ABSTRACT
<p><b>OBJECTIVE</b>To explore the clinical curative effect of anterolateral acromial approach in treating two-and three-part of proximal humeral fractures.</p><p><b>METHODS</b>Forty-two patients of proximal humeral fractures from January 2010 to June 2014 were analyzed retrospectively, including 23 males and 19 females with a mean age of 61.5 years old ranging from 40 to 76 years old. Among them, 22 cases were treated with anterolateral acromial approach and 20 cases were treated with deltopectoral approach. The operation time, intraoperative blood loss, postoperative hospitalization days, fracture healing time of two groups were compared. The shoulder pain after 1 week was assessed by the VAS score. The postoperative shoulder joint function was evaluated after 3 months and more than 6 months by Constant score.</p><p><b>RESULTS</b>The follow-up time was at final 14 months. There were significant differences in operation time(=0.003), intraoperative blood loss(=0.001), postoperative hospital day(=0.013), postoperative shoulder pain after 1 week(=0.026), postoperative Constant score after 3 months(=0.014) between the anterolateral acromial approach group and the deltopectoral approach group. There were no significant differences in clinical union time of bone(=0.462), postoperative constant score after more than 6 months(=0.204) between the anterolateral acromial approach group and the deltopectoral approach group. There were no breakage of the internal fixation and humeral head osteonecrosis.</p><p><b>CONCLUSIONS</b>It has some advantages with anterolateral acromial approach to treat Neer two-and three-part of proximal humeral fractures, such as short operation time, less intraoperative bleeding, lighter postoperative pain, quicker recovery of function.</p>
ABSTRACT
Objective:To observe influence of benazepril combined trimetazidine on blood levels of follistatin-like 1 (FSTL1)and platelet activating factor (PAF)and vascular endothelial function in patients with coronary heart dis-ease (CHD)complicated heart failure (HF).Methods:A total of 120 CHD patients with chronic heart failure were selected from our hospital.They were randomly and equally divided into benazepril group and combined treatment group (received benazepril combined trimetazidine therapy),both groups were treated for six months.Serum Blood levels of N-terminal pro brain natriuretic peptide (NT-proBNP),FSTL1 and PAF,endothelial progenitor cells (EPCs)count and fore brachial artery endothelium dependent diastolic-systolic function (FMD)before and after treatment were measured and compared between two groups.Results:Compared with before treatment,there were significant rise in left ventricular ejection fraction (LVEF),6min walking distance (6MWD),EPCs and FMD,and significant reductions in serum levels of NT-proBNP,FSTL1 and PAF after treatment in two groups,P <0.05 or <0.01;compared with benazepril group,there were significant rise in LVEF [(41.94±9.19)% vs.(46.15±10.04)%], 6MWD [(333.94±58.29)m vs.(383.14±77.84)m],EPCs [(0.059±0.029)pg/ml vs.(0.083±0.014)pg/ml]and FMD [(7.53±2.02)% vs.(8.24±1.42)%],and significant reductions in serum levels of NT-proBNP [(2.74±0.69) ng/ml vs.(2.05±0.34)ng/ml],FSTL1 [(5.38±1.29)ng/ml vs.(4.64±0.84)ng/ml]and PAF [(5.16±0.92)μg/ml vs.(4.20±1.05)μg/ml]in combined treatment group,P <0.05 or <0.01.Conclusion:Benazepril combined trimeta-zidine can effectively reduce blood levels of NT-proBNP,FSTL1 and PAF,and promote vascular endothelial function re-covery in patients with coronary heart disease complicated chronic heart failure.
