UNLABELLED: Nisoldipine is a second generation dihydropyridine calcium antagonist having characteristics of strong coronary artery dilating effect and less negative inotropic action. The purpose of this study was to evaluate the effect of nisoldipine on the cardiac function (systolic and diastolic) and the exercise tolerance, in patients with hypertrophic cardiomyopathy (HCM). SUBJECTS: Twenty-three patients with HCM were studied. METHODS: We measured the following indices using M-mode and pulsed wave Doppler echocardiography before and after nisoldipine therapy; left ventricular fractional shortening (LVFS), isometric relaxation time (IRT), deceleration half-time (DHT) of early diastolic mitral (E) flow, late diastolic mitral (A) flow and A/E ratio. Symptom-limited treadmill exercise test was performed. Exercise tolerance (EX) time was measured. Nisoldipine of 10 mg/day was orally administered. Same tests were repeated on day 14 and after 6 months. RESULTS: 1) Short-term effects; LVFS did not change (55.9 +/- 5.9%-->57.0 +/- 7.4%, NS) after 2 weeks. However, LV diastolic function significantly improved (IRT; 92.1 +/- 7.7 ms-->85.2 +/- 11.6 ms, p < 0.05, DHT; 70.7 +/- 16.2 ms-->63.3 +/- 3.7 ms, p < 0.05). EX time increased (8.9 +/- 2.6 min-->10.0 +/- 3.3 min, p < 0.05), 2) Long-term effects; LV diastolic function had a tendency toward improvement, but is statistically not significant (IRT; 91.1 +/- 7.6-->83.8 +/- 11.6 ms, DHT; 73.1 +/- 23.4-->61.0 +/- 11.4 ms, A/E; 1.26 +/- 0.29-->1.11 +/- 0.36) after 6 months. EX time was significantly increased (9.4 +/- 1.7--> 10.1 +/- 1.7 min, p < 0.05). CONCLUSIONS: Nisoldipine improved LV diastolic dysfunction and exercise tolerance in patients with HCM. These effects were similar to the first generation calcium antagonists. LV diastolic dysfunction may be improved due to the reduction of intracellular calcium concentration and the relief of myocardial ischemia by strong coronary artery dilating effect. However, nisoldipine did not affect the LV systolic function because of its less negative inotropic effect.

Adult↗

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Neuronal plasticity and Parkinson disease.

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Brain↗

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Suppression of T lymphocyte proliferation by peritoneal macrophages in chickens.

The mechanism of the suppression of lymphocyte proliferation by peritoneal macrophages (MPs) in chickens and the presence of a suppressive substance in the culture supernatant of MPs were studied. The results showed that gelatin- and peptone-induced peritoneal MPs had an inhibitory accessory function against blastogenesis of mitogen-stimulated splenic lymphocytes and that resident peritoneal MPs had an enhanced accessory function. The suppressive factor produced by gelatin-induced peritoneal MPs is a protein having a pI of 3.6 and a molecular weight of 64,000 and it is physically and chemically a relatively stable substance. Moreover, it has no cytotoxic effect against lymphocytes and it was verified that the suppressor in the culture supernatant of MPs was not prostaglandin E2 or alpha-acid glycoprotein.

Animals↗

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Frontal distribution of early cortical somatosensory evoked potentials to median nerve stimulation.

The topography of early frontal SEPs (P20 and N26) to left median nerve stimulation was studied in 30 normal subjects and 3 patients with the left frontal bone defect. The amplitudes of P20 and N26 were maximum at the frontal electrode (F4) contralateral to the stimulation and markedly decreased at frontal electrodes ipsilateral to the site of stimulation. There was, however, no latency difference of P20 and N26 between ipsilateral and contralateral frontal electrodes. These results suggest that the origin of the ipsilateral and contralateral P20 and N26 is the same. The wide distribution of P20 and N26 over both frontal areas could be explained by assuming a smearing effect from generators actually located in the rolandic fissure and motor cortex.

Adult↗

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Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions.

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23). In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.

Adolescent↗

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Cortical somatosensory potentials evoked by magnetic stimulation: effect of body height, age, and stimulus intensity.

