Aim To investigate the changes of [Ca2+]i in the pulmonary artery smooth muscle cells of PAH rats induced by MCT.Methods PAH rat model was established by MCT intraperitoneal injection.The PASMCs were primarily cultured and loaded with Fura-2/AM.Effects of Ryanodine receptor agonists on intra-cellular calcium were measured by Fluorescence microscopy Results After being given 10 nmol?L-1 Ryanodine,the concentration of [Ca2+]i in control group increased by(93.31?12.41)nmol?L-1;and the concentration in PAH group increased by(141.71?13.59)nmol?L-1(P

Humans ; Hypertension, Pulmonary ; genetics

AIM: To evaluate the clinical effect and the rotational stability of AcrySof Toric intraocular lens ( IOL ) implantation to correct preexisting corneal astigmatism in cataract surgery.
METHODS: Twenty-three patients ( 28 eyes ) were enrolled from the department of ophthalmology in the first Affiliated Hospital of Nanjing Medical University. All patients underwent similar phacoemulsification procedure combined with AcrySof Toric IOL implantation from June 2012 to December 2013. The uncorrected visual acuity ( UCVA ) , best corrected visual acuity ( BCVA ) , anticipated residual astigmatism, postoperative residual astigmatism, and Toric IOL axis were detected and measured.
RESULTS:Three months after operation, the UCVA of all eyes were 0. 75±0. 16 and the BCVA were 0. 84±0. 15, there was no significant difference between UCVA and BCVA ( t = 1. 036, P>0. 05 ). The anticipated residual astigmatism was ( 0. 28±0. 12 ) D. The actual residual astigmatism after 3mo of the operation was (0. 42±0. 17) D. There was no significant difference between anticipated and actual residual astigmatism (t=1. 259, P>0. 05). The mean axis rotation of Toric IOL was 3. 02o±1.56o (0o-7o) after 1d of operation and 3. 28o±1. 85o (0o-7o) after 3mo. Among all the eyes, 25 eyes ( 89%) rotated <5o, in 3 eyes (11%) rotated 5o-7o.
CONCLUSION: The AcrySof Toric IOL implantation shows good effectiveness, predictability and stability in correcting pre-existing astigmatism in cataract patients.

BACKGROUND: As a reliable marker of inflammation, intercellular adhesion molecule-1 (ICAM-1) plays an important role in atherogenesis. Recently, it is assumed in researches of recent years that chronic inflammation mediated by ICAM-1 is involved in hypertensive left ventricular hypertrophy probably, but there are still some objections reported. Tanshinone ⅡA is a kind of liposoluble extract from danshen(Radix Salviae Mitiorrhizae) . It is verified in animal experiment that it can inhibit hypertensive left ventricular hypertrophy.OBJECTIVE: To investigate the relationship between ICAM-1 and hypertensive left ventricular hypertrophy and the effect of tanshinone ⅡA on expression of ICAM-1.DESIGN:A randomized controlled observation was designed.SETTING: Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology.MATERIALS: The experiment was performed in the Laboratory of Emergency Department of Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology from October 2002 to January 2004. Ten male WKY rats(10 WKY rats) of 12-week-old and 20 rats with spontaneous hypertension(20 SHR rats) were employed and divided into the control group(10 WKY rats), hypertension group(10 SHR rats) and tanshinone ⅡA group(10 SHR rats).injected from caudal vein for treatment and distilled water at the same dose was injected in the other two groups. Twelve weeks later, the rats were sacrificed and myocardium was collected for specimen preparation. Haematoxylin and eosin(HE) staining, VG staining, immunocytochemical staining and myocardial ED1 labeling were applied to determine myocardial macrophage infiltration degree. The reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay(ELISA) were used to determine the expressions of ICAM-1 mRNA and protein.MAIN OUTCOME MEASURES: Degree of macrophages infiltration and the expressions of ICAM-1 mRNA and protein in myocardium in each group.RESULTS: Twelve SHR and 10 WKY rats were employed in the experiment pared with the control group, ICAM-1 mRNA and protein expressions in hypertrophic myocardium were increased significantly in hypertension group (0.176±0.087,0.537±0.195;0.104±0.011,0.173±0.027, P ＜0.01or P ＜ 0.05) . Infiltration of macrophage was significant(0. 62 ±0.07,non Ⅱ A group, the expressions of ICAM-1 mRNA and protein were decreased significantly(0. 537 ±0. 195, 0.291 ±0. 106; 0. 173 ±0.027, 0. 125± 0. 014, P ＜ 0.01 or P ＜ 0. 05); the amount of macrophages infiltration was decreased(1.85 ±0. 23, 1.16 ±0. 17, P ＜ 0.05) and the degree of cardiomyocytic hypertrophy and interstitial fibrosis was remarkably relieved.CONCLUSION: Excessive expression of myocardial ICAM-1 and its mediated inflammatory cellular infiltration plays an important role in hypertensive left ventricular hypertrophy. The inhibition of tanshinone ⅡA on left ventricular hypertrophy may be contributed to decreased expression of ICAM-1 and alleviated inflammatory cellular infiltration in myocardium.

