Using H-7, HA1001, FK506, cyclosporin A (CsA) and okadaic acid (OA), which are protein kinase and phosphatase inhibitors, we examined qualitative changes in hematopoietic precursor cells due to aging from the viewpoint of the role of protein kinases and phosphatases. Though H-7 and OA suppressed erythroid colony formation both in the elderly (age: 72-92, median: 86) and the young (age: 22-39, median: 29), no change due to aging was noted. HA1001 did not affect erythroid colony formation either in the elderly or the young. Erythroid colony formation was enhanced by FK506 and CsA in the young, however, erythroid colony formation was suppressed in the elderly. Similar examinations using cell fractions of non-T, non-macrophage, non-T+T, and CD34 positive cells were performed in both groups. Enhancement of erythroid colony formation in the young and suppression in the elderly by FK506 using unseparated MNC disappeared after removal of T cells. Enhancement of colony formation in the young and suppression of colony formation in the elderly were recovered when T cells were added again. The effects of FK506 and CsA on erythroid colony formation were thought to be the results of T cell inactivation, and the different sensitivity to FK506 and CsA in the elderly and young seemed to be the result of changes in the control mechanisms of hematopoiesis, such as the regulation of cytokine production by T cells, caused by aging.
The purpose of this study was to assess whether regimen comprehension deteriorates in the elderly without obvious mental disability. Eligible patients were elderly who could visit hospitals by themselves. We recruited 138 patients (age: 43-89, 75 males and 63 females, underlying diseases: hypertension, hyperlipidemia, arrhythmia etc.) from our outpatient clinic. The participants were tested with a regimen comprehension scale (RCS: Jpn J Geriat 1997; 34: 209-214). The differences in scores among individuals increased with age. Scores of 5 or less were recorded in 10 of 69 patients aged 65 or more, but in none of 69 patients aged less than 65 (p<0.01). The 60 patients who could not get full marks were classified into 2 groups: the tutored group (T) who were tutored by pharmacists about taking drugs, and the non-tutored group (N). Both groups were tested again with RCS to evaluate the effect of tutorial. In T-group (n=28), the second scores increased significantly (from 7.2±0.9 to 8.6±2.0 (m±SD); p<0.01). Although the second scores showed a tendency to increase in N-group (n=29), there was no statistical significance. In 7 patients who obtained less than a score of 5 on the RCS and age- and gender-matched controls who received full marks on the RCS, the HDS-R test failed to show any differences between the two groups. Thus, we concluded that even in the self-attending elderly patients, the regimen comprehension deteriorated with age, and tutorials were considered to be effective.
We examined 24 hour heart rate variability (HRV) components and baroreflex sensitivity (BRS) in elderly adults. Forty-eight subjects, aged 65-69 years old (24 men, 24 women) were examined in this study. BRS was measured in the morning (8:00-9:00) using noninvasive cross spectral analysis. There were significant correlations between BRS and low-frequency (LF) power (r=0.593, p<0.001) of HRV, and between BRS and high-frequency (HF) power (r=0.402, p<0.005). BRS values were lower in women compared with men (p<0.01), and LF/HF was significantly lower in women than in men (p<0.05).
In order to elucidate a possible mechanism for accelerated atherogenesis as well as enhanced vascular calcification observed during the normal aging process, we measured plasma osteopontin (OPN) levels and examined their relation to aging and certain disease parameters. In all cases examined, no significant relation was found between the plasma OPN level and age, body mass index, blood pressure, plasma levels of glucose and insulin, serum levels of creatinine, triglyceride, and high density lipoprotein cholesterol. On the other hand, a significant negative correlation was found between the plasma OPN level and serum total cholesterol concentration (n=78, r=-0.355, p=0.0014). The serum level of low density lipoprotein (LDL) cholesterol, calculated by the formula of Friedewald, also showed a significant negative correlation to the plasma OPN level (n=78, r=-0.301, p=0.0075). In cases without diabetes mellitus and hypertension, a significant positive correlation was found between the plasma OPN level and age (n=22, r=0.445, p=0.0378). It is postulated that OPN plays a negative regulatory role in the development of vascular calcification. Therefore, the observed negative relationship between the plasma OPN level and the serum levels of total cholesterol and LDL cholesterol, suggests a possibility that hypercholesterolemia facilitates vascular calcification by suppressing OPN synthesis. On the other hand, in non-diabetic and normotensive cases, the positive relationship between the plasma OPN level and age may reflect a defense mechanism against age-related increase of vascular calcification.
