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Biomedical subjects

D Amato

Publications and source records attributed to D Amato.

At least 91 records · Page 5Linked to original sources
PubMed1977

A review of 700 bone marrow aspirations in Papua New Guinea.

A retrospective survey of 700 marrow examinations in Papua New Guinea in a 2 1/2 year period has been carried out. Over half of the total came from the Port Moresby General Hospital. Anaemia and splenomegaly were the commonest indications. A disturbing proportion of the specimens were unsatisfactory for interpretation. Hypercellular marrows with erythroid hyperplasia were very common. Iron stores were absent or nearly absent in almost half of the evaluable specimens; this proportion rose to over 95% amongst pregnant or post-partum women with anaemia. Other relatively frequent findings included: a combination of features consistent with hypersplenism; mild degrees of eosinophilia and/or plasmacytosis; and mild degrees of megaloblastic changes. Haematological malignancies were found in over 10% of evaluable specimens. Of 611 assessable marrows from Melanesians, only 11 (1.8%) were entirely normal, but another 151 (24.7%) contained only minor abnormalities.

Adolescent↗
PubMed1977

Hereditary ovalocytosis in Melanesians.

A distinctive type of hereditary ovalocytosis has been found in Papua New Guinea and a few areas of Southeast Asia. Its main features include a high incidence among tropical lowland dwellers, autosomal recessive inheritance, specific depression of a number of red cell antigens, a characteristic morphology in blood films, and an effect on the erythrocyte sedimentation rate. Speculation has occurred as to whether the high incidence of ovalocytosis in malarious areas may be related to a selective advantage possessed by ovalocytics with regard to severe malaria. Preliminary data tend to support this hypothesis, but the evidence is not conclusive and much further work is needed.

Blood Sedimentation↗
PubMed1977

Sago haemolysis: clinical features and microbiological studies.

Severe, acute and sometimes fatal intravascular haemolysis has occurred on several occasions in Papua New Guinea families after the ingestion of apparently 'stale' sago. Earlier cases had been recorded only from the Maprik area; however, we now report the occurrence of two similar outbreaks, involving a total of 14 persons, in the Western Province. Several bacteria and fungi were isolated and identified in a sample of suspect sago from one of the outbreaks. None of these, however, to our knowledge, has ever been incriminated as a cause of haemolysis, and the aetiological agent(s) and mechanism of haemolysis thus remain to be elucidated. No mycotoxins were detected in one sample available for analysis. It is suggested that the eating of sago stored for a long time be discouraged; and further that, if a meal of sago tastes abnormal, additional mouthfuls should not be eaten and the remaining portion should be sent for analysis or discarded.

Adolescent↗
PubMed1977

Von Willebrand's disease in a Papua New Guinean.

An example of von Willebrand's disease in a Papua New Guinean female is described; this is believed to be the first time that this disorder has been documented in a Melanesian. Some salient features of the diagnosis and management of the disease are discussed. Bleeding disorders in Papua New Guinea have been found with increasing frequency in recent years, and it is not unreasonable to expect that their true incidence will be similar to those seen elsewhere.

Adult↗
PubMed1976

Erythroid colony growth in congenital hypoplastic anemia.

Four children with congenital hypoplastic anemia (Diamond-Blackfan syndrome) and 30 control children with normal erythropoiesis were studied by a cell culture method in which human marrow, grown in a plasma clot, responds to added erythropoietin (EPO) with the appearance of discrete colonies of nucleated erythroid cells. The colonies arise from EPO-responsive stem cells and are not related to the number of morphologically identifiable marrow erythroids plated. Results of studies on control marrow indicated that without EPO there was little or no colony formation. Increasing EPO doses or nucleated marrow cells per culture resulted in a linear increase in colony numbers. The optimal EPO concentration of 2.5 U/ml yielded a mean of 158 +/- 79 colonies/1 x 10(5) nucleated cells on day 7 of incubation. Even in the absence of recognizable erythroids, marrows of all four patients with anemia grew erythroid colonies. Two patients on no therapy had decreased colony numbers. The other two, on prednisone, had normal numbers. Sera from patients did not inhibit colony formation from either autologous or control marrow. In contrast, serum from an adult with acquired pure red cell aplasia produced striking inhibition of colony growth. It appears that the red cell failure in this disorder is not due to an absence of erythroid stem cells, and a serum inhibitor to erythropoiesis as seen in the acquired disease is unlikely.