ABSTRACT
Objective:To observe influence of benazepril combined trimetazidine on blood levels of follistatin-like 1 (FSTL1)and platelet activating factor (PAF)and vascular endothelial function in patients with coronary heart dis-ease (CHD)complicated heart failure (HF).Methods:A total of 120 CHD patients with chronic heart failure were selected from our hospital.They were randomly and equally divided into benazepril group and combined treatment group (received benazepril combined trimetazidine therapy),both groups were treated for six months.Serum Blood levels of N-terminal pro brain natriuretic peptide (NT-proBNP),FSTL1 and PAF,endothelial progenitor cells (EPCs)count and fore brachial artery endothelium dependent diastolic-systolic function (FMD)before and after treatment were measured and compared between two groups.Results:Compared with before treatment,there were significant rise in left ventricular ejection fraction (LVEF),6min walking distance (6MWD),EPCs and FMD,and significant reductions in serum levels of NT-proBNP,FSTL1 and PAF after treatment in two groups,P <0.05 or <0.01;compared with benazepril group,there were significant rise in LVEF [(41.94±9.19)% vs.(46.15±10.04)%], 6MWD [(333.94±58.29)m vs.(383.14±77.84)m],EPCs [(0.059±0.029)pg/ml vs.(0.083±0.014)pg/ml]and FMD [(7.53±2.02)% vs.(8.24±1.42)%],and significant reductions in serum levels of NT-proBNP [(2.74±0.69) ng/ml vs.(2.05±0.34)ng/ml],FSTL1 [(5.38±1.29)ng/ml vs.(4.64±0.84)ng/ml]and PAF [(5.16±0.92)μg/ml vs.(4.20±1.05)μg/ml]in combined treatment group,P <0.05 or <0.01.Conclusion:Benazepril combined trimeta-zidine can effectively reduce blood levels of NT-proBNP,FSTL1 and PAF,and promote vascular endothelial function re-covery in patients with coronary heart disease complicated chronic heart failure.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of estrogen on heat shock protein (HSP) 70 expression in rat masseter muscle.</p><p><b>METHODS</b>Sixty twelve-week-old female Sprague-Dawley rats were randomly divided into three groups: Sham surgery group (control group), ovariectomy group (OVX group), ovariectomy with estradiol valerate replacement treatment group (OVX/EV group). Half of the animals were sacrificed at 4 and 8 weeks respectively, then the masseter muscle was removed. Immunohistochemistry (IHC) method was employed to study the HSP70 expression in masseter muscle.</p><p><b>RESULTS</b>Compared to control group and OVX/EV group, the expression of HSP70 was significantly lower at 8 weeks in OVX group (P < 0.05). There were no significantly difference between the HSP70 expression of control group and that of OVX/EV group.</p><p><b>CONCLUSION</b>Estrogen may affect HSP70 expression in rat masseter muscle, and estrogen replacement therapy may prevent HSP70 reduction.</p>
Subject(s)
Animals , Female , Humans , Rats , Estradiol , Estrogens , HSP70 Heat-Shock Proteins , Masseter Muscle , Ovariectomy , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To investigate effects of the static magnetic field (SMF) generated by dental magnetic attachment on osteoblastic morphology and surface ultrastructure.</p><p><b>METHODS</b>The in vitro cultured rat osteoblasts were exposed continuously to 12.5 mT, 125 mT, and 250 mT static magnetic fields for 1, 3, 5, and 7 days. After exposed in SMF, osteoblasts were observed under a phase contrast microscope, and then HE stained and observed under a light microscope. In addition, the cells were observed under a scanning electron microscope (SEM).</p><p><b>RESULTS</b>By continuous exposure, the different intensities of SMF exposure did not change the vital osteoblast growth pattern or distribution. The SEM photos showed that there were certain changes in cellular microstructures for osteoblasts after exposed to 12.5 mT for 5 to 7 days, as well as 125 mT and 250 mT for 3 to 7 days. The more exposure time increased, the more microvesicles on the surfaces of cells were observed.</p><p><b>CONCLUSIONS</b>Continuous SMF-stimulation could not affect the shape, distribution, and growth pattern of osteoblasts. The SMF of magnetic attachments could lead to certain changes in surface ultrastructures of osteoblasts in this study.</p>