This study was conducted to clarify brain and carotid lesions in patients with asymptomatic carotid bruits and their characteristics. We studied 37 patients with carotid bruits, who had various diseases other than stroke and were all neurologically normal, using by brain computerized tomography (CT) and ultrasonography (US). On CT, localized low density areas (LDAs) and their distribution were assessed, as well as the grade of periventricular lucency (PVL). Carotid lesions on US were classified into 3 categories; plaque (locally thickened intima-media complex of 2.1mm or more in thickness), stenosis (narrowed lumen between 50% and 90% of the linearly measured diameter), and occlusion (severely narrowed lumen more than 90%). Ankle pressure index (API) less than 0.9 was defined as low. Mean age was 73.2 years-old and 28 of them were men. Bruits were heard bilaterally in 15 patients. CT findings showed LDA in 13 patients (35%) and severe PVL in 12 patients (32%). Twenty-three LDAs (13 in the left hemisphere and 10 in the right hemisphere) were seen and all were considered to be infarctions. Nineteen LDAs, 13 of them seen in the basal ganglia, were lacunae. Another 3 LDAs were seen in the watershed zone between the middle and posterior cerebral arteries, whereas the remaining one was a small cortical infarction in the left premotor area in the middle cerebral artery territory. Ultrasonography showed carotid lesions in 65 of 74 carotid arteries (plaque in 28, stenosis in 26, and occlusion in 11) and low API in 18 of 37 patients. Compared with patients with normal CT finding, the frequency of hypertension (92% vs 50%) and ischemic heart disease (69% vs 29%) was significantly high in 13 patients with silent infarction, although there was no difference in US findings. In the hemisphere ipsilateral to the carotid with bruits, which was frequently stenotic, the frequency of infarction was similar to that in the hemisphere ipsilateral to the carotid with no bruit. Regression analysis revealed that hypertension significantly correlated with the presence of cerebral infarction. These findings indicated that incidence of infarction in the elderly patients with asymptomatic carotid bruits was high and was associated with hypertension and advanced atherosclerosis in many organs, including the carotid and peripheral arteries. The reason for the lack of symptoms was considered to be that most of the infarctions were lacunae and located in the basal ganglia, although infarction did not significantly correlate with bruits or carotid lesions.
We attemted to clarify the temporal profile and the predisposing factors for progressing neurological disorders in the patients with acute cerebral infarction in the territory of the deep perforators of the carotid system. The subjects were 19 patients with mild hemiparesis admitted to our hospital within 24 hours of stoke onset, and their mean age was 59.9±9.1. Six of those patients (about 32%) had gradual neurological deterioration after admission (progressive cases), and they had poor outcome compared with non-progressing patients. The mean progressing period was 3.7±1.0 days. Our examination suggest that both the changes in systemic hemodynamics and the risk factors for cerebrovascular disease (hypertension, diabetes mellitus, hyperlipidemia) do not always provide a correlation with the development of progressing stroke. However, we speculate that the impairment of the microcirculation plays a major role in progressing stroke in the territory of penetrating arteries because of the result that the mean infarct size of progressive patients had a tendency to be larger than that of non-progressive patients in the chronic stage.
The causes of pituitary apoplexy are unclear. We report a case of pituitary apoplexy presenting with headache and nausea. On June 17th, 1997 a 74-year-old woman had complained of retro-orbital headache, fever and vomiting. A cold was diagnosed for which she recurred medication. In addition to the previous symptoms she was getting to lose appetite. She was admitted to our hospital for further examination and treatment on June 21. On admission neurological examination showed left pupil mydriasis, the left eye had no light reflex and the right eye had only a slight response to the light. She could hardly move both eyeballs up. Laboratory data showed a normal white blood cell count and the CRP was 16.2mg/dl. Lumbar puncture showed 97mg/dl total protein and 82 cells per μl, most of which were lymphocytes. We diagnosed viral infection based on the evidence of clinical symptoms and lumbar puncture data. The patient was treated with γ-globulin and improved. From the 16th day of sickness we recognized symptoms of oculomotor paralysis and the syndrome of inappropriate antidiuretic hormone. On the 23rd day of sickness we strongly suspected pituitary apoplexy based on transaxial MR images. After absorption of intra-tumor hemorrhage, the oculomotor symptoms recurred. We finally reached a diagnosis of pituitary apoplexy based on pathological material, MR images, symptoms and laboratory data. We must think of pituitary apoplexy when we see an aged out-patient with severe headache, nausea, vomiting and oculomotor paralysis. It was difficult to diagnose this disease in the early time course of the disease.
A 70-year-old woman with a past history of cholecystolithiasis was admitted to a local clinic because of right hypochondralgia with back pain. Since physical examination revealed Murphy's sign, this patient was diagnosed as acute cholecystitis. The ultrasonographic examination of the gallbladder showed a stone of the cystic duct with no definitive wall thickening. CT scan revealed dissection of the abdominal aorta. She was then referred to our hospital for further examinations. She was observed in the cardiac care unit to determine whether the aneurysm and cholecystitis were in an acute or chronic state. Blood examinations and enhanced CT scan showed that her clinical symptoms originated not from cholelithiasis but from acute closing aortic dissection, Stanford classification type B. Close cooperation with a highly developed medical facility is essential when diagnosing eldely patients with symptoms open to a variety of interpretation.
We report five cases of purple urine bag syndrome (PUBS). All the patients were women and they had been bed-ridden for a long period due to cerebrovascular diseases. They tended to be constipated as a result of habitual use of laxatives. Indicanuria was proven in the all urinary samples from the patients. The four assessable urinary cultures showed Proteus mirabilis contamination. Total days without evacuation per month in patients with PUBS and control subjects (5 catheterized subjects without PUBS) were 16.5±3.7 and 6.8±4.8, respectively (mean±SD), showing a significant difference (p<0.05). In each case, this syndrome was not considered to have affected their clinical course. We concluded that it is unnecessary to treat patients with PUBS aggressively. Control of evacuation and urological sanitation are important in these patients.