"Filopin" efficacy in the treatment of lymphatic filariasis.
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Biomedical subjects
Publications and source records attributed to A Kumar.
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Mild and brief electrical stimulation of sites in the pretectal nucleus of rat produced analgesia (SPA) of long duration without significant aversion. Intracerebroventricular (icv) administration of 5-HT receptor antagonists methysergide (50 micrograms) and ketanserin (50 micrograms) and the dopaminergic antagonist haloperidol (50 micrograms) had no significant effect on pretectal SPA, but alpha and beta adrenoceptor antagonists phenoxybenzamine (50 micrograms) and sotalol (50 micrograms) on icv injection significantly antagonised the pretectal SPA. The results suggest that pretectal SPA involves activation of central adrenoceptors.
Conformational studies on three DNA-oligomers (d(CGCGCGTTAATT), d(CGCGTTAA) and d(CGCGCGTT) in solution by circular dichroism spectroscopy are reported. In low salt solution, all three DNA oligomers exhibit a characteristic B-conformation. However, under the influence of high salt concentration i.e. 5M NaCl, the octamer d(CGCGCGTT) exhibits 'A' conformation whereas the decamer and dodecamer retain B-conformation. On addition of millimolar amount of NiCl2 to the 5M NaCl, solution of oligodeoxynucleotides a B-Z transition is observed in octamer, decamer and dodecamer. However, NiCl2 titrations show that mid point of transition for dodecamer is at 2.25 mM, for decamer is at 13 mM NiCl2 and for octamer is 17 mM at NiCl2. In 60% alcohol all three oligonucleotides remain in the B-conformation. The melting temperatures of oligonucleotides at various salt concentration are also reported. Thermodynamic parameters calculated by melting profile using a two state model show that dodecamer and decamer are most stable in their 5M NaCl, B-form. However, octamer is more stable in its Z form than that of its 'A' form.
Household contacts of 22 randomly selected patients with systemic lupus erythematosus (SLE) were screened for autoimmune diseases and autoantibodies. Thirty nine consanguineous and 17 nonconsanguineous household contacts were studied. In the first group symptomatic SLE was seen in 5 per cent, rheumatoid arthritis in 2.5 per cent, antinuclear antibody (ANA) in 10 per cent and rheumatoid factor (RF) in 5 per cent while anti-dsDNA, anti-nRNP and anti-Sm antibodies were not detected in any individual. The second group showed total absence of any marker of autoimmunity. In normal controls only RF was detected in 3 per cent. The occurrence of markers of autoimmunity only in consanguineous household contacts of patients with SLE further confirms the recognised role of genetic factors in the etiology of SLE.
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Two patients, one with Hodgkin's disease and the other with non-Hodgkin's lymphoma, presented with bilateral diminution of vision. Examination showed bilateral serous detachment of the macula. To our knowledge, this is only the second report in the literature of serous detachment of the macula in lymphomatous disorders.
Serum potassium and sodium changes following suxamethonium (1.5 mg/kg) administration were studied in 25 patients with septic peritonitis and 25 with no signs of peritonitis. A highly significant rise (P less than 0.001) in serum potassium (0.1-2.5 mEq/l) above the pre-induction levels was observed following suxamethonium administration in patients with septic peritonitis with maximum rise at 5 min following suxamethonium. This rise in potassium was significantly higher (P less than 0.001) in peritonitis patients at 3,5, and 10 min interval. A positive correlation was found between rise of potassium and duration of illness (P less than 0.01). No statistically significant changes were observed in serum sodium levels in both groups.
A case control study was undertaken in rural areas of Varanasi, U.P., to study the relationship of Culex quinquefasciatus landing on microfilaria--carriers and amicrofilaraemic controls. No statistically significant difference was observed in the vector landing in these two groups.
Even though a variety of adverse effects caused by sweeteners, flavorings, and dyes in susceptible individuals have been reported, there is no good single reference with information about these substances in pediatric antimicrobials. Data on sweeteners, flavorings, and dyes in 91 antimicrobial preparations were collected. Sucrose was present in 74 (85%) of 87 preparations, followed by saccharin in 30 (34%) preparations. Mannitol, lactose, and sorbitol were each present in 7 preparations. None of the preparations were free of sweeteners. Thirty-four (37%) of 91 preparations did not specify the flavoring content. While cherry was the most common flavoring used, there were 25 other flavorings. Thirteen different dyes and coloring agents were used in these antimicrobials. Red dye no. 40 was present in 45% of preparations. Tables detailing sweeteners, flavorings, and dyes in different groups of antimicrobials (amoxicillin, ampicillin, cephalosporins, erythromycin, penicillins, sulfonamides, and others) and adverse effects reported with these inert ingredients are presented. These tables should be helpful to physicians in selecting an antimicrobial containing a different sweetener and/or dye when an adverse reaction occurs.
