The specific anti-rat LH in the peroxidase anti-peroxidase (PAP) immunohistochemical method was used to demonstrate the pituitary gonadotropic cells in the pregnant rats, and then the morphometric analysis method was used to study the change of the number, size and nucleo-cytoplasmic ratio parameters of the gonadotropic cells in pregnant rats after being injected by a high dose of LHRH-A.It was observed that on 24h after injection the number of gonadotropic cells decreased, their size became smaller and their nucleo-cytoplasmic ratio larger: the cell number per mm~3 pituitary tissue was from (4.25?0.21)?10~4 to (2.49?0.14)?10~4; the cell size from 1295?35?m~3 to 895?31?m~3; the nucleo-cytoplasmic ratio from 0.144?0.005 to 0.229?0.010. On 48h after injection these changes were in the process of recovery. On 168h after injection all parameters were recovered.Our observations suggest that after being injected by a high dose of LHRH-A the change of gonadotropic cells in pregnant rats results from the exogenous high dose of LHRH-A which has stimulated gonadotropic cells to release a great amount of LH. It is believed, however, that the changes of gonadotropic cells caused by a high dose of LHRH-A can still return to normal.

Objective To investigate the clinical efficacy of exercise cupping plus acupuncture in treating acute lumbar sprain. Method Sixty-four patients with acute lumbar sprain were randomly allocated to treatment and control groups, 32 cases each. The treatment group received exercise cupping plus acupuncture and the control group, acupuncture alone. After one treatment and one course of treatment, the therapeutic effects were evaluated using the VAS for pain, lumbar joint activity and the clinical effect assessment. Result After one course of treatment, the total efficacy rate was 96.9% in the treatment group, which was significantly higher than 84.4% in the control group (P<0.05). After one treatment and one course of treatment, the VAS score was significantly lower in the treatment group than in the control group (P<0.05) and lumbar joint activity improved significantly in the treatment group compared with the control group (P<0.05). Conclusion Exercise cupping plus acupuncture is more effective than acupuncture alone in treating acute lumbar sprain.

Objective To investigate the peroxide effects of iodide excess on mitochondria in Fischer rat thyroid cell line(FRTL) in the early period.Methods After treatment with 0.0 mmol/L(control group) or 0.1 mmol/L potassium iodide(KI) for 2,4 and 24 h,respectively,changes of mitochondrial superoxide formation were assayed by flow cytometry and fluorescence microscopy using mitochondria-targeted hydroethidine(MitoSOX).The cytochrome c (cyt c) released from mitochondria to cytoplasm was detected by immunocytochemistry.The lactate dehydrogenase (LDH) released into supernatant was measured by a LDH kit using colorimetry.The percent of dead cells was assayed by flow cytometry using propidium iodide (PI).DNA with loading buffer was separated in 1％ agarose gel.Results Mitochondrial superoxide production in FRTL cells treated with 0.1 mmol/L KI was increased at 2; 4 and 24 h,especially at 2 h.The rates of cyc c protein immunity positive cells at 2,4 and 24 h in 0.1 mmol/L KI group were (35.3 ± 3.6)％,(45.8 ± 5.5)％ and (30.3 ± 6.1)％,respectively,which were significantly higher than that in control group[(14.8 ± 1.2)％,all P ＜ 0.05].The LDHs released into supernatant at 2,4 and 24 h in 0.1 mmol/L KI group were (1.85 ± 0.32),(6.63 ± 0.42) and (8.35 ± 0.34)U/mg,and these values at 4 and 24 h in 0.1 mmol/L KI group were significantly higher than that of control group[(0.89 ± 0.04)U/mg,all P ＜ 0.05].After incubation with 0.1 mmol/L KI for 2,4 and 24 h,the percentages of dead FRTL cells were 7.52％,9.29％ and 13.71％,respectively,while that of control group was 4.66％.After FRTL cells were treated with 0.1 mmol/L KI for 24 h,DNA ladder appeared.Conclusion Iodide excess (0.1 mmol/L) can cause mitochondrial peroxide injury in FRTL cells at 2 h and cell apoptosis at 24 h.

The specific anti-rat LH, anti-rat FSH and anti-hCG sera were used in the peroxidase antiperoxidase (PAP) immunohistochemical method to observe the change of pituitary gonadotropic cells in pregnant rats after being injected by a high dosage of LHRH-A. It was observed that 24 hrs after injection the immunohistochemical reaction of gonadotropic cells weakened strikingly; 48 hrs after injection the immunohistochemical reaction began to recover; and 168 hrs after injection, the recovery was still in progress. The number of LH cells of different immunoreactive intensity and their percentage in total LH cells of the control and experimental groups were calculated and tested by statistical method. It was found that the results were the same as the above. Our observations support the view that the high dosage of LHRH-A can stimulate gonadotropic cells in rat to release a great amount of LH rapidly. It inhibits the synthesis of progesterone in the ovary of pregnant rat and results in termination of pregnancy. Moreover it is believed that the effect of high dosage of LHRH-A on the secretory function of gonadotropic cells can recover themseleves.

