PubMed Health⌕ Search

Biomedical subjects

A Mithal

Publications and source records attributed to A Mithal.

At least 19 recordsLinked to original sources
PubMed1996

Learning disabilities and poor motivation to achieve due to prolonged iodine deficiency.

The effect of prolonged iodine deficiency on learning and motivation was studied. One hundred male children--matched for age, socioeconomic status, and formal education--were selected from both severely iodine-deficient (SID) and mildly iodine-deficient (MID) villages. Mean urinary iodine excretion was significantly lower in the SID than in the MID group (219.84 +/- 57.52 compared with 449.14 +/- 32.31 nmol/L, P < 0.001). The serum thyroxine concentration was significantly lower (90.36 +/- 6.46 compared with 123.70 +/- 15.42 nmol/L, P< 0.001) and serum thyroid-stimulating hormone (TSH) was significantly higher in the SID group than in the MID group (6.23 +/- 0.34 compared with 4.85 +/- 0.28 mU/L, P< 0.01). The children were administered maze, verbal, and pictorial learning tasks and a test of motivation. The results showed that SID children are slow learners compared with MID children. In both groups the rate of learning over trials was superior in younger (aged 9-12 y) children although the initial performance of older (aged 12-15 y) children was better (P < 0.01). SID children scored significantly lower than MID children on the achievement motivation scale (P < 0.01). The results are suggestive of neural impairment as well as poor sociopsychologic stimulation, resulting in learning disability and lowered achievement motivation. Unless iodine nutrition is improved in the community as a whole, these abnormalities may prevent millions of children from the SID areas from achieving their full potential even if learning opportunities are made available to them.

Achievement↗
PubMed1995

Human CD5+ B lymphocytes (B-1 cells) decrease in peripheral blood during pregnancy.

Pregnancy is a unique immunologic state where a natural homeostasis exists between antigenically different tissues. Several earlier studies have addressed the fluctuations in the number and/or function of lymphocytes, including B cells during pregnancy, but changes within the subsets of B lymphocytes, conventional (CD5-) and B-1 (CD5+), have not been addressed. Here we demonstrate that the frequency of B-1 cells decreases dramatically during pregnancy, whereas the frequency of conventional B cells remains relatively constant. The missing B-1 cells return to pre-pregnancy levels 8-10 weeks after parturition. The polyreactive autoantibodies secreted by B-1 cells have been implicated in autoimmunity and immune regulation. The possible role of B-1 cells during pregnancy will be discussed in that context.

Adult↗
PubMed1995

Non-islet cell tumour induced hypoglycaemia with acromegaloid facial and acral swelling.

The syndrome of non-islet cell tumour hypoglycaemia (NICTH) has been linked with the synthesis and secretion of 'big' IGF-II. We report a patient with a large pelvic clear cell sarcoma who developed recurrent severe hypoglycaemia and in addition presented with severe soft tissue facial swelling, skin tags and nuchal hyperpigmentation. After resection of the tumour serum 'big' IGF-II returned to normal and the acromegaloid skin changes remitted.

Acromegaly↗
PubMed1995

Expression of G protein alpha-subunits in bovine parathyroid.

A G protein-coupled Ca(2+)-sensing receptor was recently cloned from bovine parathyroid and shown to mediate divalent cation regulation of PTH secretion. To define which G proteins might be coupled to the Ca(2+)-sensing receptor in parathyroid cells, we determined which G protein alpha-subunit messenger RNAs (mRNAs) are expressed in the parathyroid. We also considered the possibility that a novel parathyroid-specific G alpha might be present. We, therefore, used the reverse transcription-polymerase chain reaction to study the expression of G alpha subunits in a bovine parathyroid mRNA preparation. Degenerate primers, corresponding to two regions conserved in every G alpha subunit, the G3 and G4 sequences, were used to amplify G alpha complementary DNA fragments that were subcloned and sequenced. We found that mRNAs corresponding to G alpha s, G alpha i2, G alpha 11, G alpha 12, and G alpha z are the predominant G alpha mRNAs expressed in the bovine parathyroid. No novel G alpha mRNA was identified. Northern blots confirmed the expression of the cloned G alpha subunits and showed lower expression of G alpha o and G alpha i1 mRNAs. Immunoblots confirmed abundant expression of G alpha s, G alpha i2, and G alpha 11 and provided evidence for expression of G alpha i1 and G alpha i3, but not G alpha o. G alpha q mRNA was not identified by the degenerate primer reverse transcription-polymerase chain reaction strategy, but the immunoblot detected G alpha q protein, albeit at considerably lower levels than G alpha 11. The abundance of G alpha 11 relative to G alpha q in bovine parathyroid is consistent with but does not prove a role for G alpha 11 in coupling the Ca(2+)-sensing receptor to phospholipase C.

Amino Acid Sequence↗
PubMed1995

Calcitonin-secreting cells of the thyroid express an extracellular calcium receptor gene.