Anemia, Aplastic↗
PubMed1976

Glanzmann's thrombasthenia in a Melanesian.

A case of Glanzmann's thrombasthenia is documented in a Melanesian child, and the diagnosis and treatment of this disorder are discussed. This is the third inherited bleeding disorder to be reported in Papua New Guinea, haemophilia A (Factor VIII deficiency) and Factor XIII deficiency having been described previously.

Blood Coagulation Disorders↗
PubMed1976

Granulopoiesis in severe congenital neutropenia.

The pathogenesis of the granulopoietic failure in three children with severe congenital neutropenia was studied. Mature neutrophils were absent from both peripheral blood and bone marrow. Assay of bone marrow granulocyte colony-forming cells (CFU-C) in a methylcellulose tissue culture system using colony-stimulating activity (CSA) from peripheral blood leukocytes demonstrated normal or increased concentrations of CFU-C compared to those from marrows of 60 age-matched controls. Colonies were of normal size and by light microscopy appeared to contain granulocytes in all stages of maturation including the mature polymorphonuclear neutrophil. CFU-C from peripheral blood of two patients were normal. Production and activity of CSA from the patients' peripheral blood leukocytes and urinary CSA excretion were normal. No serum inhibitors against CFU-C or CSA could be demonstrated using both control and autologous marrow. The defect did not appear to be due to a lack of granulocytic stem cells, a reduction of humoral stimulators of granulopoiesis, nor the presence of an inhibitor as measured by these techniques.

Agranulocytosis↗
PubMedDate not supplied

Electroencephalographic changes following low energy emission therapy.

Low energy emission therapy (LEET) is a novel approach to delivering low levels of amplitude-modulated electromagnetic fields to the human brain. The sleep electroencephalogram (EEG) effects of a 15-min LEET treatment were investigated in a double-find cross-over study to assess sleep induction. Fifty-two healthy volunteers were exposed to both active and inactive LEET treatment sessions, with a minimum interval of 1 week between the two sessions. Baseline EEGs were obtained, and 15-min posttreatment EEGs were recorded and analyzed according to the Loomis classification. A significant increase in the duration of stage B1 sleep (0.58 +/- 2.42 min [mean +/- SD], p = 0.046), decreased latency to the first 10 sec epoch of sleep (-1.23 +/- 5.32 min, p = 0.051) and decreased latency to sleep stage B2 (-1.21 +/- 5.25 min, p = 0.052) were observed after active treatment. Additionally, establishment of slow waves with progression from stages B to C was significantly more pronounced after active LEET treatment (p = 0.040). A combined analysis of these results with those of an identical study performed in Denver showed that LEET had a significant effect on afternoon sleep induction and maintenance with shorter sleep latencies (decreased latency to the first 10 sec epoch of sleep; -1.00 +/- 5.51 min, p = 0.033; decreased latency to sleep stage B2; -1.49 +/- 5.40 min, p = 0.003), an increased duration of stage B2 (0.67 +/- 2.50 min, p = 0.003), an increase in the total duration of sleep (0.69 +/- 4.21 min, p = 0.049), and a more prominent establishment of slow waves with progression to a deeper sleep stage (p = 0.006). It is concluded that the intermittent 42.7 HZ amplitude modulation of 27.12-MHz electromagnetic fields results in EEG changes consistent with shorter sleep latencies, longer sleep duration, and deeper sleep in healthy subjects.

Adult↗
PubMedDate not supplied

Cola beverage consumption induces bone mineralization reduction in ovariectomized rats.

