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Biomedical subjects

R Bose

Publications and source records attributed to R Bose.

At least 91 records · Page 5Linked to original sources
PubMed1988

Pyridine and other coal tar constituents as free radical-generating environmental neurotoxicants.

We have tested the hypothesis that chronic exposure to the principal constituents of the aqueous fraction of coal tar extracts can lead to the in vivo formation of substances which may produce neurological damage as the result of free radical generation and lipid peroxidation, these may be involved in the etiology of some neurological disorders. Artificial mixtures of the aqueous fraction of coal tar extracts were given in low concentrations to pigmented mice in their drinking water over a 3-month period. This resulted in significant increases in lipid peroxidation in the striatum, cerebellum and liver of the mice under test, the rank order being striatum greater than cerebellum greater than liver. These results are compatible with the possibility that coal tar emissions (as would be recovered or liberated in the burning, refining or beneficiation of coal) constitute a potential source of neurotoxicants with a predilection for damaging the nigrostriatal neuronal pathway. Our observations may thus have identified an important and hitherto unsuspected environmental source of neurotoxic chemicals, a possibility consistent with the proposed involvement of an environmental chemical factor in Parkinson's disease and perhaps in other neurological disorders.

Animals↗
PubMed1988

A role of calcium in altered sodium ion transport of hypertensives?

Research on the etiology of essential hypertension has led to many reports of altered ion transport in cells from hypertensive patients and animal models. Abnormalities in sodium and calcium ion gradients and transport in vascular smooth muscle, neuronal tissue, cardiac muscle as well as erythrocytes have been extensively investigated. It is not clear whether these abnormalities are of primary or secondary nature. The current knowledge of sodium and calcium ion transport in essential hypertension is briefly reviewed here. Furthermore, evidence is presented which suggests a role of calcium in the regulation of sodium transport activity.

Animals↗
PubMed1988

Effect of mannitol, nimodipine, and indomethacin singly or in combination on cerebral ischemia in rats.

The effects of mannitol, nimodipine, and indomethacin on ischemic neuronal injury were examined in 45 rats divided equally into nine groups subjected to 10 minutes of forebrain ischemia. Of two control groups, one received maintenance fluids while the other received a normal saline bolus. In the remaining seven groups, mannitol, nimodipine, and indomethacin were administered singly or in combination 5 minutes before forebrain ischemia. Seven days after ischemia, the brains were perfusion-fixed, sectioned coronally into 2.8-mm slices, and stained with hematoxylin and eosin. Ischemic neurons were directly counted on predetermined regions of standardized serial sections. Considerable amelioration of ischemic injury (ischemic neurons/total neurons) was observed with mannitol (ischemic injury, 7 +/- 5% in the hippocampal CA1/CA2 sectors and 28 +/- 17% in the CA3 sector). This is in contrast to control values of 64 +/- 11% and 80 +/- 6%, respectively, and those obtained in the normal saline group of 70 +/- 10% and 59 +/- 13%, respectively. The beneficial effect with nimodipine reached significance in only the hippocampal CA3 sector (ischemic injury, 35 +/- 21%). Indomethacin showed no significant benefit. Combining the agents resulted in significantly reduced neuronal injury compared with control groups, although the effect was not greater than that achieved with mannitol alone. The degree of ischemic injury was least when all three agents were used in combination (ischemic injury, 12 +/- 12% in the hippocampal CA1/CA2 sectors and 4 +/- 4% in the CA3 sector). Our data support the concept that successfully blocking the ischemic cascade with a single, diversely acting agent or multiple agents will evoke the best beneficial response.

Animals↗
PubMed1988

Human and murine antibodies to rye grass pollen allergen LolpIV share a common idiotope.

The possibility that a murine monoclonal antibody (mAb 12) to Rye grass pollen allergen LolpIV and LolpIV-specific antibodies in the sera of grass allergic individuals share a common idiotope (Id) was investigated. It was first established that mAb 12 and human IgE antibodies recognized the same (or similar) epitope(s) on LolpIV; i.e. mAb 12 could inhibit, to the extent of 35-60%, the binding of 125I-LolpIV to the human IgE antibodies present in the sera of grass pollen-allergic individuals. Subsequently, a rabbit anti-Id antiserum was produced against mAb 12 and rendered Id-specific by appropriate immune absorptions, and its IgG antibody fraction was isolated (Rb-aId). The specificity of Rb-aId was demonstrated by the fact that the antibodies bound only to mAb 12 and not to any other murine monoclonal antibody tested. Observations that Rb-aId inhibited the binding of 125I-LolpIV to mAb 12 indicated that the Id determinants recognized on mAb 12 were located at or near the antibody-combining sites. The Rb-aId also bound specifically to affinity-purified human anti-LolpIV antibodies isolated from human sera, but not to affinity-purified human anti-tetanus toxoid antibodies. This indicated that the human anti-LolpIV antibodies share a cross-reactive Id. The binding of Rb-aId to human anti-LolpIV antibody could also be inhibited by mAb 12. Therefore, it was concluded that the murine and human antibodies to LolpIV share a cross-reactive idiotope.

