Medical treatment of Parkinson's disease.
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Biomedical subjects
Publications and source records attributed to D L Xu.
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BACKGROUND & AIMS: Recent studies suggest that production of nitric oxide is increased in cirrhosis. This study determines to what extent this increased production contributes to arterial vasodilation and hyperdynamic circulation in cirrhosis. METHODS: Mean arterial pressure (MAP), cardiac index, and systemic vascular resistance (SVR) were determined in cirrhotic rats with ascites undergoing long-term treatment with different doses of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (3 mg or 0.5 mg.kg-1.day-1). Untreated cirrhotic rats with ascites and controls were also studied. The vascular production of NO was estimated by the aortic concentration of guanosine 3',5'-cyclic monophosphate (cGMP). RESULTS: Untreated cirrhotic rats had significantly lower MAP and SVR and higher cardiac index and aortic cGMP concentration than controls. When administrated to cirrhotic rats, an L-NAME dose of 3 mg.kg-1.day-1 induced a reduction of cGMP concentration less than normal levels. In these rats, MAP and SVR increased to greater than and cardiac index decreased to less than values in controls. By contrast, cirrhotic rats treated with 0.5 mg.kg-1.day-1 L-NAME had similar aortic cGMP concentrations as controls, suggesting a normalization of NO production. This was associated with a normalization of MAP, cardiac index, and SVR and a reduction in the elevated plasma renin activity and vasopressin concentration. CONCLUSIONS: Normalization of vascular NO production corrects systemic hemodynamic abnormalities in cirrhotic rats with ascites.
The C57Bl/6 susceptible (Bcgs) and its resistant (Bcgr) congenic mouse, previously developed by retrogressive backcrossing, were infected with 1 x 10(6) colony-forming units (CFU) of Mycobacterium avium and bacterial growth and their immune responses during the early and prolonged periods of infection were examined. There was a high proliferation in the liver and spleen of Bcgs mice, whereas no proliferation was observed in the Bcgr mice. Similarly, the sizes and weights of these organs were much higher than those of their Bcgr counterparts. The size and number of granulomas in Bcgs were also found to be higher than those of Bcgr. The CD3+ and CD4+ subsets increased dramatically in both mice during the early stage of infection. However, in the later phase of the infection, these populations decreased dramatically in Bcgs mice, but not in Bcgr mice, resulting in a depression in cell-mediated immune responses. No significant decrease in cell-mediated immune responses was observed in Bcgr mice even after prolonged infection. ELISA was performed to determine the antibody levels in both mice, and it was found that serum IgG and IgM levels in Bcgs were comparatively higher than those in Bcgr mice throughout the period of infection. The Bcg gene therefore may have an important role in the maintenance of resistance not only in the early phase but also in the later phase of Myco. avium infection.
We report five cases of cat-scratch disease encephalopathy (CSDE), with a brief review of the literature in English, in which only 96 patients of CSDE have been described up to the present. The Gram-negative bacilli demonstrated by Warthin-Starry or Dieterle silver stains are regarded as the causative agent of CSDE. Administration of antibiotics is recommended. The onset of CSDE is usually acute and the prognosis favorable.
Using molecular hybridization, left ventricular ras oncogene expression was examined in the hypertrophic heart of rat or during injection of vasopressin or alpha-receptor agonist neosynephrine. Results showed that ras oncogene expression of left ventricle could be potentiated by neosynephrine but not by vasopressin. Furthermore, expression of both nucleic oncogene myc and membrane oncogene ras were increased during chronic cardiac pressure overload, with the former occurring in early loading stage and the latter staying the whole loading stage.
Plasma concentration of ANF and expression of left ventricular ANF-gene in rats with cardiac hypertrophy induced by abdominal aortic partial ligation were analyzed by RIA and Northern blot respectively. Results showed that plasma concentration of ANF and level of left ventricular ANF-mRNA in cardiac hypertrophic rats increased markedly, indicating that the cardiac load may induce transcription and expression of left ventricular ANF-gene. This effect could be potentiated by intracellular calcium modulator taurine and inhibited by vasodilator hydralazine.
The value of an abnormal ratio of recovery systolic blood pressure to peak exercise SBP for detecting coronary artery diseases (CAD) is controversial. We evaluated the ratio in 39 patients with angiographically documented CAD and 52 patients with normal coronary artery undergoing treadmill exercise. If a response with the ratio higher than 1.0 and 0.8 at 1 and 3 min. of recovery was considered as abnormal, the sensitivity for detecting CAD was 66.7%, the specificity 73.1% and the accuracy 70.3%. If ST segment depression is combined into the criteria, the specificity and accuracy reach 94.2% and 76.9%. In CAD, the ratio at 3 min. of recovery showed significant negative correlation with resting left ventricular ejection fraction (LVEF) (r = -0.461, P < 0.01). It is suggested that low resting LVEF may be one of the mechanism of this abnormal ratio in CAD.