BACKGROUND: A significant association of cola beverage consumption and increased risk of bone fractures has been recently reported. The present study was carried out to examine the relationship of cola soft drink intake and bone mineral density in ovariectomized rats. METHODS: Study 1. Four groups of 10 female Sprague-Dawley rats were studied. Animals from groups II, III, and IV were bilaterally ovariectomized. Animals from groups I and II received tap water for drinking, while animals from groups III and IV each drank a different commercial brand of cola soft drink. After 2 months on these diets, the following were measured: solid diet and liquid consumption; bone mineral density; calcium in bone ashes; femoral cortex width; calcium; phosphate; albumin; creatinine; alkaline phosphatase; 25-OH hydroxyvitamin D, and PTH. RESULTS: Study 2. Two groups of seven ovariectomized rats were compared. Group A animals received the same management as the group III animals from study 1 (cola soft drink and rat chow ad libitum), while rats from group B received tap water for drinking and pair-feeding. After 2 months plasmatic ionized calcium, phosphate, creatinine, albumin, calcium in femoral ashes, and femoral cortex width were measured. Study 1. Rats consuming cola beverages (groups III and IV) had a threefold higher liquid intake than rats consuming water (groups I and II). Daily solid food intake of rats consuming cola soft drinks was one-half that of rats consuming water. Rats consuming soft drinks developed hypocalcemia and their femoral mineral density measured by DEXA was significantly lower than control animals as follows: group I, 0.20 +/- 0.02; group II, 0.18 +/- 0.01; group III, 0.16 +/- 0.01, and group IV, 0.16 +/- 0.01 g/cm(2). Study 2. To rule out the possibility that these calcium and bone mineral disorders were caused by decreased solid food intake, a pair-fed group was studied. Despite a lower body weight, pair-fed animals consuming tap water did not develop bone mineral reduction or hypocalcemia. CONCLUSIONS: These data suggest that heavy intake of cola soft drinks has the potential of reducing femoral mineral density.

Albumins↗
PubMedDate not supplied

Response of atrial natriuretic factor to acute extracellular fluid volume in patients with pheochromocytoma.

BACKGROUND: Patients with pheochromocytoma have been reported to show high plasmatic atrial natriuretic factor (ANF) levels. Its source may not be the atrium because blood volume, the most important physiological stimulus for ANF release, is usually reduced in these patients. METHODS: To evaluate ANF secretion functional integrity, we studied three patients with pheochromocytoma before and after surgical removal of the tumor. Extracellular fluid (ECF) volume, plasmatic ANF levels, and plasmatic renin activity (PRA) were measured. ANF was measured before and after an acute saline load of 1.5L in 90 min. RESULTS: Before surgery, ECF volume was normal or reduced, and PRA was normal but decreased after the saline load. By contrast, ANF was elevated and did not change after the saline load. After surgery ANF decreased, ECF volume rose, and the saline load induced a significant increase of plasma ANF and reduction of PRA. ANF was present in significant amounts in tumoral tissue homogenates. CONCLUSIONS: These data suggest that the tumor was the source of ANF in these patients with pheochromocytoma because high levels of ANF, despite reduced or normal ECF volume, as well as unresponsiveness to acute saline infusion, were found before surgery with subsequent normalization after tumor removal.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Left ventricular diastolic dysfunction secondary to hyperglycemia in patients with type II diabetes.

Diabetes mellitus type II, a cause of preclinical left ventricular dysfunction that can progress to cardiac insufficiency ventricular dysfunction in diabetic patients, is attributed to systemic arterial hypertension, or ischemic cardiopathy. Diastolic ventricular dysfunction takes place during the course of diabetes mellitus. The purpose of the present article is to report on the influence of hyperglycemia on the left ventricular diastolic dysfunction independently of dyslipidemia, obesity, and systemic arterial hypertension, usually present in diabetic patients. Left ventricular diastolic function was studied by Doppler echocardiography in asymptomatic type II diabetic patients without ischemic or valvular cardiopathies, cardiomegaly, or systemic arterial hypertension. Two groups of patients were integrated: patients with and without left ventricular diastolic dysfunction, i.e., groups A and B, respectively. Glycemia, cholesterol, triglycerides, and body mass index (BMI) were determined in each subject. Bivariate statistical tests (Student t, chi-square, or Mann-Whitney U tests) were applied to study the influence of the previously mentioned variables on the ventricular diastolic function. To evaluate the influence of hyperglycemia on ventricular diastolic function separately from dyslipidemia, systemic arterial hypertension, and the influence of obesity, logistic regression, and multivariate statistical analysis were applied. Independently of dyslipidemia and obesity, a relationship was found between hyperglycemia and diastolic dysfunction of the left ventricle in patients belonging to group A (p <0.05, odds ratio [OR] 12.1). No statistical significance was found between glycemia and the diastolic function of the left ventricle in group B patients. Even in type II diabetic patients without cardiopathy, uncontrolled hyperglycemia provokes diastolic left ventricular dysfunction.

Adult↗