Acupuncture Points ; Acupuncture Therapy ; Adult ; Combined Modality Therapy ; Female ; Humans ; Intervertebral Disc Displacement ; therapy ; Male ; Massage ; Middle Aged ; Young Adult

Adult ; Cardiac Catheterization ; instrumentation ; Ductus Arteriosus, Patent ; therapy ; Equipment Failure ; Female ; Humans ; Male ; Young Adult

Acupuncture Therapy ; Adult ; Cervical Vertebrae ; injuries ; Combined Modality Therapy ; Female ; Humans ; Male ; Massage ; Middle Aged ; Pharyngitis ; etiology ; therapy ; Spinal Diseases ; complications ; Young Adult

OBJECTIVETo observe the effect of β₃adrenoceptors (β₃-AR) activation on rat thoracic aorta smooth muscle contractility and the possible related mechanism.

METHODSThe endothelium removed thoracic aorta was pre-contracted with 30 mmol/L KCl physiological saline solution (PSS). Then the tension of the thoracic aorta was recorded in presence of BRL37344 (BRL) to determine the action of β₃-AR. The tension of the thoracic aorta was also recorded in the presence of Propranolol (PRA), SR59230A (SR), L-NNA, H-89 and Iberiotoxin (IBTX) respectively to reveal the underling mechanism of β₃-AR activation on rat vascular smooth muscle. Immunohistochemistry was adopted to confirm the existence and the distribution of β₃-AR in rat thoracic aorta.

RESULTSThe results showed that: (1) The thoracic aorta was relaxed by β₃-AR activation, with a relaxation percentage of (10.59 ± 0.79). (2) β₃-AR was expressed in both endothelial and smooth muscle layer in thoracic aorta sections of rats. (3) PRA did not block the effect of BRL on the thoracic aorta. The relaxation actions of BRL could be antagonized by pre-incubating the thoracic aorta with SR. (4) L-NNA (a NOS inhibitor) and H-89 (a PKA inhibitor) reversed the relaxation effect of BRL on vascular smooth muscle. (5) The effect of BRL was decreased after application of Ibriotoxin (IBTX), a large conductance calcium dependent potassium channel blocker.

CONCLUSIONThe results confirmed that activation of β₃-AR led to relaxation of thoracic aorta smooth muscle. The relaxation action of β₃-AR on smooth muscle of rat thoracic aorta was related to activation of NOS and PKA signaling pathway. Large conductance Ca²⁺-K⁺ channels were involved in the relaxation action of β₃-AR activation on rat thoracic aorta smooth muscle.

Animals ; Aorta, Thoracic ; physiology ; In Vitro Techniques ; Isoquinolines ; Large-Conductance Calcium-Activated Potassium Channels ; physiology ; Muscle Contraction ; Muscle Relaxation ; Muscle, Smooth, Vascular ; physiology ; Nitroarginine ; Peptides ; Propanolamines ; Propranolol ; Rats ; Receptors, Adrenergic, beta-3 ; physiology ; Signal Transduction ; Sulfonamides

Objective To investigate the distribution and severity of cerebral artery stenosis and the prognosis in elderly patients with acute cerebral infarction using digital subtraction angiography (DSA). Methods The 432 elderly patients with acute cerebral ischemia infarction underwent DSA,and they were divided into two groups: elderly group (n= 320) and non-elderly group (n= 112). The characteristics of distribution and severity of cerebral artery stenosis, the relationship between artery stenosis and relative risk factors, and the prognosis of acute cerebral infarction were analyzed.Results In elderly group, 270 cases (84.3%) had intra- and extra- cranial artery stenosis, of which 98 patients (30.6%) with pure extracranial arterial stenosis, 132 patients (41.3%) with combined extra- and intra-cranial artery stenosis. They were both significantly higher than the corresponding data in non-elderly group [23 cases (20.5%) and 28 cases (25%), P＜0.05 and 0.01]. The prevalences of moderate and severe cerebral artery stenosises were higher in elderly group than in nonelderly group [224 locations (52.1%) vs. 51 locations (40.8%), P＜0. 05]. The number of patients with previous history of cerebrovascular disease was much more and the prognosis was much worse in elderly group than in non-elderly group (both P＜0.05), Conclusions The elderly patients with cerebral infarction have severer cerebral artery stenosis, increased proportion of multivessel disease and poor prognosis. So it is very important to take aggressive treatment as soon as possible, and to make secondary prevention and effective rehabilitation so as to improve their prognosis.

Objective To study the molecular mechanism of renal injury of chronic arsenic poisoning rats induced by the expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cells.Methods Sixty healthy SD rats were divided into three groups,high-,low-dose group,and control group,n =20 in each group.The rats in high and low dose groups were treated with As203 through drinking water,10.0 and 0.4 mg/kg,respectively.The control rats were given distilled water.Four months later,serum and urinary arsenic level was determined,and kidney specimens were taken.The expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cells was detected by histological technique-HE staining and SABC immunohistochemistry.In addition,cell number counting and image analyses were used in the study.Results The number of caspase-8 positive cells of renal proximal tubule in control group,low-and high-dose group was 3.33±1.32,31.14±8.02 and 46.50±7.20 cell number/visual fields,respectively,which was increased with dose increasing(all P ＜0.05);the average gray value was 151.34±6.40,133.58±4.63 and 128.34±16.28,respectively,decreased with dose increasing(all P ＜0.05).The number of P53 positive cells was 3.17±1.59,26.29±4.23 and 47.00±6.22 cell number/visual fields,respectively,increased with dose increasing (all P ＜ 0.05) ; the average gray value was 142.54±8.06,121.48±5.68 and 101.89±6.35,respectively,decreased with dose increasing (all P ＜ 0.05).Conclusion The increase of caspase-8 and P53 positive cells is one of the molecular mechanisms of renal injury induced by arsenic poisoning.