Hepatitogenicity of three plaque purified mutant strains of mouse hepatitis virus, designated as MHV-2S, -2M and -2L, isolated from MHV-2 infected SR-CDF1-DBT cells was studied. After intraperitoneal inoculation with 2 x 10(5) PFU of parental MHV-2 and its mutants to 4-week-old female ICR mice, 40% of mice inoculated with MHV-2S and 20% of mice with -2M died in one week, whereas with -2L all mice survived. All mice inoculated with MHV-2 died in 3 days postinoculation (p.i.). Virus titer of the liver of mice inoculated with MHV-2, -2S and -2M reached peaks (MHV-2:10(7) PFU/0.2 g, -2S: 10(5) PFU/0.2 g and -2M: 10(6) PFU/0.2 g) at 96 hr p.i., while with -2L a peak titer (10(3) PFU/0.2 g) was shown at 48 hr p.i. Immunofluorescence revealed MHV specific antigen in the liver of MHV-2S infected mice in and around necrotic areas though less extensive than that of parental MHV-2 infected mice. With MHV-2M specific fluorescence was restricted in degenerated hepatocytes in the small necrotic foci. In mice inoculated with MHV-2L only faint fluorescence was detected. Histopathologically, in the liver of MHV-2S infected mice zonal necrosis and cell infiltration were observed. There were spotty necrosis and focal cell infiltration in the liver of MHV-2M infected mice and only small inflammatory foci were seen in MHV-2L infected mice. Large number of extracellular virions were detectable in MHV-2S but not in -2M and -2L infected mice by electron microscopy.
After local surgical exposure, we administrated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) directly into the right common carotid artery of 5 rhesus monkeys. All the monkeys manifested akinesia, rigidity and postural tremor of the contralateral limbs, and spontaneous circling toward the MPTP treated side. These disturbances began to appear 3-4 days after injection, peaking at one month, and continued until the day of sacrifice. After treatment with madopar and apomorphine, marked improvements of the motor impairments appeared and a striking reversal of the direction of rotation away from the MPTP-treated side occurred in a dose-dependent manner. The ipsilateral neurotoxicity was confirmed biochemically by 99% reduction in the caudate-putamen dopamine levels and histologically by selective cell loss in the substantia nigra of the MPTP-treated side. It is concluded that this primate model of hemiparkinsonism is easy to reproduce and life is maintained with good health otherwise. So it may be more feasible for behavioral and pharmacological studies of Parkinson's disease.
T-lymphocyte subsets, B-lymphocyte, immunoglobulins and complement were studied in 38 children with Henoch Schonlein Purpura (HSP) in the acute stage. They had significantly lower CD3 percentage and lymphocyte blastogenesis rate, greater CD8 variation coefficient and B-lymphocyte percentage and higher levels immunoglobulins (IgA, IgG, IgM) and complement 3 than the controls. 21 (55%) of them had a low CD8 percentage. The results indicated that children with HSP had low T-lymphocyte percentages and function, increased B-lymphocyte percentage and function, high immunoglobulins, normal or elevated complement. On the other hand, no significant differences were found in the T-lymphocyte subsets values among healthy children aged 7-11 years. The normal values of T cell subsets in 35 normal controls were CD3 66-70%, CD4 37-41%, CD8 28-32%, respectively.
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The administration of MPTP to man and monkey has been shown to cause a neurotoxic effect on the nigrostriatal dopamine system. MPTP was injected in C57-BL black mice, 36 mg per kg for 7 days, which resulted in permanent reduction of dopamine and serotonin levels in the striatum. In the mice pretreated with PLG, although the striatal dopamine level was also reduced, mean dopamine and serotonin levels were significantly higher than in mice given MPTP alone. It is concluded that PLG could protect at least partially the neurotoxic effect of MPTP.
PLG potentiates the action of levodopa in 6-OH-DA-treated rats. PLG plus levodopa is more effective than levodopa alone. PLG-treated rats have a decreased concentration of Leu-enkephalin in the caudate nucleus as compared with the control. Preliminary results of using PLG (400 mg/day) for 10 days for treating PD are satisfactory. The mode of action of PLG with relation to dopamine-enkephalin interaction is discussed.