24 h(all P

OBJECTIVE: To analyze the latency of posture evoked response of normal lower limb muscle in different stimulations and explore its influencing factors. METHODS: The normal lower limb was induced to produce postural evoked response by the dynamic posturography through two kinds of perturbations, the supporting surface rotation stimulation (Toes-up and Toes-down) and the horizontal perturbation stimulation (Forward and Backward). The latencies of tibialis anterior muscle and gastrocnemius muscle were recorded by surface electromyography acquisition system. The differences of the left and right limb, gender and height on the latency of postural evoked response were analyzed. RESULTS: (1) Under the Toes-up and Backward perturbation, the latency of tibialis anterior muscle was longer than gastrocnemius muscle; under the Toes-down and Forward perturbation, the latency of gastrocnemius muscle was longer than tibialis anterior muscle. (2) The latencies of left limb and right limb had no significant difference. (3) The latency in male was longer than that in female. (4) The latency gradually increased with the increase of height. CONCLUSION In the postural evoked response, different perturbations, gender and height have significant impacts on the latency of posture evoked response of lower limb muscle. However, the effect of height and gender should be not considered referring to the same individual.
Electromyography ; Female ; Humans ; Lower Extremity ; Male ; Muscle, Skeletal/physiology* ; Posture

Twelve flavonoids were isolated from an ethanol extract of Machilus wangchiana by a combination of various chromatographic techniques including column chromatography over silica gel and Sephadex LH-20 and reversed-phase flash chromatography and HPLC. Their structures were identified by spectroscopic data analysis (IR, MS, and NMR) as (+)-catechin (1), (-)-epicatechin (2), 3'-O-methyl-(+)-catechin (3), 3'-O-methyl-(-)-epicatechin (4), 3, 5, 7, 2', 5'-pentahydroxy flavan (5), (-)-naringenin (6), (-)-eriodictyol (7), (-)-liquiritigenin (8), (2R,3R)-(+)-dihydrokaempferol (9), (2R,3S)-(-)-dihydro- kaempferol (10), (2R, 3R)-(+)-taxifolin (11), and quercetin (12). Compounds 1-10 are isolated from the genus Machilus for the first time.
Drugs, Chinese Herbal ; chemistry ; Flavonoids ; chemistry ; Lauraceae ; chemistry ; Mass Spectrometry ; Molecular Structure ; Plant Roots ; chemistry

OBJECTIVETo investigate the effect of salidroside on hypoxia-induced apoptosis of corpus cavernosum smooth muscle cells (CCSMCs) in rats.

METHODSRat CCSMCs were cultured in vitro by the enzyme digestion method and identified by immunofluorescent staining of anti-alpha-SMA and anti-Desmin. The non-toxic dose of salidroside was determined by MTT assay. Low-oxygen mixed gas (1% O2, 5% CO2, and 94% N2) was piped into a modular incubator chamber to induce hypoxia. The CCSMCs were divided into a normal, a hypoxia, and a 32 microg/mL salidroside intervention group. The apoptosis of the CCSMCs was detected by flow cytometry and the expression of the caspase-3 protein determined by Western blot.

RESULTSThe majority of the CCSMCs were positive for alpha-SMA and Desmin at immunofluorescent staining. Salidroside at < 32 microg/ml produced no obvious toxicity to CCSMCs. Compared with the normal control group, the rates of early and late apoptosis of CCSMCs were both increased significantly in the hypoxia group ([12.77 +/-1.41]% vs [18.69 +/- 1.29]%, P < 0.01 and [14.63 +/- 2.00]% vs [21.03 +/- 1.530]% , P < 0.05). Western blot showed a markedly increased expression of cleaved caspase-3 (P < 0.01). Intervention with 32 microg/ml salidroside significantly reduced hypoxia-induced early apoptosis of CCSMCs ([13.46% +/- 1.87]%, P < 0.01) and decreased the expression of cleaved caspase-3 (P < 0.01).

CONCLUSIONSalidroside can reduce the expression of cleaved caspase-3 and inhibit hypoxia-induced apoptosis of CCSMCs in rats.

