Acquired Immunodeficiency Syndrome ; prevention & control ; Adult ; Burnout, Professional ; Chi-Square Distribution ; Female ; Humans ; Male ; Medical Staff ; Middle Aged ; Rural Population ; Surveys and Questionnaires ; Young Adult

OBJECTIVETo develop an HPLC for determination of aglycone of momordicoside L in Momordica charantia.

METHODA Kromasil C18 (4.6 mm x 150 mm, 5 microm) column was used. The mobile phase was acetonitrile-H2O (64:36), the flow rate was 1.0 mL x min(-1) and the UV detection wavelength was set 203 nm.

RESULTThe calibration curves were linear from of 0.025 microg to 1 microg (r =0.9911), the contents of aglycone of momordicoside L in Shandong, Henan, Hebei, Jiangxi are 0.211, 0.033, 0.013, 0.007 mg x g(-1), respectively.

CONCLUSIONThe method is simple and reliable for determination of aglycone of momordicoside L in M. charantia.

Calibration ; Chromatography, High Pressure Liquid ; methods ; Momordica charantia ; chemistry ; Saponins ; analysis

Objective To study the clinical and electrophysiological features of myasthenia gravis (MG)accompanied by myogenic lesion.Methods The data of the patients who were diagnosed MG accompanied by myogenic lesion from 1998 to 2006 were collected in EMG Room, Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and were retrospectively analyzed.Results In this group of 53 patients, myogenic lesion was found more often in patients with early-onset MG than those with late-onset(69.81% vs 30.20%), and among the early-onset patients the frequency of female was significantly higher than male(26 vs 11,X~2=5.281, P

Objective To investigate the clinical significance of myasthenia gravis (MG) associated autoantibodies.Methods Titin,ryanodine receptor (RyR)and acetylcholine receptor (AChR) antibodies were examined in the sera of 74 myasthenia gravies patients by ELISA.Results AChR,Titin, RyR antibodies were detected in 77.0% (57/74),39.2% (29/74) and 32.4% (24/74) of the MG patients,respectively.For thymoma MG,AChR,Titin and RyR antibodies were detected in 76.2% (16/21),71.4% (15/21) and 52.4% (11/21) respectively.For late onset MG,Titin and RyR antibodies were detected in 77.3% (17/22) and 50.0% (11/22) respectively.With respect to the modified Osserman classification,the positve rate for Titin and RyR antibodies is much higher in more severe patients (X~2= 16.094,P=0.001;X~2=11.226,P=0.011).Titin antibodies was significantly related with RyR antibodies (r=0.380,P=0.001).Conclusions Titin and RyR antibodies show high sensitivity for thymoma MG,and the combination of serological and radiological testing can increase both sensitivity and specificity in diagnosis of thymoma MG.The levels of the two antibodies may serve as important prognosis markers in MG.The induction of the immune response against Titin and RyR and the possible pathogenic effects of the two antibodies will be further studied.

Adolescent ; Adult ; Analgesics ; administration & dosage ; Anesthetics, Intravenous ; administration & dosage ; Flurbiprofen ; administration & dosage ; Humans ; Hypnotics and Sedatives ; administration & dosage ; Midazolam ; administration & dosage ; Middle Aged ; Molar, Third ; Pain Measurement ; Pain, Postoperative ; prevention & control ; Patient Satisfaction ; Preoperative Care ; Prospective Studies ; Tooth Extraction ; Young Adult

OBJECTIVETo clarify the effects of repetitive transcranial magnetic stimulation (rTMS) on rat motor cortical excitability and neurofunction after cerebral ischemia-reperfusion injury.

METHODSAfter determined awake resting motor threshold (MT) and motor evoked potentials (MEPs) of right hindlimbs, 20 Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) reperfusion injury, then rTMS were applied to rTMS group (n=10) at different time, while control group (n=10) received no stimulation. A week later, MT and MEPs were evaluated again, as well as neurological deficits and infarct volume. The effects of rTMS and MCAO reperfusion injury on these parameters were analyzed.

RESULTSAfter MCAO reperfusion, both MT level and neurological deficit scores increased, distinct focal infarction formed, and latency of MEP elongated. Compared with the control group, the increased extent of MT and neurological scores of rats receiving rTMS were significantly lower (P < 0.05), as well as the infarct volumes reduced significantly (P < 0.05). But MEP was not affected by rTMS obviously. There was a positive linear correlation between postinjury MT and infarct volume (r = 0.64, P < 0.05).

