Tuberculosis of the CNS presenting as mass lesions.
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Adult↗
Biomedical subjects
A R Kumar
Publications and source records attributed to A R Kumar.
Phase II study of procarbazine, CCNU, and vincristine combination chemotherapy in the treatment of malignant brain tumors.
Forty-eight patients with primary or metastatic malignant tumors of the central nervous system (CNS) were treated with combination chemotherapy, consisting or procarbazine (100 mg/m2 X 14 days), CCNU (75 mg/m2), and vincristine (1.4 mg/m2 X 2, 1 week apart) (PCV) every 4 weeks. Most patients had undergone initial resection of primary tumors, postoperative radiotherapy, and a post irradiation interval of 3 months or more. Other patients harbored unbiopsied, newly-discovered primary or metastatic tumors. All patients were deteriorating neurologically when treatment began. Overall response rate for PCV combination therapy was 44%, no better than results obtained with single agent procarbazine or BCNU, the most effective drugs used alone in previous brain tumor chemotherapy studies.
Brain Neoplasms↗
Comparative rates of dead tumor cell removal from brain, muscle, subcutaneous tissue, and peritoneal cavity.
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Animals↗
Surfactant protein-A: new insights into an old protein--Part I.
Pulmonary surfactant is a lipoprotein substance that lines the lungs and helps reduce surface tension. Surfactant associated protein-A (SP-A) is the most abundant non-serum protein in pulmonary surfactant. This complex glycoprotein aids in the synthesis, secretion and recycling of surfactant phospholipids, and facilitates the reduction of surface tension by surfactant phospholipids. Recent evidence has highlighted the role of SP-A in the innate immune system present in the lung. SP-A may play a major role in defense against pathogens by interacting with both infectious agents and the immune system. Factors that affect fetal lung maturation, e.g., gestational age and hormones, regulate SP-A gene expression. Mediators of immune function also regulate SP-A levels. A number of lung disorders, including infectious diseases and respiratory distress syndrome are associated with abnormal alveolar SP-A levels. SP-A can no longer be called a lung-specific protein, since it has recently been detected in other tissues. In most species, SP-A is encoded by a single gene, however in humans it is encoded by two, very similar genes. Models for the structure of the human SP-A protein molecule have been proposed, suggesting that the mature alveolar SP-A molecule is composed of both gene products. The study of SP-A may provide information helpful in understanding disease processes and formulating new treatment modalities.
Gene Expression↗
Surfactant protein-A: new insights into an old protein--II.
Pulmonary surfactant is a lipoprotein substance that lines the lungs and helps reduce surface tension. Surfactant associated protein-A (SP-A) is the most abundant non-serum protein in pulmonary surfactant. This complex glycoprotein aids in the synthesis, secretion and recycling of surfactant phospholipids, and facilitates the reduction of surface tension by surfactant phospholipids. Recent evidence has highlighted the role of SP-A in the innate immune system present in the lung. SP-A may play a major role in defense against pathogens by interacting with both infectious agents and the immune system. Factors that affect fetal lung maturation, e.g. gestational age and hormones regulate SP-A gene expression. Mediators of immune function also regulate SP-A levels. A number of lung disorders, including infectious diseases and respiratory distress syndrome are associated with abnormal alveolar SP-A levels. SP-A can no longer be called a lung-specific protein, since it has recently been detected in other tissues. In most species, SP-A is encoded by a single gene, however in humans it is encoded by two, very similar genes. Models for the structure of the human SP-A protein molecule have been proposed, suggesting that the mature alveolar SP-A molecule is composed of both gene products. The study of SP-A may provide information helpful in understanding disease processes and formulating new treatment modalities.
Gene Expression↗
Familial truncus arteriosus: a possible autosomal-recessive trait.
Truncus arteriosus is a relatively uncommon congenital malformation. It accounts for approximately 1% of congenital heart diseases. The defect occurs sporadically but 22q11 deletion is frequently noted in such patients with conotruncal defects. We studied six cases of TA in four closely related families. Analysis of karyotypes in these cases was normal. Family 1 has one affected male infant who was born in 1998. Family 2 has two affected children (one male and one female) who were born in 1989 and 1995, respectively. They have four other normal children. Family 3 has two affected children (one male and one female) who were born in 1981 and 1984, respectively. They have three other normal children. Family 4 has one affected male born in 1998 and another healthy child. All parents of all affected children are double cousins. The data in this study are compatible with an autosomal-recessive inheritance, but multifactorial inheritance may also play a role.
Chromosome Aberrations↗
Hypothalamic digoxin and neural regulation of blood pressure and vascular thrombosis.
The isoprenoid pathway produces three key metabolites--digoxin (membrane sodium-potassium ATPase inhibitor and regulator of neurotransmitter/aminoacid transport), dolichol (regulates N-glycosylation of proteins) and ubiquinone (free radical scavenger). This was assessed in patients with essential hypertension, familial hypotension, acute coronary artery disease and acute thrombotic strokes. The pathway was also assessed in patients with right hemispheric, left hemispheric and bihemispheric dominance for comparison. In patients with acute coronary artery disease, acute thrombotic stroke, essential hypertension and right hemispheric dominance, there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels and low ubiquinone and high free radical levels. There was also an increase in tryptophan catabolites, reduction in tyrosine catabolites, increase in cholesterol-phospholipid ratio and a reduction in glycoconjugate level of RBC membrane in this group of patients as well as in those with right hemispheric dominance. In patients with familial hypotension and left hemispheric dominance, the patterns were reversed. The role of a dysfunctional isoprenoid pathway and endogenous digoxin in the pathogenesis of essential hypertension and familial hypotension and in thrombotic vascular disease in relation to hemispheric dominance is discussed.
Aged↗
Hypothalamic digoxin and irritable bowel syndrome.
BACKGROUND: The hypothalamus produces an endogenous membrane Na+-K+ ATPase inhibitor digoxin that can modulate neurotransmitter transport and may play a role in hemispheric dominance. It can also modulate glycoconjugate synthesis and thus affect synaptic connectivity in the bowel wall. Digoxin could play a role in the genesis of irritable bowel syndrome (IBS). AIM: To study digoxin status in IBS and to correlate it with hemispheric dominance. METHODS: The isoprenoid pathway, tryptophan/tyrosine catabolic patterns and glycoconjugate metabolism were assessed in patients with IBS and in right hemispheric dominant/left hemispheric dominant/bihemispheric dominant individuals. RESULTS: The isoprenoid pathway was upregulated in IBS, with increased HMG CoA reductase activity (0.8 [0.07] vs 0.4 [0.06] in controls; p<0.01), serum digoxin (14.8 [1.0] vs 29.0 [1.2] ng/dL; p<0.01) and dolichol levels (63.8 [3.0] vs 120.3 [3.6] mg/dL; p<0.01). RBC membrane Na+-K+ ATPase activity (3.0 [0.2] vs 1.0 [0.1] microg/p/mg protein; p<0.01), serum magnesium (1.7 [0.1] vs 1.0 [0.1] mg/dL; p<0.01) and ubiquinone (86.4 [5.9] vs 39.8 [1.2] microg/dL; p<0.01) were reduced. There was increase in tryptophan catabolites and reduction in tyrosine catabolites. Serum total glycosaminoglycan and carbohydrate component of glycoproteins were increased in IBS. The activity of glycosaminoglycan degrading enzymes and glycohydrolases were increased. This pattern correlated with those obtained in right hemispheric chemical dominance. CONCLUSION: Hypothalamic digoxin and right hemispheric dominance could play a role in the genesis of irritable bowel syndrome.
Biomarkers↗