Subject(s)
Animals , Rats , Cells, Cultured , Denture Precision Attachment , Electromagnetic Fields , Osteoblasts , Radiation Effects , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of metoprolol on cardiac function and myocyte calcium regulatory protein expressions in rabbits with heart failure.</p><p><b>METHODS</b>Rabbit heart failure model was established by aortic insufficiency induced volume overload followed 14 days later by pressure overload induced by abdominal aorta constricting (HF, n = 11), another 8 rabbits with heart failure were treated with metoprolol (ME) for 6 weeks, sham-operated rabbits (n = 11) served as control. Cardiac function was measured by echocardiography at the end of study. Caffeine-induced calcium transients of myocytes loaded by Fluo-3/AM were observed under Laser scanning confocal microscope. Calcium regulatory protein expression was determined by Western blot analysis.</p><p><b>RESULTS</b>Compared to control animals, the ejection fractions [EF, (45.7 +/- 3.0)% vs. (72. 6 +/- 5.0)%, P < 0.01] and the amplitude of caffeine-induced calcium transients [(16.0 +/- 3.5) FI vs. (43.5 +/- 6.2) FI, P < 0.01] were significantly decreased while its time to peak was significantly prolonged [(129.8 +/- 14.5) s vs. (52.2 +/- 7.4) s, P < 0.01] in HF rabbits. The RyR2 (0.106 +/- 0.007 vs. 0.203 +/- 0.021, P < 0.01) and the ratio of SERCA2a and NCX (1.22 +/- 0.23 vs. 1.96 +/- 0.12, P < 0.01) were also significantly reduced in myocytes of HF rabbits. Metoprolol significantly attenuated the decrease of EF [(60.2 +/- 5.1)%], the amplitude of calcium transient [(32.8 +/- 5.4) FI], the RyR2 expression (0.164 +/- 0.016) and the ratio of SERCA2a and NCX (1.68 +/- 0.17, all P < 0.05 vs. HF rabbits) and attenuated the increase of the time to peak of caffeine-induced calcium transients [(91.4 +/- 10.9) s, P < 0.05 vs. HF rabbits].</p><p><b>CONCLUSION</b>Metoprolol could improve the cardiac function possibly by preventing the alterations of calcium regulatory proteins and increasing calcium transients in failing heart.</p>
Subject(s)
Animals , Rabbits , Aortic Valve Insufficiency , Drug Therapy , Metabolism , Calcium , Metabolism , Calcium-Binding Proteins , Metabolism , Disease Models, Animal , Heart Failure , Drug Therapy , Metabolism , Metoprolol , Pharmacology , Therapeutic Uses , Myocytes, Cardiac , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of the static magnetic field (SMF) generated by dental magnetic attachments on osteoblastic proliferations, cell cycle distribution, and apoptosis ratio.</p><p><b>METHODS</b>By simulating those of the closed-field, the closure process and the open-field Magnedisc 800 magnetic attachments respectively, the in vitro cultured rat osteoblasts were exposed continuously to 12.5, 125, 250 mT SMF. The effects of the SMF on the proliferation of the cells were examined. MTT colorimetry test was performed to detect the effect of the SMF on the vitalities of cells. Flow cytometry was utilized to analyze the cell cycles and cell apoptosis rates.</p><p><b>RESULTS</b>The SMF exposure didn't change the vital osteoblasts number, the cell cycle distribution and proliferation activities of osteoblasts. The cell apoptosis situation were not observed statistical differences.</p><p><b>CONCLUSION</b>No matter the closed-field, the closure process and the open-field magnetic attachments respectively, continuous simulating SMF-stimulation of magnetic attachments couldn't change osteoblasts proliferation activity, cell cycle distribution, and apoptosis ratio.</p>
Subject(s)
Animals , Rats , Apoptosis , Cell Cycle , Cell Proliferation , Electromagnetic Fields , Magnetic Fields , Magnetic Phenomena , Magnetics , OsteoblastsABSTRACT