Cognitive impairment is a common complication of diabetes. Hippocampus plays an important role in cognitive function. In hyperglycemia, synaptophysin, a crucial synaptic vesicle membrane protein in hippocampus neuron is found to be down-regulated. Recent evidences have shown that angiotensin IV can facilitate memory acquisition and recovery. However, whether it can also improve cognitive functions of diabetic rats with cognitive disorder, and the possible mechanisms are uncertain. Hence, the objectives of this study. Forty fi ve Sprague Dawley male rats were randomly divided into three groups: Control, diabetic group and diabetes with angiotensin IV treatment group. The cognitive functions, mainly learning and memory of the rats were evaluated using Morris water maze task. The synapses ultrastructure, relative mRNA concentrations and protein expression levels of synaptophysin in hippocampus CA1 area were estimated using transmission electron microscope, RT-PCR, immunohistochemistry and western blotting, respectively. Our study showed that in the diabetic rats with angiotensin IV treatment, the cognitive impairment as measured by Morris water maze task improved, the ultrastructure of synapses in hippocampus reversed, the relative mRNA concentrations and protein levels of synaptophysin in hippocampus signifi cantly increased, when compared with diabetic rats. We conclude that angiotensin IV plays an important role in improving cognitive function of diabetic rats. The possible mechanisms are up-regulating the expression of synaptophysin and normalizing the ultrastructure of synapses in hippocampus.

Dietary restriction (DR) can delay senescence,prolong lifespan of mammals and improve their learning-memory activity.The purpose of the study was to explore the effects of DR on hypolipidemic action and liver function of mice with hyperlipidemia.To investigate these effects,hyperlipidemia mouse models were established with high-fat diet (HFD) (34％ of energy),then randomly divided into HFD group,DR30％ group and DR50％ group.Mice in DR30％ and DR50％ group were respectively supplied with HFD as much as about 70％ and 50％ of the consumption of HFD in the mice of HFD group.Rats in control group were fed routinely.After DR for 5 weeks,the average body weight,liver weight,liver index,serum lipids and glucose levels in both DR groups decreased significantly as compared with the HFD group (P＜0.05 or P＜0.01),so did alanine aminotransferase (ALT),aspartate aminotransferase (AST),lactate dehydrogenase (LDH) levels and the ratio of LDL-C/HDL-C in the DR50％ group (P＜0.05 or P＜0.01).Histopathology examination of liver tissues further proved ameliorative effect of DR on liver function.Western blotting showed that DR significantly increased the expression of silent mating type information regulation 2 homolog 1 (SIRT1) in liver and adipose,while notably decreased the expression of peroxisome proliferators-activated receptors-gamma (PPARγ) in adipose (P＜0.05 or P＜0.01).The increase of SIRT1 and decrease of PPARγ may be a mechanism by which DR reduces blood lipids and ameliorates liver function.

OBJECTIVETo investigate the expression of Plexin A1 in gastric cancer(GC) and its relationship with angiogenesis and proliferation of GC.

METHODSPlexin A1 mRNA expression in 20 cases of GC specimens and matched resected normal gastric tissue were examined by RT-PCR. Plexin A1, Ki-67, vascular endothelial growth factor(VEGF) protein expression and microvessel density (MVD) in 50 cases of GC specimens and 20 cases of normal gastric mucosa were detected by immunohistochemistry.

RESULTSRT-PCR showed that the expression of Plexin A1 in GC was significantly higher than that in normal gastric mucosa(0.71 +/- 0.37 vs 0.60 +/- 0.25, P < 0.05). MVD within tumor tissue increased significantly with Plexin A1 mRNA expression(r=0.8736, P < 0.01) and Plexin A1 protein expression (P < 0.01). The Plexin A1 expression was positively correlated with the proliferation index (Ki-67) of cancer cells (r=0.4851, P < 0.01). However, the Plexin A1 expression level had no relationship with the VEGF expression level.

CONCLUSIONPlexin A1 plays an important role in the occurrence and development of GC. Plexin A1 may regulate angiogenesis, and promote the proliferation of GC cells.

Adult ; Aged ; Cell Proliferation ; Female ; Humans ; Ki-67 Antigen ; metabolism ; Male ; Middle Aged ; Neovascularization, Pathologic ; Nerve Tissue Proteins ; metabolism ; Receptors, Cell Surface ; metabolism ; Stomach Neoplasms ; metabolism ; pathology ; Vascular Endothelial Growth Factor A ; metabolism

Adolescent ; Antigens, Viral ; blood ; Child ; Child, Preschool ; Cytomegalovirus ; immunology ; Cytomegalovirus Infections ; diagnosis ; Female ; Flow Cytometry ; Hepatitis, Viral, Human ; diagnosis ; virology ; Humans ; Infant ; Male ; Phosphoproteins ; blood ; Viral Matrix Proteins ; blood