL patients have clinical features similar to CLL. Interphase FISH can play an important role in the diagnosis of MCL.

Aged ; Chromosomes, Human, Pair 11 ; genetics ; Chromosomes, Human, Pair 14 ; genetics ; Female ; Humans ; In Situ Hybridization, Fluorescence ; methods ; Lymphoma, Mantle-Cell ; diagnosis ; genetics ; Male ; Middle Aged ; Translocation, Genetic

Objective:To explore the risk factors affecting the occurrence of lower extremity deep venous thrombosis in patients with acute cerebral hemorrhage during intensive care unit (ICU) period.Methods:One hundred and thirty-five patients with acute cerebral hemorrhage who were transferred to ICU of our hospital from December 2016 to August 2019 were enrolled. The clinical data were collected, including gender, age, Glasgow coma scale (GCS) scores, hematoma volume, body mass index (BMI), systolic pressure, D-dimer, activated partial thromboplastin time, surgery before transfer, unplanned surgery during ICU period, and so on. According to occurrence of lower extremity deep venous thrombosis, these patients were divided into thrombosis group and non-thrombosis group; univariate analysis was used to compare the differences in clinical data between the two groups, and multivariate Logistic regression analysis was used to screen the independent risk factors for lower limb deep vein thrombosis, and the predictive efficacy was evaluated using receiver operating characteristic (ROC) curve.Results:Thirteen patients (9.63%) were diagnosed as having lower extremity deep venous thrombosis. There were statistical differences between two groups in GCS scores at admission, hematoma volume, BMI, D-dimer, platelet count, surgery before admission, unplanned surgery during ICU period, and hemostasis treatment ( P<0.05). Results of multivariate Logistic regression analysis showed that BMI, D-dimer, and unplanned surgery during ICU period were independent risk factors for lower extremity deep venous thrombosis ( OR=1.868, 95%CI: 1.147-3.043, P=0.012; OR=1.004, 95%CI: 1.000-1.008, P=0.037; OR=0.019, 95%CI: 0.001-0.446, P=0.014). ROC curve showed the area under the curve by combining these three factors was 0.982 ( P=0.000), with sensitivity of 92.31% and specificity of 96.72%. Conclusion:Acute cerebral hemorrhage patients with high BMI, high D-dimer level, and unplanned surgery during ICU period are more likely to have low extremity deep venous thrombosis during ICU period; these patients should be alerted in clinical process.

Aim To investigate the effect of exogenous growth differentiation factor 11(GDF11)on vascular re-modeling in hypertensive rats through regulating the endoplasmic reticulum stress pathway mediated by lectin-like oxidized low density lipoprotein receptor-1(LOX-1).Methods Rats were randomly divided into control group,model group(Ang Ⅱ-induced hypertension rat model group),r-GDF11 group,Ab-LOX-1 group,r-GDF11+r-LOX-1 group,with 10 rats in each group.The changes of caudal arterial blood pressure in rats were detected by animal non-invasive blood pres-sure meter;the morphology of aortic vessels was evaluated by hematoxylin-eosin(HE)staining;the collagen deposition in aortic tissue was evaluated by Masson staining;the expression of GDF11,LOX-1 and endoplasmic reticulum(ER)stress related proteins in aortic tissues were detected by Western blot.Results Compared with the control group,the blood pressure of rats in the model group was increased,the media thickness(MT)and MT/lumen diameter(LD)of aortic tis-sue were increased,and the LD of aortic tissue was decreased(all P＜0.05);Collagen volume fraction(CVF)value,the expression of glucose regulated protein 78(GRP78)and activating transcription factor 6(ATF6)protein,the ratio of phosphorylated PKR-like endoplasmic reticulum regulating kinase(p-PERK)/PERK and phosphorylated inositol requiring enzyme 1α(p-IRE1α)/IRE1α in aortic tissue were increased(all P＜0.05).Compared with the model group,the blood pressure of rats in the r-GDF11 group and Ab-LOX-1 group was decreased,the MT and MT/LD of aortic tissue were de-creased,and the LD of aortic tissue was increased(all P＜0.05);CVF value,the expression of GRP78 and ATF6 protein,p-PERK/PERK and p-IRE1α/IRE1α in aortic tissue were decreased(all P＜0.05).Compared with the r-GDF11 group,the blood pressure of rats in the r-GDF11+r-LOX-1 group was increased,the MT and MT/LD of aortic tissue were increased,and the LD of aortic tissue was decreased(all P＜0.05);CVF value,the expression of GRP78 and ATF6 protein,the p-PERK/PERK and p-IRE1α/IRE1α in aortic tissue were increased(all P＜0.05).Conclusion Exogenous GDF11 im-proves vascular remodeling in hypertensive rats through inhibiting LOX-1-mediated endoplasmic reticulum stress pathway.