CONCLUSIONrTMS may facilitate neurofunction recovery after cerebral ischemia-reperfusion. Postinjury MT could provide prognostic information after MCAO reperfusion injury.

Animals ; Behavior, Animal ; physiology ; Brain ; pathology ; Evoked Potentials, Motor ; Hindlimb ; physiopathology ; Infarction, Middle Cerebral Artery ; pathology ; physiopathology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; pathology ; physiopathology ; Transcranial Magnetic Stimulation

OBJECTIVETo analyze the relationship between tumor necrosis factor-alpha (TNFalpha) gene promoter -308 polymorphism and myasthenia gravis (MG) in Chinese and analyze secretion of TNFalpha in peripheral blood mononuclear cells (PBMC) in MG patients.

METHODSA biallelic polymorphism at position -308 in the promoter of TNFalpha gene was screened by PCR amplification and NcoI recognition site. One hundred and twenty-three MG cases and 115 healthy controls were included in this study. MG patients were classified to different groups according to clinical type, age at onset, and sex respectively. PBMC were isolated from 20 patients and 20 healthy controls, and then cultured in the presence or absence of phytohemagglutinin (PHA) and acetycholine receptors (AchR). The supernatants were harvested after incubation and stored until TNFalpha was assayed by enzyme-linked immunosorbent assay.

RESULTSThe frequency of TNFalpha-308 allele 2 (A) was found significantly increase in MG patients and showed a trend especially in late onset (> or =40 years) and male patients (P < 0.05). The allele A had no relationship with thymic pathogenesis in MG patients. But frequency of allele A was significantly higher in general type than in ocular type (P < 0.05). MG patients had a higher inducible level of TNFalpha by PHA and AchR, and could be down regulated after treatment.

CONCLUSIONPolymorphism in TNFalpha gene promoter -308 is associated with onset of MG. The microsatellite allele TNFalpha2 confer risk for the development of MG in Chinese patients. MG patients have a higher inducible level of TNFalpha.

Adolescent ; Adult ; Aged ; Cells, Cultured ; Child ; Child, Preschool ; Female ; Gene Frequency ; Genotype ; Humans ; Immunosuppressive Agents ; therapeutic use ; Leukocytes, Mononuclear ; pathology ; secretion ; Male ; Middle Aged ; Myasthenia Gravis ; drug therapy ; genetics ; metabolism ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Tumor Necrosis Factor-alpha ; genetics ; secretion

BACKGROUNDSingle-fiber electromyography (SFEMG) has been suggested as a quantitative method for supporting chronic partial denervation in amyotrophic lateral sclerosis (ALS) by the revised EI Escorial criteria. Although concentric needle (CN) electrodes have been used to assess jitter in myasthenia gravis patients and healthy controls, there are few reports using CN electrodes to assess motor unit instability and denervation in neurogenic diseases. The aim of this study was to determine whether quantitative changes in jitter and spike number using CN electrodes could be used for ALS studies.

METHODSTwenty-seven healthy controls and 23 ALS patients were studied using both CN and single-fiber needle (SFN) electrodes on the extensor digitorum communis muscle with an SFEMG program. The SFN-jitter and SFN-fiber density data were measured using SFN electrodes. The CN-jitter and spike number were measured using CN electrodes.

RESULTSThe mean CN-jitter was significantly increased in ALS patients (47.3 ± 17.0 μs) than in healthy controls (27.4 ± 3.3 μs) (P < 0.001). Besides, the mean spike number was significantly increased in ALS patients (2.5 ± 0.5) than in healthy controls (1.7 ± 0.3) (P < 0.001). The sensitivity and specificity in the diagnosis of ALS were 82.6% and 92.6% for CN-jitter (cut-off value: 32 μs), and 91.3% and 96.3% for the spike number (cut-off value: 2.0), respectively. There was no significant difference between the SFN-jitter and CN-jitter in ALS patients; meanwhile, there was no significant difference between the SFN-jitter and CN-jitter in healthy controls.

CONCLUSIONCN-jitter and spike number could be used to quantitatively evaluate changes due to denervation-reinnervation in ALS.

