Acetylcholine ; Amygdala ; Cues ; Fear

It is known that in myasthenia gravis(MG) the plasmapheresis therapy removes the acetylcholine receptor (AChR) antibodies and other toxins in the serum to cause clinical improvement temporarily. To know the effects of plasmapheresis on AChR antibody and clinical courses the authors checked serially the AChR antibody titers and clinical stages in myasthenia gravis. The plasmapheresis were performed for the therapeutic purposes in seven and elective purposes in three MG subjects. After two, three or four cycles of plasmapheresis, the myasthenic symptoms have dramatically improved in all subjects. However the AChR antibody titers decreased in only four out of ten and the decremental ratio in each case uas rather smaller than being expected. Thus the effects of plasmapheresis could not be explained solely by the decreasing phenomena of AChR antibody titers in MG subjects. Therefore the authors assumed that the clinical severities of MG could be correlated with other types of AChR antibodies that are not checked by the routine @-bungarotoxin binding technique, or the AChR antibodies are secondarily produced in large amount by the mechanism of rebound enhancing activity.
Acetylcholine* ; Antibodies ; Myasthenia Gravis* ; Plasmapheresis*

Sometimes it is not easy to make the diagnosis of myasthenia gravis (MG). The aim of our study was to understand the diagnostic sensitivities of tensilon, repetitive nerve stimulation (RNS), single fiber EMG (SFEMG) tests, acetylcholine receptor (AChR) antibodies (Ab), and to know their comparative significances for making diagnosis of MG. Those tests were safely completed in 40 myasthenia gravis, which consisted of 17 ocular, 21 generalized, 1 acute severe, 1 late severe MG. In all 40 subjects at least one of the tests was abnormal. The positive rates of tensilon, RNS tests, SFEMG, AChR Ab were 92.5%, 65.0%, 90.0%, and 82.5% respectively. The sensitivities of each tests were high in severe MG group, compared with those in mild MG group, because the positive rates were decreased from 100.0% to 89.2% in tensilon tests, from 83.3% to 57.1% in RNS test, from 100.0% to 89.2% in SFEMG tests and 91.7% to 78.6% in AChR Ab test. The positive results of RNS test was increased from 32.5% on abductor digiti quinti (ADQ) to 65.0% on orbicularis oculi (OOC). Among 3 cases with negative tensilon test, the RNS test in 1 case, the SFEMG tests were positive in all 3 cases, and the AChR Ab assay 1case. Among 3 cases with negative SFEMG, the tensilon tests were positive in 3 all cases, the RNS test in 1case and the AChR Ab assay in 1 cases. Among 5 cases, with negative RNS teses and negative AChR Ab assay, the tensilon tesrs wre positive in 3 cases and the SFEMG tests in 3 cases. Therefore we conclude that tensilon and SFEMG tests were more sensitive than RNS tests and AChR Ab assay. SFEMG test would be indicated to diagnose MG, especially in those mild MG cases with negative stensilon test. Also AChR Ab assay could improve diagnostic yields.
Acetylcholine ; Antibodies ; Diagnosis ; Edrophonium ; Myasthenia Gravis*

PURPOSE: This study was undertaken to evaluate the clinical usefulness of Tensilon test, repetitive nerve stimulation test(RNST), single fiber EMG(SFEMG) test and acetylcholine receptor antibody(AchR Ab) assay for making diagnosis of myasthenia gravis(MG). METHOD: These tests were performed in 21 MG patients which were classified into 11 ocular, 5 mild generalized, 4 moderate generalized, and 1 chronic severe MG. RESULT: The overall positivity of Tensilon test, SFEMG and AchR Ab was 95%, 87%, and 76% respectively. The overall positivity of RNST was 67%; 38% on flexor carpi ulnaris, 43% on adductor digiti quinti and 62% on orbicularis oculi muscles. The positivity of each test was higher in generalized MG group than in ocular MG group. But we could observe the statistically significant difference only in the RNST(p<0.05). CONCLUSION: Tensilon test showed the highest positivity in all MG groups. So we would like to recommend the Tensilon test for the diagnosis of MG at first, followed by RNST and AchR Ab assay, and SFEMG would be indicated to MG group which showed relatively low postivity in other tests.
Acetylcholine ; Diagnosis* ; Edrophonium ; Humans ; Muscles ; Myasthenia Gravis*

The authors have measured the anti-AChR antibody concentration in sera of 20 myasthenia gravis and of 17 normal or other neurological diseases, to establish the radioimmunoassay(RIA) system for the AChR antibody test and to evaluate the possible relationships between changes in AChR antibody titer and clinical severity of myasthenia gravis. Significant AChR antibody titers(more than 0.04 pmol/ml) were found in 17 out of 20 myasthenia gravis (85.0%) and in 1 out of 17 norrnal or other neurological diseases (5.9%). When those 20 myasthenia gravis were classified into Ossennan's clinical stage, the AchR antibody titer rarlged from 0 to 059 pmole/ml in grade I, from 0.01 to 0.68 pmole/ml in grade IIA, from 0.15 to 1.05 pmole/ml in grade II and from 0.22 to 1.03 pmol/ml in grade III, and showed relatively good correlation with clinical severity of myasthenia gravis (Pearson correlation coef{icient 0.76). However the correlation proved to be better when the AChR antibody titers were compared with the functional activities of myasthenia gravis according to Drachman s proposal. Also the authors thought that the AChR antibody tests would be invaluable in the diagnosis of myasthenia gravis and that the extensive studies would be needed to establish the normal value of the binding AChR antibody in our laboratory.
Acetylcholine* ; Diagnosis ; Myasthenia Gravis* ; Reference Values