Calcitonin (CT) secretion by parafollicular cells of the thyroid (C cells) is regulated by small changes in the concentration of extracellular calcium ([Ca2+]e). Elevation of [Ca2+]e elicits a rise in the C cell cytoplasmic calcium concentration and stimulates CT release. The molecular entity through which C cells detect changes in [Ca2+]e and modulate hormone secretion is unknown. Recently, an extracellular calcium-sensing receptor (CaR) complementary DNA was isolated from bovine parathyroid gland. To assess whether parathyroid cells and C cells use similar mechanisms to detect changes in ambient Ca2+, rat, human, and sheep C cells were examined for expression of the parathyroid CaR or a related receptor isoform. Reverse transcription-polymerase chain reaction analysis identified CaR transcripts in rat and human thyroid gland. Northern blot analysis demonstrated CaR messenger RNA (mRNA) in rat thyroid gland, a human medullary thyroid carcinoma (MTC) isolate, and a highly enriched preparation of sheep C cells. Rat MTC 44-2 cells, a cell line responsive to changes in [Ca2+]e, express abundant levels of CaR mRNA. Human TT cells, a C cell line lacking the extracellular calcium-sensing function, have undetectable levels of CaR mRNA by Northern blot analysis. Western blot analysis, using antiserum specific to the parathyroid CaR, detected CaR protein in rMTC 44-2, but not TT cells. Immunostaining of both dispersed sheep C cells and rat thyroid gland sections identified C cell-specific expression of the CaR protein, and in situ hybridization analysis confirmed the C cell-specific expression of CaR mRNA in the intact rat thyroid. The nucleotide sequence of the coding region of the rMTC 44-2 CaR transcripts was found to encode the same CaR protein as that expressed in the parathyroid and kidney. The results demonstrate that C cells express the same extracellular calcium-sensing receptor that is found in parathyroid and kidney, and the presence of this receptor protein in C cell lines correlates with the extracellular calcium-sensing function. This CaR is likely to represent the primary molecular entity through which C cells detect changes in [Ca2+]e and control CT release, suggesting that activation of the same receptor can either stimulate or inhibit hormone secretion in different cell types.

Amino Acid Sequence↗
PubMed1995

The reduced responsiveness of cultured bovine parathyroid cells to extracellular Ca2+ is associated with marked reduction in the expression of extracellular Ca(2+)-sensing receptor messenger ribonucleic acid and protein.

PTH secretion from dispersed bovine parathyroid cells maintained in culture becomes progressively less responsive to changes in the extracellular Ca2+ concentration (Ca2+o) over several days. We have now investigated whether this change in secretory control is associated with alterations in the expression of the Ca2+o-sensing receptor (BoPCaR) recently cloned from bovine parathyroid, which plays a central role in Ca2+o-regulated PTH secretion. BoPCaR messenger RNA levels dropped rapidly in cultured bovine parathyroid cells, as assessed by Northern analysis, decreasing by 78% within 18 h and remaining low for at least 4 days. The level of receptor protein decreased to a comparable extent (approximately 72-82%) after 3-4 days in culture, as determined by immunocytochemistry with specific antibodies directed at the extracellular domain of the receptor. The half-time for the reduction in receptor protein (approximately 2 days) was considerably longer, however, than that for BoPCaR messenger RNA, but was comparable to that for the loss of sensitivity of PTH secretion to Ca2+o. Indeed, there was a close linear correlation between maximal suppressibility of PTH secretion and the intensity of staining for the receptor protein (r = 0.88; P = 0.004). We conclude that alterations in the expression of BoPCaR could explain much of the reduced responsiveness of cultured bovine parathyroid cells to Ca2+o.

Animals↗
PubMed1993

Radiological spectrum of endemic fluorosis: relationship with calcium intake.

Skeletal fluorosis continues to be endemic in many parts of India. Osteosclerosis and interosseous membrane calcification have long been regarded as hallmarks of this disease. Our study showed in addition a wide variety of radiological patterns: coarse trabecular pattern, axial osteosclerosis with distal osteopenia and diffuse osteopenia. Subjects with osteopenic changes had a significantly lower dietary intake of calcium than those groups having normal radiological findings, predominant osteosclerosis or coarse trabecular pattern (p < 0.001, p < 0.01, and p < 0.01 respectively). This suggests the role of calcium intake in determining the skeletal changes in endemic fluorosis.

Adolescent↗
PubMed1993

Reversible impairment of glucose tolerance in patients with endemic fluorosis. Fluoride Collaborative Study Group.