AIM　To study the effects of superoxide anion (O.2) on Ca2+ homeostasi and contractility in cultured bovine aortic smooth muscle cell. METHODS　Using Fura-2 fluorescence technique to determine Ca2+ level and collagen gel contraction system to analyze muscle contractility. RESULTS　ATP (10 μmol*L-1 )-induced Ca2+ transient was smaller in xanthine oxidase treated cells(X/XO) than control. The mean peak increment of ［Ca2+］i(△［Ca2+］i peak) and the time integral of the elevated ［Ca2+］i(∫△［Ca2+］i dt) for 5 min were decreased from (206.1±10.2) to (147.4±14.7) nmol·L-1,and from (12.2±0.5) to (9.8±0.8) μmol·L-1·s-1. Δ［Ca2+］i peak induced by thapsigargin（1 μmol·L-1 ）in Ca2+-free solution was not affected by X/XO, but was decreased from (27.3±1.0) nmol·L-1 to (13.5±1.0) nmol·L-1 in Ca2+-containing solution because of the activation of CRAC(△［Ca2+］i CRAC). X/XO accelerated the velocity of thapsigargin-induced Ca2+ leak from (78.7±3.4) s to (64.8±4.40) s. Gel contraction area in X/XO-treated cells induced by ATP or thapsigargin (in Ca2+ free solution and in Krebs solution)was decreased from 23.6%±4.6% to 7.4%±0.2%, from 3.5%±0.6% to -1.0%±0.5%, and from 7.9%±1.4% to -0.5%±0.7%, respectively. CONCLUTION　O.2 attenuats smooth muscle contraction by impairing some of Ca2+ mobilization pathways.

Adult ; Fluoroscopy ; Foreign Bodies ; therapy ; Humans ; Male ; Trauma, Nervous System ; therapy ; Wounds, Penetrating ; therapy

Adolescent ; Alkanes ; poisoning ; Alkenes ; poisoning ; Daphne ; chemistry ; Humans ; Male

Administration, Oral ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Male ; Middle Aged ; Peracetic Acid ; administration & dosage ; poisoning ; Poisoning ; diagnosis ; therapy

0.05).The activity of Na~+-K~+ ATPase in SMO group was significantly higher than that in HTK group at 72 h(P

Aim To investigate the effects of monocrotaline pyrrole on production of nitric oxide and expression of eNOS protein of cultured pulmonary artery endothelial cells and on contractility of cultured pulmonary artery smooth muscle cells.Methods DAF-2 fluorescence technique was used to determine NO level,Western blot analysis was performed to determine the level of eNOS protein,and collagen gel contraction system was adopted to analyze muscle contractility.Results NO production induced by ACh and expression of eNOS protein were obviously inhibited by monocrotaline pyrrole compared with those of control group and gel contraction area in MCTP-treated cells induced by Thapsigargin obviously decreased.Conclusions monocrotaline pyrrole could inhibit the level of the ACh-induced production of NO and expression of eNOS protein,and enhance the contractility of pulmonary artery smooth muscle cells,which may be one of the possible mechanisms of MCTP-induced pulmonary artery hypertension.