Forty-seven patients with probable dementia of the Alzheimer type (DAT) and 30 healthy age-matched controls were scanned using [18F]-2-fluoro-2-deoxy-D-glucose on a Scanditronix PC 1024-7B tomograph (inplane resolution = 6 mm, axial resolution = 10 mm). Patients and controls were scanned in the resting state with their eyes patched and ears occluded. The regional cerebral metabolic rates for glucose (rCMRglc) in most major neocortical and subcortical gray matter regions, and certain metabolic ratios (rCMRglc/ calcarine rCMRglc), quantitatively discriminated even the mildly demented patients from healthy controls. The association neocortices showed metabolic abnormalities that were more severe than those in the sensorimotor and calcarine regions. All demented groups showed significant neuropsychological disturbances when compared to healthy controls. These data demonstrated widespread metabolic disturbances, particularly in the association areas, relatively early in Alzheimer's disease, and more profound involvement with disease progression.
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An IL-4-dependent T cell clone (LD8) was isolated from the murine IL-2-dependent cytotoxic T cell line C30.1. This clone has lost the capacity to proliferate in response to IL-2 after long-term culture in IL-4. LD8 cells express the p70, but not the p55, subunit of the IL-2R on their cell surface. The number of p70 IL-2R molecules on LD8 cells is comparable with the number of high-affinity IL-2R on the parental C30.1 cell line. LD8 cells can efficiently internalize IL-2 through the p70 IL-2R subunit. Following stimulation by IL-2, LD8 cells up-regulate p70 IL-2R mRNA, but do not express p55 IL-2R mRNA. IL-2-dependent proliferation of LD8 cells was reconstituted after introduction and expression of a human p55 IL-2R cDNA. To further investigate the role of p70 IL-2R, we have measured IL-2-induced proliferation of C30.1 cells in the presence of three anti-p55 IL-2R mAb (5A2, PC61, and 7D4) that recognize different epitopes. Under the experimental conditions used, the combination of anti-p55 IL-2R mAb prevents the formation of high-affinity IL-2R, but does not affect the binding of IL-2 to p70 IL-2R or IL-2 internalization. However, these three mAb inhibit proliferation of C30.1 cells even in the presence of IL-2 concentrations sufficient to saturate p70 IL-2R. Together these results demonstrate that p70 IL-2R alone is not sufficient to transmit IL-2-induced growth signals and that formation of p55-p70 IL-2R complex is required for IL-2-dependent proliferation of murine T cells.
Rhesus monkey erythrocytes were subjected to heating at 50 degrees C for 5-15 min, and the heat-induced effects on the membrane structure were ascertained by analysing the membrane phospholipid organization and membrane skeleton dynamics and interactions in the heated cells. Membrane skeleton dynamics and interactions were determined by measuring the Tris-induced dissociation of the Triton-insoluble membrane skeleton (Triton shells), the spectrin-actin extractability at low ionic strength, spectrin self-association and spectrin binding to normal monkey erythrocyte membrane inside-out vesicles (IOVs). The Tris-induced Triton shell dissociation and spectrin-actin extractability were markedly decreased by the erythrocyte heating. Also, the binding of the heated erythrocyte membrane spectrin-actin with the IOVs was much smaller than that observed with the normal erythrocyte spectrin-actin. Further, the spectrin structure was extensively modified in the heated cells, as compared to the normal erythrocytes. Transbilayer phospholipid organization was ascertained by employing bee venom and pancreatic phospholipases A2, fluorescamine, and Merocyanine 540 as the external membrane probes. The amounts of aminophospholipids hydrolysed by phospholipases A2 or labeled by fluorescamine in intact erythrocytes considerably increased after subjecting them to heating at 50 degrees C for 15 min. Also, the fluorescent dye Merocyanine 540 readily stained the 15-min-heated cells but not the fresh erythrocytes. Unlike these findings, the extent of aminophospholipid hydrolysis in 5-min-heated cells by phospholipases A2 depended on the incubation time. While no change in the membrane phospholipid organization could be detected in 10 min, prolonged incubations led to the increased aminophospholipid hydrolysis. Similarly, fluorescamine failed to detect any change in the transbilayer phospholipid distribution soon after the 5 min heating, but it labeled greater amounts of aminophospholipids in the 5-min-heated cells, as compared to normal cells, after incubating them for 4 h at 37 degrees C. These results have been discussed to analyse the role of membrane skeleton in maintaining the erythrocyte membrane phospholipid asymmetry. It has been concluded that both the ATP-dependent aminophospholipid pump and membrane bilayer-skeleton interactions are required to maintain the transbilayer phospholipid asymmetry in native erythrocyte membrane.
A1 is a major core protein of the mammalian hnRNP complex, and as a purified protein of approximately 34 kDa, A1 is a strong single-stranded nucleic acid binding protein. Several lines of evidence suggest that the protein is organized in discrete domains consisting of an N-terminal segment of approximately 22 kDa and a C-terminal segment of approximately 12 kDa. Each of these domains as a purified fragment is capable of binding to both ssDNA and RNA. We report here that A1 and its C-terminal domain fragment are capable of potent strand-annealing activity for base-pair complementary single-stranded polynucleotides of both RNA and DNA. This effect is not stimulated by ATP. Compared with A1 and the C-terminal fragment, the N-terminal domain fragment has negligible annealing activity. These results indicate that A1 has biochemical activity consistent with a strand-annealing role in relevant reactions, such as pre-mRNA splicing.