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Biomedical subjects

A J Blotcky

Publications and source records attributed to A J Blotcky.

At least 19 recordsLinked to original sources
PubMed2001

Coexisting independent sodium-sensitive and sodium-insensitive mechanisms of genetic hypertension in spontaneously hypertensive rats (SHR).

Some essential hypertensive patients and genetic hypertensive rat strains have less than the normal levels of Mg2+ tightly bound to the plasma membranes of their erythrocytes and other cells, i.e., the magnesium binding defect (MgBD). This binding defect appears to cause increased passive permeability of the membrane to Na+ and thereby its increased intracellular concentration, particularly if the Na+-extrusion enzyme systems of the cell are also defective. The Na+-Ca2+ exchange system in the cell membrane exports Na+ and imports Ca2+, increasing the tone of the smooth muscle cell and thus producing hypertension (HTn). This HTn is Na+-sensitive. Evidence supporting this postulate was obtained by determining the intraerythrocyte total concentrations of Na+, Ca2+, K+, and Mg2+ in two strains of spontaneously hypertensive rats (SHR and SS/Jr rats, having the MgBD together with the other requisites of the Na+-sensitive pathway) and their respective controls (WKY and SR/Jr rats, in which this complete pathway is absent). The Na+ and Ca2+ concentrations in the hypertensive rats were increased, and that of K+ was decreased. The concentrations of these cations were very similar in the two hypertensive strains. The level of membrane tightly bound Ca2+ in SHR erythrocyte membranes was significantly higher than those in the other three rat strains, which were not statistically different from each other. These results support previously reported evidence of the existence of a novel HTn-generating mechanism in the SHR rat, in which the intracellular Ca2+ concentration is increased as the result of the enhanced diffusion of this ion into the cell and the accompanying deficiency of the Ca2+ extrusion enzyme systems. This pathway is therefore Na+-insensitive, i.e., Ca2+-sensitive.

Animals↗
PubMed1997

Brain mercury in neurodegenerative disorders.

BACKGROUND: Trace element neurotoxicity has long been invoked as an etiologic factor for Alzheimer's disease. This study was conducted to determine the concentrations of mercury in seven different brain regions from deceased patients histologically confirmed with Alzheimer's disease or multiple sclerosis as compared to control subjects without known central nervous system and renal disorders. Brain mercury concentrations in all deceased subjects can arise from amalgam restorations, diet, and the working environment. METHODS: Autopsy frozen specimens (control, Alzheimer's disease and multiple sclerosis) from seven brain regions, which included frontal cortex, temporal cortex, occipital cortex, putamen, hippocampus, corona radiata and corpus callosum were assayed for the concentrations of selenium using instrumental neutron activation analysis and mercury using radiochemical neutron activation analysis. RESULTS: We found that the concentrations of mercury and the mercury/selenium molar ratios were significantly lower in the hippocampi of multiple sclerosis patients as compared to aged-matched controls. However, no statistically significant differences were detected for the concentrations of mercury and the mercury/ selenium molar ratios for the remaining six brain regions among these groups. CONCLUSIONS: Since brain mercury concentrations from deceased subjects with either Alzheimer's disease or multiple sclerosis are not significantly higher than controls, the present study provides no scientific support that mercury plays a significant role in the pathogenesis of these neurologic disorders.

Aged↗
PubMed1995

Determination of blood mercury concentrations in Alzheimer's patients.

Trace element neurotoxicity can be an etiologic factor for Alzheimer's disease. This cross sectional clinical study determined blood mercury in patients with diagnosed Alzheimer's disease as compared to control subjects without known central nervous system and renal disorders. Unique within the confines of a nursing home, all subjects were exposed to the same environment and consumed a diet without fish and seafood for a period of three months prior to the study. The results of this study show that blood mercury concentrations detected in subjects with Alzheimer's disease were not statistically different than that of control subjects. Ratios of blood mercury to blood selenium were also determined and no statistical difference was found between these two groups.

Aged↗
PubMed1993

Selenium in peritoneal fluid.

Selenium (Se) has been identified in reproductive tissues, including human endometrium and decidua. However, no information regarding its presence in peritoneal fluid or any subsequent correlation with a reproductive clinical condition has been reported. This research endeavored to determine the presence of Se in peritoneal fluid in 30 women undergoing diagnostic laparoscopy for an infertility evaluation. Semen analysis, postcoital tests, endometrial biopsy and hysterosalpingography were performed on each patient preoperatively; normal results were a prerequisite. Except in three cases, samples from all patients undergoing diagnostic laparoscopy were obtained during the luteal phase of the menstrual cycle. Se was assayed quantitatively by instrumental neutron activation analysis. It was identified in all peritoneal fluid samples but did not specifically correlate with any clinical infertility findings.

Adolescent↗
PubMed1992

Determination of aluminum by chemical and instrumental neutron activation analysis in biological standard reference material and human brain tissue.

Since aluminum is an extremely difficult element to determine reliably in biological samples, no National Institute of Standards and Technology (NIST) biological standard reference material for tissue has yet been certified for aluminum. A chemical neutron activation analysis procedure employing anion-exchange chromatography was developed. The procedure proved successful in decontaminating radioactivatable sodium and chlorine and phosphorus which can produce aluminum via a fast neutron bombardment. For bovine liver (NIST SRM 1577 a) a value of 2.1 +/- 0.2 micrograms of aluminum/g of sample was determined, comparing favorably to the uncertified value 2 micrograms/g sample. For freeze-dried urine (NIST SRM 2670) a value of 0.18 +/- 0.01 micrograms of aluminum/mL of urine was observed. Its uncertified value is 0.18 micrograms of aluminum/mL of sample. Twenty three individual samples in three different human brains were analyzed for their aluminum content.