Objective To investigate the roles of myeloid differentiation factor 88 (MyD88) and TIR domain-containing adaptor inducing interferon-β (TRIF) in sepsis-induced myocardial dysfunction, and to analyze whether strain rate (SR) can be early sensitive evaluation for septic heart failure.Methods Sixty-four healthy male C57BL/6 mice were divided into four groups by random number table (n = 16 in each group): sham group, cecum ligation and puncture (CLP)-induced sepsis model group, anti-MyD88 group and anti-TRIF group. The anti-MyD88 group and anti-TRIF group were injected with 5μL/g of anti-MyD88 antibody or anti-TRIF antibody through the tail veins 2 hours before CLP. Eight animals in each group were used to observe the survival of 24 hours, and the other 8 myocardial tissues were harvested for examination. The cardiac function was evaluated by echocardiography before and 6 hours and 12 hours after operation. The mRNA expressions of MyD88, TRIF and inflammatory factors in myocardium were measured by polymerase chain reaction (PCR) at 24 hours after operation, and the degree of neutrophils infiltration was detected by myeloperoxidase (MPO) activity.Results The number of 24-hour survive in anti-MyD88 group and anti-TRIF group were higher than that in CLP group (number: 4, 3 vs. 2,P = 0.044,P = 0.047). Compared with sham group, the cardiac function was significantly decreased, the mRNA expressions of myocardial tissues MyD88, TRIF, interleukin (IL-1, IL-6) and tumor necrosis factor-α (TNF-α) were significantly increased, and the infiltration of neutrophils were obvious in CLP group. Compared with CLP group, the left ventricular short axis fractional shortening rate (FS) and SR were significantly increased after 12 hours in anti-MyD88 group and anti-TRIF group [FS: (49.52±1.78)%, (49.89±1.49)%vs. (41.11±1.63)%, SR (s-1): 17.63±2.16, 17.85±1.64 vs. 12.55±1.84]; the mRNA expressions of MyD88, TRIF and inflammatory factors were significantly decreased [MyD88 mRNA (A value): 0.463±0.046, 0.505±0.048 vs. 0.638±0.102, TRIF mRNA (A value): 0.413±0.031, 0.410±0.021 vs. 0.625±0.057, IL-1 mRNA (A value):0.569±0.101, 0.570±0.091 vs. 0.946±0.171, IL-6 mRNA (A value): 0.551±0.143, 0.431±0.157 vs. 0.850±0.194, TNF-α mRNA (A value): 0.471±0.082, 0.444±0.093 vs. 0.707±0.094]; and the infiltration of neutrophils were significantly decreased [MPO (U/L): 62.34±2.60, 60.87±2.40 vs. 73.83±4.90], with statistically significant differences (allP < 0.05). There was no statistical difference in above parameters between the anti-MyD88 group and anti-TRIF group (allP > 0.05).Conclusions Blocking MyD88 and TRIF expression play significant and similar roles in protecting cardiac deterioration from sepsis by attenuating cytokine release, reducing neutrophil infiltration. SR can sensitively assess septic cardiac dysfunction.

ObjectiveTo investigate the effects of simvastatin preconditioning on the expression of inducible and endothelial nitric oxide synthase ( iNOS,eNOS) in thoracic aorta in a rat model of sepsis.Methods Eighty pathogen-free female Wistar rats aged 4 months weighing 200-250 g were randomly divided into 4 groups:group normal control (group Ⅰ,n =8) ; group sham operation (group Ⅱ,n =8) ; group sepsis (group Ⅲ,n =32) and group simvastatin preconditioning (group Ⅳ,n =32).Sepsis was induced by cecal ligation and puncture (CLP) in groups Ⅲ and Ⅳ.In group Ⅳ simvastatin 20 mg/kg was given via a gastric tube once a day for 2 weeksbefore CLP.The thoracic aorta specimens were taken at 3,6,24 and 48 h after CLP (n =8 at each time point)for detection of iNOS and eNOS protein expression by Western blot analysis.ResultsCLP significantly up-regulated iNOS expression and down-regulated eNOS expression in group Ⅲ as compared with groups Ⅰ and Ⅱ.Simvastatin pretreatment significantly attenuated CLP-induced increase in iNOS expression and decrease in eNOS expression in group Ⅳ as compared with group Ⅲ.ConclusionSimvastatin preconditioning can protect vascular endothelial cells from septic injury by down-regulating iNOS expression and up-regulating eNOS expression in vascular endothelial cells.

Objective To investigate the effect of simvastatin on endothelial cell function in a rat model of sepsis. Methods Ninety-six pathogen-free female Wistar rats aged 4 months weighing 200-250 g were randomly divided into 3 groups (n = 32 each): group sham operation (group Ⅰ ); group sepsis (group Ⅱ )and group simvastatin + sepsis(group Ⅲ ) . Sepsis was induced by cecal ligation and puncture (CLP). In group Ⅲ simvastatin 20 mg/kg was given via a gastric tube once a day for 2 weeks. Blood samples were taken from carotid artery at 3,6, 24 and 48 h ( n = 8 at each time point) for WBC count and measurement of serum E-selectin concentration (by ELISA) . Results CLP significantly increased WBC count and serum E-selectin concentration in group Ⅱ as compared with group Ⅰ . The peak values were reached at 6 h after operation. Simvastatin pretreatment attenuated the sepsis-induced increase in WBC count and serum E-selectin concentration in group Ⅲ. Conclusion Protection of endothelial cell function is involved in the mechanism of treatment of sepsis with simvastatin.