It is well known that estrogen can inhibit bone absorption, decrease bone turnover and preserve bone mass. Some studies indicated that the effect of estrogen on calcium and bone is relative to vitamin D system, while others also reported that this effect of estrogen is independent of vitamin D. The genomic effect of 1alpha, 25(OH)(2)D(3)is mediated by the nuclear vitamin D receptor (VDR) in a ligand-dependent manner. Hypocalcemia, hyperparathyroidism and osteomalacia are developed in VDR gene knockout mice. To determine whether the effect of estrogen on calcium and bone is dependent on VDR, this study examined the effect of exogenous estrogen on calcium and bone homeostasis in VDR gene knockout mice. Male and female wild type (WT) and VDR gene knockout heterozygous mice were mated each other and the genotyping of their offsprings were determined by PCR. At age of 21-day, WT and knockout mice were weaned and treated by one of three different regimens: (1) WT-vehicle group: the WT mice were injected with normal saline; (2) VDR KO-vehicle group: the VDR gene knockout mice were injected with normal saline; (3) VDR KO-E group: the VDR gene knockout mice were subcutaneously injected with estradiol, 0.2 mug per mouse, once daily for 1 month. The bone mineral density (BMD) of mice was measured using dual-energy X-ray absorptiometry. All mice were sacrificed at age of 50-day. Blood was taken by heart puncture under anesthesia and serum calcium was measured by autoanalyser.Tibiae were removed, fixed and embedded with the methylmethacrylate (MMA), and undecalcified sections were cut. These sections were stained for mineral with the von Kossa staining procedure and counterstained with toluidine blue. Static histomorphometric analyses were performed on those stained sections. The results showed that the serum calcium level was (2.10+/-0.37) mmol/L in the VDR KO-vehicle mice and rose to (2.80+/-0.41) mmol/L in the VDR KO-E mice although it was still lower than WT-vehicle mice [(3.10+/-0.48) mmol/L]. BMD and mineralized trabeculer volume were increased significantly in VDR KO-E group compared with that in VDR KO-vehicle group. These results suggest that exogenous estrogen can improve calcium absorption and skeletal mineralization in a VDR-independent manner.
Subject(s)
Animals , Female , Mice , Bone Density , Calcification, Physiologic , Calcium , Metabolism , Estrogens , Pharmacology , Gene Knockout Techniques , Homeostasis , Mice, Knockout , Receptors, Calcitriol , GeneticsABSTRACT
<p><b>AIM</b>To investigate the effects of 1 alpha hydroxylase and serum calcium on the expression of 24-hydroxylase gene in mice kidney.</p><p><b>METHODS</b>Mice with targeted deletion of the 25-hydroxyvitamin D 1 alpha hydroxylase gene(1alpha (OH)ase-/-), and the vitamin D receptor gene (VDR-/-) were used. The study of each mutant had two groups which were (1) mutant with high calcium diet, which maintained fertility but left mice hypocalcaemia; (2) mutant with high lactose diet, which normalized calcium in two mutant. Mice in same litter were as control. There were six groups in total and each group had five mice. All mice were killed at 10-week-old. Serum calcium was determined by an autoanalyzer. RNA was isolated from mouse kidney and the express of 1 alpha hydroxylase gene and 24-Hydroxylase gene were studied by RT-PCR.</p><p><b>RESULTS</b>On the high calcium intake, all mutant animals were hypocalcaemia (1alpha (OH)ase-/- (78 +/- 10.4) mg/L, P < 0.05; VDR-/- (68 +/- 9.8) mg/L, P < 0.05. WT (111 +/- 16.5 mg/L), but when the high lactose diet was administered, serum calcium levels in two mutant mice rose to wild-type levels. The 1 alpha hydroxylase gene was expressed at very higher levels in the vitamin D receptor mutant mice than in wild-type mice when animals received a high calcium intake; This was reduced by eliminating hypocalcaemia with the high lactose diet. Expression of the 24(OH)ase gene was extremely down-regulated in two mutant mice on the high calcium diet but was restored to wild-type levels on the high lactose diet.</p><p><b>CONCLUSION</b>The express of 24-hydroxylase gene was directly regulated by serum calcium rather than 1 alpha-hydroxylase. These studies indicate that both the serum calcium and 1 alpha-hydroxylase exert effects on the expression of 24-hydroxylase gene, but 1 alpha-hydroxylase take the effects by elevated the concentration of serum calcium. There are no direct interaction between 1 alpha-hydroxylase gene and 24-hydroxylase gene.</p>