Animals ; Apoptosis ; drug effects ; physiology ; Caspase 3 ; metabolism ; Cell Hypoxia ; physiology ; Cells, Cultured ; Glucosides ; pharmacology ; Humans ; Male ; Myocytes, Smooth Muscle ; cytology ; drug effects ; enzymology ; Penis ; cytology ; drug effects ; Phenols ; pharmacology ; Rats

Fatty Liver ; diagnosis ; therapy ; Humans ; Non-alcoholic Fatty Liver Disease ; Practice Guidelines as Topic ; United States

Nitrobenzene is one of the toxic compounds. Much work had focused on biodegradation of it sofar. Two main pathways for nitrobenzene biodegradation, oxidative and partial reductive pathways, were reviewed in this article. The mechanism of these pathways including involved enzymes and genes was introduce in details. Comparative analysis of the pathways would provide basis for the development and application of biodegradation technology for nitrobenzene and other organic pollutants.

AIM To investigate the effect of fenofibrate and simvastatin on the serum free fatty acids of alcoholic fatty liver in rats. METHODS The rat model of alcoholic fatty liver was reproduced by chronic ethanol ingestion plus olive oil diet. The model rats were divided into three groups as follows: finofibrate treatment group(finofibrate 80 mg?kg -1 po, once a day),simvastatin treatment group (simvastatin 4 mg?kg -1 po, once a day)and control group without either above-mentioned treatment. Experimental rats were treated for four weeks and then sacrificed for blood sampling. Serum free fatty acids were analyzed by gas chromatography. RESULTS Fenofibrate significantly ameliorated the decrease in polyunsaturated fatty acids induced by ethanol [oleic acid:(38.212?7.788) ?g?L -1 vs (31.620?6.142) ?g?L -1,linoleic acid:(37.269?8.065) ?g?L -1 vs (30.254?9.063) ?g?L -1,arachidonic acid:(11.646?2.601) ?g?L -1 vs (9.012?1.236) ?g?L -1] accompanied by the improvement of the fat infiltration of the liver, but demonstrated no effect on the increase in serum saturated fatty acids by ethanol. In the contrast, simvastatin can aggravate the decrease in polyunsatrurated fatty acids and significantly increase the levels of satrurated fatty acids in serum induced by ethanol along with the pathological aggravation of alcoholic fatty liver. CONCLUSION The results of present study revealed that fenofibrate and simvastatin exerted different effect on the serum free fatty acids of alcoholic fatty liver. Polyunsatrurated fatty acids in the serum play an important role in the pathogenesis and treatment response of alcoholic fatty liver.

Objective To evaluate the differential expression of lysophosphatidic acid receptor (LPAR) in breast cancer (BC), and its relationship with clinicopathological features of BC patients. Methods The qRT-PCR and immunohistochemical staining were used to detect the LPAR expression in 37 normal tissues, 55 benign disease tissues and 82 BC tissues, besides, the correlation of LPAR expression with clinicopathological data was also analyzed. Results The expression levels of LPAR2 and LPAR3 mRNA and protein in BC tissues were higher than those in normal benign tissues (all P<0.05). LPAR1 mRNA expression had no difference in three tissues (χ2 =1.908, P >0.05). LPAR1 expression was not associated with clinicopathological features in BC tissues (P>0.05). LPAR2 expression in postmenopausal patients was higher than that in premenopausal patients (χ2=4.821, P<0.05). LPAR3 expression was significantly associated with nodal metastasis, estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) in BC tissues (all P<0.05). Conclusion LPAR in BC tissues has differential expression, which is associated with nodal metastasis, ER, PR and HER2.

The clinical characteristics of patients who presented in poor clinical grade due to ruptured middle cerebral artery aneurysms (MCAAs) associated with large sylvian hematomas (SylH) were analyzed and an ingenious designed prophylactic hinged craniectomy was introduced. Twenty-eight patients were graded into Hunt-Hess grades IV-V and emergency standard micro-neurosurgeries (aneurysm clipping, hematoma evacuation and prophylactic hinged craniectomy) were performed, and their clinical data were retrospectively analyzed. 46.43% of the patients reached encouraged favorable outcomes on discharge. The favorable outcome group and the poor outcome group significantly differed in terms of patients' anisocoria, Hunt-Hess grade before surgery, extent of the midline shift and time to the surgery after bleeding (P<0.05). There were no significant differences in age, sex, volume and location of the hematoma, size of aneurysm between the favorable and poor groups (P>0.05). However, ingenious designed prophylactic hinged craniectomy efficiently reduced the patients' intracranial pressure (ICP) after surgery. It was suggested that preoperative conditions such as Hunt-Hess grading, extent of the midline shift and the occurrence of cerebral hernia affect the prognosis of patients, but time to the surgery after bleeding and prophylactic hinged craniectomy are of significant importance for optimizing the prognosis of MCAA patients presenting with large SylH.