Objective To investigate right ventricular(RV) dyssynchrony in patients with pulmonary hypertension(PH)by strain imaging.Methods Sixty PH patients were divided into three groups according to the pulmonary artery systolic pressure(PASP),20 healthy volunteers served as control group.RV structures parameters included RV end-diastolic area(RVEDA),end-systolic area(RVESA),the ratio of RV diameter and LV diameter(RVTD/LVTD).RV function parameters included RV fractional area change (RVFAC)and Tei index.RV strain parameters included the maxmal differences of the peak systolic strain(Max-ΔPST)and the maxmal differences of the time to peak systolic strain(Max-ΔT_(Q-S))of each segment.Results Compared with control group, Max-ΔT_(Q-S) and Max-ΔPST of PH groups were significantly larger (P<0.01).Max-ΔT_(Q-S) had strong correlations with PASP and RV structure and function parameters(P<0.01).Max-ΔPST had good correlations with PASP and Tei-index(P<0.05,P<0.01).Conclusions PH patients exhibit right ventricular dyssynchrony which correlates with right ventricular function and structure parameters.Right ventricular dyssynchrony parameters could evaluate right ventricular function in PH patients early by strain imaging.

Circular RNA (circRNA) is a novel endogenous noncoding RNA (ncRNA).CircRNA has been widely concerned in recent years and is a hotspot in the field of ncRNA research owing to stable structure,high abundance and organization specificity.More and more studies have shown that circRNA plays a vital role in the regulation of gene expression.It will be more important in the development and progression of neurological diseases.This review will focus on the formation,characteristics and biological functions of circRNA,as well as the possible mechanism by which it modulates neurological diseases.

OBJECTIVEThe exact mechanisms of defect closure in patients with perimembranous ventricular septal defect (PMVSD) remain unknown. We hypothesized that the expression of urokinase type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) may mediate extracellular matrix (ECM) remodeling in aneurysms.

METHODSeven normal heart tricuspid septal leaflet and 33 aneurysms were collected in Shanghai Renji Hospital and Shanghai Children's Medical Center from January 2008 to June 2010. Immunohistochemical expression of uPA and PAI-1 in 4 normal heart valvular tissues and 15 aneurysms was detected with immunohistochemical methods. The expression of uPA and PAI-1 mRNA in 3 normal heart valvular tissues and 7 aneurysms was studied by real time fluorescent PCR; the protein expression of uPA and PAI-1 in 4 normal heart valvular tissues and 11 aneurysms was tested with Western blotting.

RESULTThe surface of the aneurysms were completely covered by endothelial cells. Two types of granulation tissue, myxoid and fibrous, were associated with the aneurismal formation. uPA were recognized predominantly in valvar interstitial cells (VICs) which located mainly in regions adjacent to the endothelium and smooth muscle cells of blood vessels. PAI-1 was found in both VICs which located mainly in granulation tissue and endothelial cells. Nine aneurysms expressed a higher uPA activity than 4 normal valvular tissues ((74.6±11.8)% vs. (49.5±7.4)%; t = 3.87, P = 0.003) and six aneurysms expressed a low uPA activity ((10.3±3.1)% vs. (49.5±7.4)%; t=11.78, P=0.000) and a high PAI-1 activity ((55.2±1.7)% vs. (50.8±3.8)%; t=2.55, P=0.034) using immunohistochemical methods. uPA / PAI-1 ratio of protein expression tested by Western blot was 0.88±0.22 in four normal heart vavular tissues; five aneurysms expressed high uPA activity and low PAI-1 activity and uPA/PAI-1 ratio was 4.26±2.04; while the other 6 cases expressed low uPA activity and high PAI-1 activity and uPA/PAI-1 ratio was 0.30±0.07; the difference among the three groups was statistically significant (P<0.05). The rate of uPA/PAI-1 in relative copy of mRNA expression among normal heart valvular tissue, high uPA expressed aneurysms and low uPA expressed aneurysms are also significantly different (2.14±0.17 vs. 0.45±0.04; 2.14±0.17 vs. 4.38±1.41, P<0.05) respectively.

CONCLUSIONThe expression of uPA and PAI-1 in VICs suggests that interactions among these molecules contribute to the aneurysm formation and development. This provides a potential mechanism for defect closure in patients with PMVSD.

Aneurysm ; pathology ; Blotting, Western ; China ; Endothelial Cells ; cytology ; Extracellular Matrix ; metabolism ; Granulation Tissue ; pathology ; Heart Septal Defects, Ventricular ; pathology ; Humans ; Immunohistochemistry ; Plasminogen Activator Inhibitor 1 ; metabolism ; RNA, Messenger ; Urokinase-Type Plasminogen Activator ; metabolism