Aluminum↗
PubMed1983

Red blood cell and serum selenium concentrations as influenced by age and selected diseases.

Red blood cell and serum selenium concentrations were investigated to determine normal concentrations for our geographic area and if potential differences existed in patients with selected diagnoses (hepatic, renal, malignant, and chronic diseases). Selenium was quantified in samples of red blood cells, serum and urine by neutron activation analysis. The results were analyzed by comparing 1) pooled data from all ages for each disease with normal values, and 2) normal values with age-matched patients in each disease category. Decreases in red blood cell selenium concentrations (P less than 0.05) occurred in normal subjects over 60 years of age without concurrent significant decreases in serum selenium. Although differential results were noted in age-matched groups, overall results showed that decreased concentrations of selenium in both red cells and in serum occurred with alcoholic cirrhosis, malignancies, and chronic renal failure (P less than 0.025). Red blood cell selenium concentrations also were decreased in patients with stable chronic disease. Decreased serum selenium concentrations were positively correlated with albumin concentrations in patients with cirrhosis. There was no correlation between serum selenium and bilirubin concentrations in patients with liver disease or between serum selenium and creatinine concentrations in patients with chronic renal failure whose urinary excretion of selenium was far below control levels.

Adult↗
PubMed1980

The relationship of dietary selenium and breast cancer.

An inverse relationship exists between dietary selenium (Se) concentrations and the incidence of human breast cancer. The addition of Se to the diet has been shown to decrease the incidence of spontaneous murine mammary tumors. We compared the serum Se concentrations in breast cancer patients with those of women without breast cancer. Serum was collected from 35 women with breast cancer. Nineteen of these women had infiltrating ductal carcinoma and two had Paget disease of the nipple. Nine women had lymph nodal metastases at the time of mastectomy, four had definite evidence of metastatic disease when the blood samples were drawn, and the disease process of one patient was unclassified. Samples from 27 women known to be free of breast cancer were used as controls. The difference noted between the mean serum Se concentrations of breast cancer patients and controls were found to be significant.

Adult↗
PubMed1980

Inhibition of cadmium-induced hypertension in rats.

In a low cadmium environment, adding 10 parts per million (ppm) of cadmium to the drinking water of rats for 3 to 18 months induced increases in systolic pressure averaging 12 to 18 mm Hg. The pressor effect of the cadmium was inhibited by adding 3.6 ppm of selenium or 200 ppm of zinc to the drinking water or by dissolving the cadmium in hard water rather than deionized water. A second experiment with 2.5 ppm of cadmium and smaller amounts of selenium and zinc was confirmatory. Exposure to 10 ppm of cadmium increased renal, hepatic, and cardiac cadmium many fold from barely detectable control levels; however, the increases were much less when the cadmium was dissolved in hard water. Cadmium exposure also increased tissue zinc by 30 to 60%. The addition of selenium to cadmium further increased cardiac cadmium, but the addition of zinc to cadmium had no further effect on tissue cadmium. Tissue selenium concentrations were suggestively but not significantly higher following selenium exposure. Cadmium alone, or combined with selenium or zinc, increased renal copper; while the combination of cadmium and selenium increased hepatic copper.

Animals↗
PubMed1979

Serum levels of selenium, calcium, copper magnesium, manganese and zinc in various human diseases.

Serum selenium as well as serum zinc, copper, magnesium, calcium and manganese were investigated in a control group of adult males and in 11 groups of patients in various disease states. Not only the change of each trace element but also the possible association between elements was studied in the various groups. All patients were fasting when sampled and studied only after the acute phase of the disease was corrected. Trace metal determinations were performed by atomic absorption spectrophometry (Mg, Ca, Cu, Zn) and by neutron activation analysis (Se, Mn). All patients showed low serum zinc when compared to controls. Cirrhotic patients had a low serum selenium level as well as low calcium, magnesium and zinc. Emphysemia and cancer patients had an elevated serum copper concentration while copper and manganese levels were elevated in congestive heart failure, infection and pschoses. To our knowledge this is the first time low serum selenium values have been demonstrated to be associated with the low serum zinc, calcium and magnesium levels found in cirrhotic patients.

Adult↗
PubMed1978

Serum selenium and reticuloendothelial tumors.

Serum selenium levels were determined by neutron activation analysis on 59 patients with a variety of reticuloendothelial neoplasms. Correlations were attempted between the widely variable range in the serum concentrations of the trace element with the parameters employed in this study. Therapy, particularly less than six weeks initiation, produced elevations in the serum selenium levels.

Female↗
PubMed1977

Evidence of aluminum absorption from the gastrointestinal tract and bone deposition by aluminum carbonate ingestion with normal renal function.

The question of whether aluminum is toxic in patients ingesting large oral loads, either for phosphate binding in renal dialysis or as an antacid for peptic ulcer, has been raised. The permeability of the gut barrier for aluminum has not been established because of the lack of precise analytical techniques. Urine aluminum was measured in this study before and during oral aluminum carbonate loading in six subjects with normal renal function, one of which had peptic ulcer disease and a 25-year history of high oral aluminum ingestion. The analytical procedure involved destructive neutron activation analysis. Aluminum was present in the urine in all instances before loading and rose in every case from 4-fold to 10-fold. Bone aluminum was measured in six autopsy specimens, three dialysis patients, three nondialysis patients, and in an iliac crest biopsy from the peptic ulcer patient who had osteoporosis. The bone biopsy aluminum level in the ulcer patient was intermediate between those of "normal subjects" and patients on dialysis. These results show that the gut barrier is permeable to heavy aluminum load and suggest that bone aluminum deposition occurs in humans with normal renal function.

Adult↗