Objective: To explore the effects of hypoxia inducible factor-1α (HIF-1α) on P311 and its influence on the migration of murine epidermal stem cells (ESCs) under hypoxia in vitro. Methods: Two kinds of murine ESCs were isolated and obtained from 15 neonatal wild-type C57BL/6J mice and 5 congeneric source P311 gene knock-out mice, respectively. The first passage of cells were used in the following experiments after morphologic observation and detection of expression of cell surface markers CD71 and CD49f with flow cytometer. (1) After cell scratch assay, according to the random number table (the same dividing method below), ESCs of P311 gene knock-out mice were divided into normoxia group (cells were cultured with complete medium in normoxic carbon dioxide incubator, and the subsequent normoxic treatments were the same) and hypoxia group (cells were cultured in hypoxic carbon dioxide incubator containing 1% oxygen, and the subsequent hypoxic treatments were the same), with 12 inserts in each group. ESCs of wild-type mice were divided into normoxia group, pure hypoxia group, dimethyl sulfoxide (DMSO) control group (2 μL DMSO solvent was added for 1 h of normoxia treatment before hypoxia treatment), HIF-1α inhibitor group (cells were treated with 11 μmol/L HIF-1 inhibitor of 2 μL under normoxia condition for 1 h before hypoxia treatment), HIF-1α stabilizer group (the cells were treated with 2 μmol/L FG-4592 of 2 μL under normoxia condition for 1 h before hypoxia treatment), with 12 inserts in each group. Three inserts of each time point in each group were adopted respectively to measure the residual width of scratch under inverted phase contrast microscope at post scratch hour (PSH) 0 (immediately), 12, 24, and 48. (2) After hypoxia treatment, the protein level of HIF-1α in ESCs of wild-type mice was detected by Western blotting at post hypoxia hour (PHH) 0, 12, 24, and 48. (3) ESCs of wild-type mice were divided into pure hypoxia group, DMSO control group, HIF-1α inhibitor group, and HIF-1α stabilizer group as that of experiment (1) with the same treatment. The mRNA expression of P311 and expression of P311 in ESCs were determined by real-time fluorescent quantitative reverse transcription polymerase chain reaction and immunocytochemical staining, respectively, at PHH 0 (immediately), 12, 24, and 48 (with sample numbers of 12). (4) The second passage of human embryonic kidney 293 (HEK-293) cells were divided into empty vector hypoxia group (cells were cultured under hypoxia condition after being transfected with empty vector plasmid), P311 normoxia group (cells were cultured under normoxia condition after being transfected with P311 reporter gene plasmid), P311 hypoxia group (cells were cultured under hypoxia condition after being transfected with P311 reporter gene plasmid), P311 hypoxia+ HIF-1α inhibitor group (cells which were incubated with HIF-1α inhibitor were cultured under hypoxia condition after being transfected with P311 reporter gene plasmid). The luciferase activity was detected at post culture hour (PCH) 0 and 12, respectively, and then the P311 transcriptional regulatory binding site of HIF-1α and the promoter sequence of P311 were predicted and searched by bioinformatics methods. Data were processed with factorial design variance analysis, one-way analysis of variance, LSD test and Bonferroni correction. Results: (1) The results of ESCs. The cells showed cobblestone-like pattern and different clonal morphology due to the different cell proliferation potential. The proportion of CD71^-CD49f⁺ cells accounted for about 85%. The identification results indicated that the cells showed strong stem cell properties and high purity. Compared with those in cells of normoxia group of P311 gene