Animals↗
PubMed1988

Relaxant effect of amiloride on canine tracheal smooth muscle.

Amiloride, a K+-sparing diuretic, relaxed canine tracheal smooth muscle strips contracted isometrically with high potassium (KCl), carbachol, serotonin and histamine. This indicated that relaxation was not linked to an interaction with an agonist specific receptor. Amiloride-induced relaxation was also not mediated through the production of relaxant prostaglandins, or by the endogenous release of catecholamines. During potassium contractions, amiloride addition produced a slow monophasic, dose-dependent relaxation (IC50 = 12.3 microM). In carbachol contracted strips, 1 and 10 microM amiloride induced a slow monophasic relaxation. With 35 to 250 microM, an initial rapid phase (IC50 = 75.5 microM) was superimposed onto this slow phase (IC50 = 23.5 microM), producing a biphasic relaxation. The rates of relaxation decreased with increased external [Na+] regardless of stimulus, suggesting possible competitive inhibition of a sodium-dependent process. Exposure caused a rapid decline in tension followed by a recovery phase. Tension maintenance during potassium contraction decreased transiently upon the addition of acid to a much lesser extent. Amiloride (100 microM) depressed tension recovery after acid exposure in both cases. Based on the known actions of this drug, inhibition of the Na+-H+ antiporter appears to be consistent with these data. This suggests amiloride may well belong to a new class of smooth muscle relaxants.

Airway Resistance↗
PubMed1987

Ethanol-induced acute gastric injury in mast cell-deficient and congenic normal mice. Evidence that mast cells can augment the area of damage.

The authors used stereomicroscopy and planimetry to measure the area of glandular stomach mucosa acutely injured by oral ethanol in mast cell-deficient and congenic normal (+/+) mice, and examined the damaged areas in 1-mu sections. Ethanol caused degranulation and/or disruption of gastric mucosal mast cells, and, at certain concentrations of ethanol, mast cell-deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice developed significantly less (43-90% less) acute gastric injury than either congenic +/+ mice or WBB6F1-W/Wv mice whose mast cells were restored by bone marrow transplantation from WBB6F1-+/+ mice. Nevertheless, ethanol produced detectable, and in some cases substantial, gastric injury even in the complete absence of mast cells. Thus, ethanol can produce some damage to the gastric mucosa independently of mast cells. But these data suggest that under certain circumstances mast cells can augment the area of acute gastric injury induced by ethanol.

Alcoholic Intoxication↗
PubMed1986

The influence of antibody affinity on the radioallergosorbent test (RAST) and in vitro histamine release. Studies with hapten-specific monoclonal IgE antibodies.

Four murine monoclonal IgE antibodies specific for the hapten, 4-hydroxy-3-nitrophenylacetyl (NP), had been previously found to be heteroclitic in nature in that they bound the crossreacting hapten, 4-hydroxy-3-iodo-5-nitrophenylacetyl (NIP), with greater affinity than NP. The influence of antibody affinity on the results of two commonly used assays for IgE, namely the radioallergosorbent test (RAST) and histamine release from rat peritoneal mast cells, was studied using these antibodies. In general, in agreement with previous reports, it was found that affinity influences both RAST and histamine release; however, the affinity constants deduced from equilibrium dialysis measurements for the reactions with monovalent haptens were not directly related to the activities of the antibodies as reflected in assays using multivalent hapten protein conjugates.

Animals↗
PubMed1986

The antiproliferative properties of tamoxifen and phenothiazines may be mediated by a unique histamine receptor (?H3) distinct from the calmodulin-binding site.

N,N-diethyl-2-[(4-phenylmethyl)-phenoxy]-ethanamine HCl (DPPE), a novel histamine antagonist (?H3), which selectively binds with high affinity to the antiestrogen-binding site (AEBS/?H3), inhibits the activity of calmodulin-dependent myosin light chain kinase (MLCK) only at concentrations greater than 1 mM, as opposed to tamoxifen (TAM), which has an IC50 = 4 microM in the same assay. This suggests that the antiestrogen-binding site is distinct from the site on calmodulin which binds TAM and phenothiazines. However, at an in vitro concentration of 1 X 10(-6) M, the antiproliferative effects of DPPE and several phenothiazines, which also compete for binding to AEBS/?H3, are about equal; this suggests that affinity for AEBS/?H3 rather than that for the calmodulin-binding site may correlate with clinically relevant antigrowth effects of these compounds.

Animals↗
PubMed1986

Mechanisms of frequency-induced potentiation of contractions in isolated rat atria.