Endemic fluorosis is a condition resulting from prolonged ingestion of drinking water which contains excess fluoride. Studies on rats have suggested that fluoride toxicity may produce glucose intolerance and abnormalities in insulin secretion. We studied glucose and insulin profiles following an oral glucose load in patients with endemic fluorosis. Twenty-five young adults (age range, 15-30 years) with endemic fluorosis, and an equal number of matched healthy control subjects with normal fluoride intake were studied. Impaired glucose tolerance was demonstrated in 10 of 25 (40%) patients with endemic fluorosis. Patients with impaired glucose tolerance had significantly higher fasting serum immunoreactive insulin (p < 0.05), higher fasting serum fluoride (p < 0.001), and a significantly lower fasting glucose to insulin ratio than that in patients with normal glucose tolerance (p < 0.001) or control subjects (p < 0.05). The fasting serum fluoride levels correlated positively with the area under the glucose curve (r = 0.80, p < 0.01) in patients with impaired glucose tolerance. Interestingly these abnormalities could be reversed when the village was provided drinking water with fluoride levels within acceptable limits. The present study shows that chronic fluoride toxicity in humans could result in significant abnormalities in glucose tolerance which are reversible upon removal of the excess fluoride.

Adolescent↗
PubMed1993

Skeletal scintigraphic findings in endemic skeletal fluorosis.

Endemic skeletal fluorosis is characterized by bone, joint and muscle pain, progressive ankylosis of various joints and crippling deformities. Whole body skeletal scintigraphy with 99Tcm-methylene diphosphonate was performed for 17 symptomatic subjects suffering from this disorder. The fluoride content of drinking water ranged from 4.1 to 12.9 mg l-1 (normal < 1 mg l-1). Urinary and serum fluoride levels were markedly elevated. Serum calcium (total and ionized), inorganic phosphorus, creatinine and albumin were essentially normal while serum alkaline phosphatase was elevated in six subjects (mean +/- S.D. 206 +/- 106; range 22-1072 IU l-1). Skeletal radiology revealed a wide spectrum of bony abnormalities. Skeletal scintigraphy revealed a picture similar to metabolic 'superscan' in all subjects, i.e. increased tracer uptake in axial and appendicular skeleton, reduced soft tissue uptake, poor or absent renal images, prominent costochondral junction and 'tie' sign in sternum. Increased uptake was present in all subjects irrespective of age, water fluoride content, serum alkaline phosphatase level and radiological abnormalities. Our findings suggest the presence of a high bone turnover state in endemic skeletal fluorosis irrespective of other variables.

Adolescent↗
PubMed1993

Hyperkalemic periodic paralysis associated with thyrotoxicosis.

A 32 year old male presented with episodic pure motor weakness for 1 1/2 months. On evaluation he was found to be thyrotoxic. Hyperkalemic challenge test provoked similar weakness with raised serum potassium (6 meq/L). He responded to treatment with neomercazole. Till he became euthyroid, he responded to the addition of acetazolamide to his medication. He is symptom free on antithyroid drug alone over 8 months of follow up.

Acetazolamide↗
PubMed1992

Glucocorticoid-dependent transformation by human papillomavirus type 16 E7 coding and 3' noncoding sequences.

The establishment of transformation of primary rodent cells by human papillomavirus (HPV) type 16 DNA requires glucocorticoid hormones (Pater et al., Nature 335, 832-835, 1988). Here we provide evidence by mutational analysis that, in the context of the hormone-regulated HPV 16 promoter/enhancer, the only protein coding sequences of HPV 16 required are those of the E7 gene. Moreover, additional sequences adjacent to the 3' end of E7 coding sequences are also essential for the establishment of the transformed phenotype. Splice donor sites, especially an E7 ORF 3' proximal one, are implicated for this cis-acting function, since specific deletion mutations of these splice sites greatly or completely reduced the frequency of transformation and the level of E7 RNA.

Animals↗
PubMed1992

Idiopathic oedema.

Explore the source record for details and available documents.

Autonomic Nervous System Diseases↗
PubMed1991

Malignant insulinoma presenting with recurrent episodic loss of consciousness.

A 57 year old male presented with episodic behavioural abnormalities and loss of consciousness for 2 years. His fasting blood glucose was 20 mg/dl and corresponding insulin level 119 uU/ml. His EEG showed intermittent rhythmic delta activity. Abdominal CT scan revealed an enhancing mass in the tail of the pancreas and secondaries in the liver. After distal pancreatectomy, resection of the left lobe of the liver and chemotherapy, the hypoglycaemic spells subsided. Histopathology revealed an islet cell tumour with metastases in the liver. Episodic neurobehavioural dysfunction should alert towards the possibility of hypoglycaemia.

Humans↗
PubMed1988

Late-onset adrenal hyperplasia in north Indian hirsute women.

The occurrence of late-onset congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency was studied in 60 consecutive hirsute women by means of adrenocorticotrophin (ACTH)-stimulated serum 17-hydroxyprogesterone (17-OHP) levels. Five (8.3%) women had an exaggerated response (ACTH-stimulated 17-OHP 3,160 +/- 560 ng/dl). All of them had regular periods and 3 were virilized. The other 2 were indistinguishable from those with idiopathic hirsutism or polycystic ovarian disease.

17-alpha-Hydroxyprogesterone↗