Objective To investigate the effects of angiotensin Ⅱ (Ang Ⅱ) on the expression of TLR4 and its role in lipopolysaccharide (LPS)-induced NF-κB activation and CD40 expression in rat peritoneal mesothelial cells (RPMCs). Methods RPMCs were harvested from Spragne-Dawley rat peritoneal cavity and maintained under defined in vitro condition. The cells were treated with Ang Ⅱ at different concentrations (10-9, 10-8, 10-7, 10-6 mol/L) and exposed to Ang Ⅱ (10-7 mol/L) for different times (1, 2, 4, 8, 12, 24, 48 h for mRNA and 6, 12, 24, 36, 48 h for protein, respectively). Meanwhile, the influence of AT1 receptor antagonist (AT1R, losartan, 10-5 mol/L) and AT2 receptor blocker (AT2R, PD123177, 10-5 mol/L) on the TLR4 induced by Ang Ⅱ was observed. After synchronization for 24 hours, the cells were randomly assigned to four groups: the control group, the Ang Ⅱ (10-7 tool/L) group, the LPS (1 mg/L) group, the Ang Ⅱ (10-7 mol/L) plus LPS (1 mg/L) group, which were used to investigate the effects of Ang Ⅱ on the NF-κB activation and CD40 expression induced by LPS. The mRNA expression of TLR4 and CD40 was measured by RT-PCR and the protein abundance of TLR4, NF-κB p65, phospho-p65, IKBα and phospho-IκBα were analyzed by Western blot. Immunofluorescence was performed to determine the subcellular localization of p65 subunit of NF-κB. Results (1) Treatment of RPMCs with Ang Ⅱ resulted in a concentration-dependent increase in the expression of TLR4. Ang Ⅱ at 10-9, 10-8, 10-7 and 10-6 mol/L increased TLR4 mRNA expression by 70.5%, 89.5%, 102.9%, and 121.9%, respectively and protein expression by 12.1%, 27.7%, 51.2%, and 41.6%, respectively (P<0.01). Treatment of RPMCs with 10-7 mol/L Ang Ⅱ resulted in a time-dependent increase in the expression of TLR4, with the peak of mRNA expression at 8 and 12 h (P<0.01) and the protein expression at 12 and 24 h (P<0.01). (2) Losartan antagonized Ang Ⅱ-stimulated expression of TLR4 by 33.5% (P<0.05), PD123177 had no such effect (P0.05). (3) Treatment of RPMCs with LPS (1 mg/L) for 60 rain significantly increased the ratio of phospho-IκBα to IκBα by 362.6% (P< 0.01) , phospho-p65 to p65 by 67.4% (P<0.05), and LPS (1 mg/L) for 4 h significantly increased the expression of CD40 mRNA by 299.9% (P<0.01) compared to the control group. In comparison to the LPS (1 mg/L) group, preincubation of RPMCs with AngⅡ (10-7 mol/L) for 24 h then treated with LPS (1 mg/L) for 60 rain significantly increased the ratio of phospho-IκBα to IκBα by 49.1% (P<0.01), phospho-p65 to p65 by 29.3%(P<0.05), and LPS (1 mg/L) for 4 h significantly increased the expression of CD40 mRNA by 56.8%(P<0.01). (4) The p65 subunit of NF-κB was dominantly distributed in the cytoplasm in the control and Ang Ⅱ group. Following exposure to LPS for 60 min, p65 subunit labeling was upregulated and translocated into the nuclei. A significantly increased nuclear staining of p65 in ceils treated with Ang Ⅱ plus LPS were observed. Conclusions Ang Ⅱ induces the expression of TLR4 in dose- and time-dependent manner in RPMCs, resulting in enhanced NF-κB signaling and induction of CD40 expression, Locally produced Ang Ⅱ in the peritoneum may play an amplified role in LPS-induced peritoneal inflammation.