Mechanisms underlying the potentiation of contractions after periods of high frequency stimulation (post-stimulation potentiation; PSP) and periods of rest (rest potentiation; RP) were investigated in isolated rat atria. Transmembrane action potentials were not changed during PSP and RP and were superimposable upon the pre-test action potentials. However, the 45Ca content of atrial strips was significantly increased during PSP, which indicates a net gain in intracellular Ca. 45Ca content was not changed during RP. PSP and RP were increased in magnitude in atria pre-treated with gallopamil (2.5 mumol/l). This effect was due to a greater depression by gallopamil of the pre-test contractions than the potentiated post-test contractions. In contrast, PSP was abolished in atria exposed to 7.5 mmol/l [Ca]o and a transient depression of the post-test contractions was seen. RP was also abolished by high Ca medium, but contractions were not depressed after periods of rest. RP, but not PSP, was unmasked when gallopamil was added to high Ca medium to decrease the size of the basal contractions. Conversely, ryanodine (100 mmol/l) abolished RP but did not affect PSP. With ryanodine present, PSP was greatly increased when the extracellular Ca concentration was increased to 5 mmol/l, whereas RP remained abolished. These results suggest that PSP may reflect an increased transsarcolemmal influx of extracellular Ca, possibly mediated through Na-Ca exchange. In contrast, the mechanism suggested for RP is a transient increase in contractile Ca resulting from an intracellular redistribution of Ca to release sites in the sarcoplasmic reticulum.

Action Potentials↗
PubMed1986

Production and characterization of mouse monoclonal antibodies to allergenic epitopes on LolpI (Rye I).

This study describes the production and characterization of mouse monoclonal antibodies (Mab) to LolpI (Rye I), the major allergen of rye-grass pollen. Hybridoma cell lines were screened for the secretion of Mab, the binding of which to labelled LolpI could be inhibited by pooled human sera containing IgE and IgG anti-LolpI antibodies. Twenty monoclonal hybridoma cell lines were expanded, and their product was purified and characterized. Each Mab bound to LolpI but not to unrelated antigens. Cross-inhibition studies allowed the grouping of these 20 Mab into five families differing by their epitope specificity. One representative Mab of each family was tested for its ability to inhibit human IgE/IgG anti-Lolp-I from 15 allergic donors as well as for its inhibition by affinity-purified anti-LolpI antibodies isolated from 14 donors. The results indicated that each family of Mab was specific for an epitope that was identical or close to that recognized by some human anti-LolpI antibodies. It is further shown that human IgE/IgG anti-LolpI are heterogeneous with some patients reacting preferentially with one or two epitopes defined by the Mab LolpI, and others reacting with epitopes different from those identified by the Mab LolpI.

Allergens↗
PubMed1986

Mu- and delta-opioid modulation of electrically-induced epileptic seizures in mice.

Graded seizure responses to suprathreshold cerebral electroshock in mice were modified by drugs acting at mu- and at delta-opioid receptors. Morphine exerts a proconvulsant effect at a non-mu opioid receptor and may exert a simultaneous anticonvulsant effect at a mu-opioid receptor. Delta-opioid receptor blockade increases seizure severity, suggesting a predominantly anticonvulsant nature of the delta-opioid system in the seizure model tested here.

Animals↗
PubMed1986

Anti-idiotypes to anti-Lolp I (Rye) antibodies in allergic and non-allergic individuals. Influence of immunotherapy.

Anti-idiotypes (aId) reacting with anti-Lol I (Lolp I; Rye I) antibodies were detected by their ability to bind to radioiodinated F(ab')2 anti-Lol I. Sera were tested after removal of anti-Lol I and anti-heavy and light chain activity by adsorption on Lol I-Sepharose 4B and normal human serum Sepharose 4B. The binding of aId to Id was inhibited by affinity purified anti-Lol I but not by certain unrelated immunoglobulins; in some sera this binding was also inhibited by Lol I. The levels of aId were measured in serial bleedings collected over a 1 year period from Lol I-sensitive patients, allergic donors not sensitive to Lol I and non-allergic persons. In Lol I-allergic patients the levels of aId were significantly influenced by seasonal exposure to pollen and by immunotherapy with extracts of grass pollen. Moreover, in 12 out of 16 cases, there was also a significant inverse relationship between changes in serum levels of aId and of IgG or IgE anti-Lol I. Most interestingly, aId were also detected in non-allergic individuals; in this case, the levels of aId were not influenced by the pollen season. The data suggest that Id-aId interactions may play a role in the regulation of anti-Lol I antibody production.

Allergens↗
PubMed1985

In utero immunization of the fetus to tetanus by maternal vaccination during pregnancy.

We tested 36 pairs of umbilical cord blood and maternal sera collected at the time of delivery by radioimmunoassay and by Western blot analysis for IgG or IgM antitetanus antibodies (anti-TT). Twenty-one participants had received a recall injection of tetanus toxoid at various periods during pregnancy. Maternal vaccination in the last trimester of pregnancy was associated with the presence of IgM anti-TT in the cord blood sera; these were not detected in neonatal sera from mothers who were not vaccinated during pregnancy or who received the booster injection during the first two trimesters of gestation. The results could not be ascribed to artifacts such as the contamination of neonatal sera by maternal blood, the contamination of the anti-IgM antisera by antiidiotypes, or by the presence of neonatal IgM rheumatoid factor binding to immune complexes made of maternal IgG anti-TT and radiolabelled TT. Hence, it is concluded that maternal vaccination during the last trimester of pregnancy may induce in utero active immunization of the fetus.

Female↗