Phytochemical investigation from the stem bark of Beilschmiedia pulverulenta resulted in the isolation of five lignans, (+)-yangambin (1), (+)-sesartemin (2), (+)-excelsin (3), (+)-sesamin (4), and (+)-syringaresinol (5), together with lupeol (6), lupenone (7), β-sitosterol (8), and β-sitostenone (9). Their structures were established by the analysis of their spectroscopic (1D and 2D NMR) and spectrometric (MS) data, as well as by comparison with those reported in the literature. The isolated lignans were tested for their anticholinesterase (AChE: acetylcholine esterase and BChE: butyryl cholineesterase) and anti-inflammatory (COX-2: cyclooxygenase-2 and LOX: lipoxygenase) activities. All the isolated lignans (1 – 5) exhibited significant inhibition activities in AChE/BChE and COX-2/LOX assays with IC50 values ranging from 168.8 – 504.2 µM and 21.0 – 59.4 µM, respectively.
Acetylcholine ; Cyclooxygenase 2 ; Inhibitory Concentration 50 ; Lignans

This study was performed to evaluate the titer of serum acetylcholine receptor antibody (AChR-Ab), the correlation between AChR-Ab titer and clinical state, clinical response to thymectomy and histopathologic finding of thymus in myasthenia gravis. Twenty-seven patients with various clinical grades of myasthenia gravis and twenty-three norrnal controls were included in this study. Mean AChR-Ab titers were 4.21+4.27nM in myasthenia gravis and 0.05+0.06nM in control group(p<0.05). Mean AChR-Ab titers of each clinical grade were 0.80+1.67nM in grade I, 5.05+3.42nN in grade Iia, 8.37+4.50nM in grade Iib, 6.67nM in grade m and 10.89nM in grade IV. There were significant correlation between clinical grade and level of AChR-AB titer. There were no correlation between degree of clinical improvement and changes of serum AChR-Ab titer after thymectomy in myasthenia gravis. There were also no correlation between level of AChR-Ab titers and histopathologic findings of thymus.
Acetylcholine ; Humans ; Myasthenia Gravis* ; Thymectomy ; Thymus Gland

This study was performed to evaluate the titer of serum acetylcholine receptor antibody (AChR-Ab), the correlation between AChR-Ab titer and clinical state, clinical response to thymectomy and histopathologic finding of thymus in myasthenia gravis. Twenty-seven patients with various clinical grades of myasthenia gravis and twenty-three norrnal controls were included in this study. Mean AChR-Ab titers were 4.21+4.27nM in myasthenia gravis and 0.05+0.06nM in control group(p<0.05). Mean AChR-Ab titers of each clinical grade were 0.80+1.67nM in grade I, 5.05+3.42nN in grade Iia, 8.37+4.50nM in grade Iib, 6.67nM in grade m and 10.89nM in grade IV. There were significant correlation between clinical grade and level of AChR-AB titer. There were no correlation between degree of clinical improvement and changes of serum AChR-Ab titer after thymectomy in myasthenia gravis. There were also no correlation between level of AChR-Ab titers and histopathologic findings of thymus.
Acetylcholine ; Humans ; Myasthenia Gravis* ; Thymectomy ; Thymus Gland

The aim of this study was to investigate the relationship between the acetylcholine concentration in the blood and gelsenicine-induced death in mice. Kunming mice were given intraperitoneal injections of normal saline, gelsenicine or different doses of acetylcholine chloride. Atropine was given to the mice which received gelsenicine or medium dose acetylcholine chloride injection. The blood was sampled immediately when the mice died or survived for 20 min after injection. The acetylcholine concentration and acetylcholinesterase activity in the blood were measured by the testing kits, and the mortality was calculated and analyzed. The results showed that half lethal dose of gelsenicine (0.15 mg/kg) reduced the acetylcholinesterase activity and increased the blood acetylcholine concentration. The blood acetylcholine concentration of the dead mice in the gelsenicine group was increased to 43.0 μg/mL (from 31.1 μg/mL in the control), which was lower than that (53.9 μg/mL) of the dead mice in the medium dose acetylcholine chloride group, but almost equal to that (42.7 μg/mL) of the survival mice in the medium dose acetylcholine chloride group. Atropine could successfully rescue the mice from acetylcholine poisoning, but its efficiency of rescuing the mice from gelsenicine intoxication was weak. These results suggest that gelsenicine can inhibit acetylcholinesterase activity and increase blood acetylcholine concentration, but the accumulation of acetylcholine may not be the only or main cause of the death induced by gelsenicine in mice.
Acetylcholine ; Animals ; Death ; Indole Alkaloids ; Mice

The cholinergic anti-inflammatory pathway (CAP) is a neuro-immunomodulatory pathway,in which acetylcholine (ACh) released by the interaction of vagal nerves with α7 nicotinic acetylcholine receptor (α7nAChR),which prevents the synthesis and release of pro-inflammatory cytokines and ultimately regulates the local or systemic inflammatory response in a feedback manner. It has been shown that there are many possible effective treatments for sepsis, including vagus nerve stimulation by physical therapy, drugs such as acetylcholine receptor agonist and ultrasound therapy.
Acetylcholine ; Humans ; Inflammation ; Neuroimmunomodulation ; Sepsis ; Vagus Nerve Stimulation ; alpha7 Nicotinic Acetylcholine Receptor