Cortical somatosensory evoked potentials elicited by non-invasive magnetic stimulation at Th10, Th12, and L5 vertebral levels and at mid-gluteus and ankle were studied in 45 normal controls varying in body height and age. Peak latencies of P2 evoked by ankle, mid-gluteus and L5 stimulation were correlated with body height. However, P2 latencies evoked by Th10 and Th12 stimulation were independent of body height. In contrast, all N2 latencies evoked by Th10, Th12, L5, mid-gluteus and ankle were correlated with body height. There were no correlations between latencies of P3 and N3 and body height. No peak latencies of cortical components were affected by age within the age group studied (15-67 years). In the intensity study, N2 showed double peaks when low to moderate stimulus intensities were applied to Th12 vertebra. Furthermore, in 2 patients with mild somatosensory dysfunction of lumbar roots or cord, N2 evoked by L5 stimulation revealed double peaks with prolonged interpeak latencies between the first peak of N2 and P3, which might be related to the temporal dispersion of the afferent fibers. These data suggest that the N2 component is induced by both fast and slow afferent fibers.

Adolescent↗

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Clinical comparison of Alzheimer's disease in pedigrees with the codon 717 Val-->Ile mutation in the amyloid precursor protein gene.

Alzheimer's disease (AD) is the most common cause of dementia (32). Although the majority of cases of AD are sporadic, the most consistent risk factor detected in several epidemiological studies has been a positive family history of the disease (14,21). In addition, many large pedigrees have been described in which AD appears to be inherited as an autosomal dominant disorder. In one such pedigree (F23) a point mutation within the beta-amyloid precursor protein (APP) gene at codon 717 was identified and hypothesized to be pathogenic (10). The mutation results in a valine to isoleucine change in APP (APP717 Val-->Ile). Subsequent screening has revealed four other pedigrees, detailed in this study, in which this mutation co-segregates with AD (13,26,37). In addition, one other pedigree (Tor3) with this mutation has been described (15) and detailed clinical, neuropsychological, and neuropathological data are reported. Tor3 is discussed below in comparison to the findings in the families in this study. The five families we report with the mutation were identified in Britain (1 family), the United States (1 family), and Japan (3 families). The mutation has not been reported in the general population of any of these countries (3,13,26,33). On this basis alone it seems this mutation is pathogenic. Other APP codon 717 mutations have been identified which co-segregate with the disease (4,25). Also, a double mutation in APP at codons 670/671 has been shown to cosegregate with the disease in two large Swedish pedigrees (22). In all cases, there is complete co-segregation of the APP mutation with early onset AD, providing overwhelming statistical evidence that these mutations are pathogenic. We present the clinical features and limited neuropathology of AD in these families with the APP 717 Val-->Ile mutation.

Adult↗

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Functional imaging for the analysis of the mucosal blood hemoglobin distribution using electronic endoscopy.

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Animals↗

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Homologous complement activation on drug-induced apoptotic cells from a human lung adenocarcinoma cell line.

Activation of the alternative pathway of homologous complement (C) was observed in a human lung adenocarcinoma cell line, CADO 43, after the cells had become apoptotic following treatment in vitro with vincristine and predonisolone. Deposition of C3b and C3bi on the serum-treated apoptotic cells was revealed by flow cytometry with anti-C3b and -C3bi-specific antibodies and immunoblotting with anti-C3 antibody immunoprecipitates extracted from solubilized fractions of serum-treated apoptotic cells. Two molecular mechanisms were found to be responsible for this post-apoptotic C-activation. Firstly, all C regulators, decay accelerating factor (DAF), membrane cofactor protein (MCP) and C3b/C4b receptor (CR1), were diminished on the cell surface concomitantly with the apoptotic process. Secondly, unidentified molecules which potentially activate homologous C and accept C3b/C3bi fragments became expressed on the cell surface during the apoptotic process. These findings may explain the mechanism whereby tumor cells are efficiently eliminated through chemotherapy.

Adenocarcinoma↗

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mtDNA polymorphisms in Japanese sporadic Alzheimer's disease.

We screened 92 Japanese patients with sporadic AD (clinically diagnosed: 72 cases; autopsy-confirmed: 20 cases) and 59 age-matched controls for mitochondrial polymorphisms previously reported to be associated with increased risk in Caucasian AD. The polymorphisms in tRNA(Gln) (nt. 4336), 16S rRNA (nt. 3196), and ND1 (nt. 3397) were not found in either in Japanese AD or age-matched controls. The frequencies of these polymorphisms in Japanese seems to be very rare if not absent, indicating that these three mutations are not likely to be genetic risk factors of Japanese AD. In the analysis of polymorphisms of 12S rRNA, however, we identified two novel mutations, an insertion of three cytosines and an A to G transition at nt. 856, which have not been described before. The insertion of three cytosines was observed in one of the 90 AD cases, but not in 59 normal controls. The A to G transition at nt. 856 was found in 2 of the 90 AD cases, but not in 59 normal controls. These results raise the possibility that the mutations in the 12S rRNA are genetic risk factors for AD in Japanese population.

Adult↗