Amyotrophic Lateral Sclerosis ; physiopathology ; Electrodes ; Electromyography ; Humans ; Middle Aged ; Needles ; ROC Curve

This study is to investigate the protection effect of schisandrin B (Sch B) against oxidation stress of HK-2 cells induced by cisplatin and the mechanisms involved. HK-2 cells were cultured and divided into different groups: solvent control group, cisplatin exposure group, positive group, Sch B treatment group. Cell viability and toxicity were evaluated by MTT and LDH assay. GSH level and SOD enzymes activities were also measured. DCFH-DA as fluorescence probe was used to detect ROS level by fluorescence microplate reader. Nrf2 translocation was detected by Western blotting. Real time Q-PCR was used to detect expressions of NQO1, HO-1 and GCLC mRNA level. The results showed that Sch B could significantly inhibit the decline of cell viability induced by cisplatin treatment (P < 0.05) and the protective effect was in a dose dependent manner. Furthermore, Sch B treatment significantly inhibited the increase of ROS level induced by cisplatin and reversed the decrease of GSH level (P < 0.05). When Sch B concentration was up to 5 micromol x L(-1), SOD enzyme activities were also enhanced significantly compared with that of the cisplatin group (P < 0.05). It was shown that Sch B could cause nuclear accumulation of Nrf2 in association with downstream activation of Nrf2 mediated oxidative response genes such as GCLC, NQO1 and HO-1. These results suggested Sch B could protect against the oxidative damage of HK-2 cells induced by cisplatin via the activation of Nrf2/ARE signal pathway.
Antineoplastic Agents ; toxicity ; Antioxidants ; isolation & purification ; pharmacology ; Cell Line ; Cell Survival ; drug effects ; Cisplatin ; toxicity ; Cyclooctanes ; isolation & purification ; pharmacology ; Glutamate-Cysteine Ligase ; genetics ; metabolism ; Glutathione ; metabolism ; Heme Oxygenase-1 ; genetics ; metabolism ; Humans ; Kidney Tubules, Proximal ; cytology ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Lignans ; isolation & purification ; pharmacology ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; metabolism ; NF-E2-Related Factor 2 ; genetics ; metabolism ; Polycyclic Compounds ; isolation & purification ; pharmacology ; RNA, Messenger ; metabolism ; Reactive Oxygen Species ; metabolism ; Schisandra ; chemistry ; Signal Transduction ; Superoxide Dismutase ; metabolism

BACKGROUNDMotor dysfunction is common in stroke patients. Clinical electrophysiological studies suggest that transsynaptic degeneration occurred in the lower motor neurons, while pathological evidence is lacked. This study aimed to combine the electrophysiological and pathological results to prove the existence of transsynaptic degeneration in the motor system after stroke.

METHODSModified neurologic severity score, electrophysiological, and pathological assessments were evaluated in rats before middle cerebral artery occlusion (MCAO), and at 24 hours, 7 days, and 14 days after MCAO. Paired and independent-sample t-tests were applied to assess the changes of electrophysiological and pathological data.

RESULTSCompound motor action potential amplitude in the paretic side was significantly lower than the nonparetic side at both 24 hours (61.9 ± 10.4 vs. 66.6 ± 8.9, P < 0.05) and 7 days (60.9 ± 8.4 vs. 67.3 ± 9.6, P < 0.05) after MCAO. Motor unit number estimation of the paretic side was significantly less than the nonparetic side (379.0 ± 84.6 vs. 445.0 ± 89.5, P < 0.05) at 7 days after MCAO. Until 14 days after stroke, the pathological loss of motor neurons was detected. Motor neurons in 14-day MCAO group were significantly decreased, compared with control group (5.3 ± 0.7 vs. 7.3 ± 1.8, P < 0.05).

CONCLUSIONSBoth electrophysiological and pathological studies showed transsynaptic degeneration after stroke. This study identified the asynchronization in changes of electrophysiology and pathology. The abnormal physiological changes and function impairment can be detected in the early stage and recovered quickly, while the pathological loss of motor neuron can be detected only in a later stage.

Animals ; Electrophysiology ; Infarction, Middle Cerebral Artery ; pathology ; physiopathology ; Male ; Motor Neurons ; pathology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; pathology ; physiopathology