knock-out mice, the residual widths of scratch of cells in pure hypoxia group were smaller at PSH 12 and 24 (with P values below 0.05), and those in hypoxia group, normoxia group of wild-type mice, DMSO control group, HIF-1α inhibitor group, and HIF-1α stabilizer group were smaller at PSH 12 (with P values below 0.05). Compared with those in cells of normoxia group of wild-type mice, the residual widths of scratch of cells in hypoxia group, pure hypoxia group, and DMSO control group were smaller at PSH 12 and 24 (with P values below 0.05), and the residual width of scratch of cells in HIF-1α stabilizer group was smaller at PSH 12 (P<0.05). Compared with those of cells in pure hypoxia group, the residual widths of scratch of cells in hypoxia group were wider at PSH 12 and 24 (with P values below 0.05), and the residual width of scratch of cells in HIF-1α inhibitor group was wider at PSH 12 (P<0.05), and those of cells in HIF-1α stabilizer group were smaller at PSH 12 and 24 (with P values below 0.05). There was no obvious difference in the width of scratch in cells among the 7 groups (F=19.02, P>0.05). The protein levels of HIF-1α in ESCs of wild-type mice at PHH 0, 12, 24, and 48 were respectively 1.02±0.05, 2.56±0.09, 1.60±0.17, and 1.17±0.03. Compared with that at PHH 0, the protein level of HIF-1α at PHH 12 was significantly enhanced (P<0.01). It began to decline at PHH 24 but was still higher than that at PHH 0 (P<0.05), and the protein level of HIF-1α at PHH 48 was close to the normoxia level (P>0.05). Compared with those of cells in pure hypoxia group, the mRNA expressions of P311 of cells in HIF-1α inhibitor group were significantly decreased at each time point (with P values below 0.05), and those in HIF-1α stabilizer group were significantly increased at PHH 12 and 24 (with P values below 0.05). Compared with those of cells in HIF-1α inhibitor group, the mRNA expressions of P311 of cells in DMSO control group and HIF-1α stabilizer group were significantly increased at PHH 0, 12, and 24 (with P values below 0.05). Compared with those of cells in pure hypoxia group, the expressions of P311 of cells in HIF-1α inhibitor group were significantly decreased at each time point (with P values below 0.05), while those in HIF-1α stabilizer group were significantly increased at PHH 12 and 24 (with P values below 0.05). Compared with those of cells in HIF-1α inhibitor group, the expressions of P311 of cells in DMSO control group and HIF-1α stabilizer group were significantly increased at PHH 12 and 24 (with P values below 0.05). (2) The results of HEK-293 cells. At PCH 0, there was no significant difference in the luciferase activity among cells of empty vector hypoxia group, P311 normoxia group, P311 hypoxia group, and P311 hypoxia+ HIF-1α inhibitor group (F=13.33, P>0.05). At PCH 12, the luciferase activity of cells in P311 hypoxia group was higher than that in empty vector hypoxia group (P<0.01). The luciferase activity of cells in hypoxia group was higher than that in P311 normoxia group (P<0.05), while that of cells in P311 hypoxia+ HIF-1α inhibitor group was lower than that in P311 hypoxia group (P<0.01). Conclusions HIF-1α may increase the migration of murine ESCs through inducing the expression of P311 at the early stage of hypoxia.

The incidence of stroke increases year by year.It seriously affects the quality of life in patients.The pathogenesis of stroke is related to a variety of factors,involving genetic polymorphisms,biochemical mechanisms,and inflammatory effect.Among them,vascular endothelial growth factor (VEGF) has become one of the hotspots of research on the pathogenesis of stroke in recent years.This article reviews the correlation between VEGF gene polymorphism and stroke.