Intake of arsenic from water, food composites and excretion through urine, hair from a studied population in West Bengal, India.

To evaluate the main intake source of arsenic by the villagers from arsenic-affected families in Jalangi and Domkol blocks in Mushidabad district, West Bengal-India, we determined the concentrations of arsenic in tube-well water and in food composites, mainly including vegetables and cereals collected from the surveyed families which were cultivated in that region. The daily dietary intakes of arsenic by the villagers were estimated and the excretions of arsenic through urine and hair were determined. The arsenic concentrations in hair and urine of the studied population living in mild (2.78 microg/L), moderate (30.7 microg/L) and high (118 microg/L) arsenic-affected families were 133, 1,391 and 4,713 microg/kg and 43.1, 244 and 336 microg/L, respectively. The linear regressions show good correlations between arsenic concentrations in water vs hair (r(2)=0.928, p<0.001) and water vs urine (r(2)=0.464, p<0.01). Approximately 29.4%, 58.1% and 62.1% of adult population from mild, moderate and high arsenic-affected families were suffering from arsenical skin manifestations. The mean arsenic concentrations of food composites (vegetables and cereals) in high arsenic-affected families are not significantly different from mild arsenic-affected families. The daily dietary intakes of arsenic from water and food composites of the studied population, living in high, moderate and mild arsenic-affected families were 568, 228 and 137 microg, respectively. The linear regressions show good correlations between arsenic concentrations in hair vs daily dietary intake (r(2)=0.452, p<0.001) and urine vs daily dietary intake (r(2)=0.134, p<0.001). The water for drinking contributed 6.07%, 26.7% and 58.1% of total arsenic in our study from mild, moderate and high arsenic-affected families. The result suggested that the contaminated water from high arsenic-affected families should be the main source for intake of arsenic. On contrary, the contribution of arsenic-contaminated food composites from mild and moderate arsenic-affected families might be the main source for intake of arsenic. The Food and Agriculture Organization/World Health Organization (FAO/WHO) provisional tolerable weekly intake (PTWI) values of arsenic in our study were 3.32, 5.75 and 12.9 microg/kg body weight/day from mild, moderate and high arsenic-affected families, respectively, which is higher than the recommended PTWI value of arsenic (2.1 microg/kg body weight/day).     

Immunohistochemical and immunoelectron microscopical characterization of cerebrovascular and senile plaque amyloid in aged dogs'' brains

Immunohistochemical and immunoelectron microscopical studies were carried out on 28 aged dogs' brains. Amyloid deposits were seen in the arteries and capillaries in the leptomeninges and in superficial areas of the cortices in 19 (67.9%) of the 28 dogs (10-22 years of age). Immunohistochemically, these amyloid deposits were reactive for anti-beta/A4 antibody. Additionally, a variable number of parenchymal deposits with diffuse beta/A4-immunoreactivity (diffuse plaques) was also noted throughout the cerebral cortex in 24/28 dogs (85.7%). However, these plaque lesions were undetectable in Congo red staining. Electron microscopically, amyloid fibrils, measuring 10 nm in width, were located mainly in the tunica media of the arteries, and in less involved vessels they tended to be present among collagen fibres in the adventitia and smooth muscle cells in the outer layer of the media. The plaque lesions appeared to contain sparse aggregations of amyloid fibrils. In immunoelectron microscopical examinations, all amyloid fibrils in both blood vessels and plaques were selectively labelled by gold particles. These findings indicate that aged dogs can provide a useful experimental model for research into the beta/A4-type of cerebral amyloidosis commonly seen in Alzheimer's disease.     

MRI of the brain in chronic carbon monoxide poisoning

We examined 13 patients with chronic carbon monoxide (CO) poisoning by magnetic resonance imaging (MRI); all of them had been in an explosion in a coal mine 25 years previously. Symmetrical globus pallidus lesions were observed in 12, as was degeneration of the white matter, with focal cortical atrophy. The temporal parietal and occipital lobes were usually affected, the parietooccipital region being the most frequently and extensively damaged. Of the 12 patients with white matter degeneration 7 had definitely asymmetrical cortical and subcortical lesions. There were 6 patients with dilated temporal horns, probably due to atrophy of the hippocampal gyri. A history of CO inhalation and an awareness of the typical distributions of lesions are important for recognition of the effects of CO poisoning, especially when patients are in the chronic stage.     

Early seizures after acute ischemic stroke]

In order to determine predictive factors of early seizures (ES) after acute stroke and to estimate prognosis, we retrospectively examined clinical data of 1,743 consecutive patients with acute ischemic stroke. The subjects were divided into two groups; an ES group (19 patients) and a non-ES group (1,724 patients). Multivariate statistical analysis revealed that the NIH-Stroke Scale score on admission (/10, OR, 1.1: 95% CI 1.04 to 1.13) and positive past history of cerebrovascular disease or brain injury (OR, 3.85: 95% CI 1.49 to 9.95) are significant factors to predict ES. There was no significant difference in the outcome between the two groups. A recurrence of seizures, after follow up for 4 to 40 months, was observed only in one patient with a history of ES.     

Nucleolus-associated J chains in myeloma cells: clinical significance

Bone marrow aspirates from 20 patients with multiple myeloma (MM), 4 with smoldering multiple myeloma (S-MM), 1 with idiopathic Bence Jones proteinuria (I-BJP), and 6 with primary macroglobulinemia (PMG) were examined for nucleolus-associated J chain. The incidence of nucleolar J chain-positive (J+) cells among nucleolated cells producing M-component was measured. This incidence (94.0-100%) in terminal MM was significantly higher than that (0-58.0%) in non-terminal MM. Judging from a low incidence in the remission phase, chemotherapy might cause a selective elimination of less differentiated myeloma cells with J+ nucleoli and might have some effect on J chain synthesis. The incidence of nucleolar J+ cells was very low in S-MM. The IgM cells in PMG, where J chain is present in a disulfide-linked form, had no or few J+ nucleoli. No correlation between the incidence of nucleolar J+ cells among nucleolated plasma cells and the percentage of nucleolated cells or that of J+ cells was found. Large J+ nucleoli seemed to be another morphological feature indicating anaplastic myeloma cells. A high incidence of nucleolar J+ cells may be one of the indicators for progressive disease.     

Late-onset hemorrhagic infarction in patients with patent foramen ovale: reports of two cases]

We presented here two patients with hemorrhagic infarction occurred during subacute phase of brain embolism. The patients were 71-year-old and 73-year-old men who suffered from brain infarction of the left posterior cerebral artery and right middle cerebral artery territory, respectively. Both of them were diagnosed as having cryptogenic stroke and patent foramen ovale. After transferred to rehabilitation hospitals taking aspirin for a secondary prevention of stroke, they developed hemorrhagic infarction at day 17 and day 19, respectively. Their blood pressure remained within normal range throughout acute and subacute phase. Although most of hemorrhagic infarction occurs within 24 hours of stroke onset, some patients develop symptomatic hemorrhagic infarction even after 10 days. We need to be careful about late-onset hemorrhagic infarction, because many patients are now transferred early to rehabilitation hospitals to facilitate dedicated systematic rehabilitation.