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Biomedical subjects

A Haque

Publications and source records attributed to A Haque.

At least 91 records · Page 5Linked to original sources

Environmental fate and distribution of sodium [14C] pentachlorophenate in a section of urban wasteland ecosystem.

An urban terrestrial microecosystem has been used under outdoor conditions to study the transfer of chemical residues within the system components. The microecosystem consisted of soil monoliths obtained from a site with an established vegetation cover dominated by goldenrod, Solidago gigantea. The microecosystem contained integrated food chain elements composed of primary producers, herbivores and carnivores. The system was stocked with indicator insect species, snails (Cepaea nemoralis) and earthworms (Allolobophora caliginosa), captured from the original site. Evaluation of the system was made using radiolabelled sodium pentachlorophenate (PCP-Na) which was applied as a single application at an equivalent rate of 5 kg ha-1. The mass balance revealed that, after 131 days, in the autumn, and after 222 days, in the winter, that 43 and 39% radiocarbon, respectively, was recoverable from the microecosystem. The unaccounted radiocarbon was very probably removed through volatilization and photomineralization of the compound. PCP residues on foliage decreased rapidly, 50% of which were metabolised within 15 days. Most of the radiocarbon remaining in the system after 131 days was in the top soil and plant litter, transmitted mainly through washing off by rain and leaf litter fall. There was a variation in the uptake of PCP-Na residues in the food chain organisms, where the total radiocarbon concentrations during the first 19 days of exposure ranged, e.g. in snails, from 3 to 0.6 micrograms g-1, in springtails from 5 to 105; in beetles (Amara fusca) from 3 to 1, in spiders from 13 to 11, and in harvestman from 31 to 77 micrograms g-1. The ecological magnification indices (EM) of all the organisms with respect to their main food source, i.e. plant litter, demonstrated no bioconcentration effects. This is attributed to the metabolism of PCP-Na by the organisms and its rapid excretion. The urban wasteland ecosystem contained in outdoor lysimeters employed as a model gives valuable information and has considerable value in predicting the ecological fate of industrial chemicals.

Animals↗

Terrestrial model food chain and environmental chemicals. I. Transfer of sodium [14C]pentachlorophenate between springtails and carabids.

A model soil food chain of a ruderal ecosystem has been constructed in order to study the uptake, transfer, and accumulation of [14C]pentachlorophenate (PCP-Na). The model was based on three food levels, viz. baker's yeast, collembola, and carabid beetles, and the contaminant chemical introduced was via initial food. Continuous exposure of the organisms to the test chemical resulted in a significant uptake and transfer of radiocarbon into the food chain elements. Bioaccumulation of radiocarbon in the body tissues of the organisms was low, as large amounts taken up were quickly eliminated through the excrements. The radiocarbon level of prey animals was about 100 times higher than that of their predators, but there was only small difference in concentration between collembolas and yeast. This was probably because of a faster excretion of the chemical by the beetles than by the collembolas. During the test period no conversion of [14C]PCP-Na took place in the yeast, but the collembolas and beetles metabolized 50 and 59%, respectively. Criteria are proposed for successful implementation of food chain models.

Animals↗

Lathyrism.

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Amino Acids, Diamino↗

Studies on the mechanism of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU)-induced hepatotoxicity. II. Biochemical and morphological characterization of the injury and its prevention by phenobarbital.

The present study characterizes the biochemical, morphological, and histological sites of CCNU-induced hepatotoxicity and investigates the effect of modifiers of drug metabolism on this toxicity. A single oral dose (100 mg/kg) of CCNU caused four- and ninefold increases in serum GOT and GPT respectively 48 h after administration in rats. A 25-fold rise in serum bilirubin, a total loss of bile flow, and a decrease in BSP clearance were also observed. Cytochrome P-450 content and EM-N-demethylase activity were significantly decreased to 88% and 66% of control values respectively. A histopathological time course study of CCNU-induced injury showed a progression of acute inflammation, edema, and fibrin deposition in portal areas over 24 h with necrosis and sloughing of bile duct epithelium at 24 and 36 h. Treatment of rats with PB (40 mg/kg/day for 4 days, i.p.) 24 h prior to CCNU administration protected against CCNU-induced hepatotoxicity. Thus, the levels of serum GOT, GPT, and bilirubin were only 2.5 and 4 times higher than in untreated or PB-treated controls. Histopathological examination also showed reduced severity of bile duct lesions in PB-pretreated animals. In rats receiving both PB and CCNU, bile flow was restored and BSP clearance was increased compared to the CCNU-treated rats. The mixed-function oxidase activity in PB + CCNU-treated rats was not significantly different from that in PB-treated controls. It is concluded that pretreatment of rats with PB can markedly suppress the hepatotoxic manifestations, including histopathological changes, the rise in serum bilirubin, and the cholestasis observed in CCNU-treated rats.

Alanine Transaminase↗

Platelet mediated killing of larvae from different filarial species in the presence of Dipetalonema viteae stimulated IgE antibodies.

The platelets from normal rats interact with microfilariae of Dipetalonema viteae in vitro in the presence of antibodies leading to the killing of the parasite. The antibody involved in this reaction is identified as IgE because the absorption of immune rat serum on anti-rat IgE column or the pretreatment of platelets with anti-Fc epsilon receptor resulted in a significant reduction in the percentage of killing of microfilariae. This antibody, which mediates platelet activity towards microfilariae, appears early in the secondary infection and persists for a short period of time. This short-lasting IgE antibody is not apparently present in the form of large complexes since the supernatant but not the pellet after ultracentrifugation was able to mediate killing of microfilariae by platelets. IgE-dependent platelet-mediated parasite killing is neither stage- nor species-specific because the microfilariae (LI) of Brugia malayi or of Loa loa and infective larvae (L3) of D. viteae or of B. malayi were killed when they were incubated with the serum obtained from rats at day 8 after secondary infection with adult D. viteae worms. The results of the present study suggest that platelets can actively participate in the immunological killing of filarial larvae.

Animals↗

Resistance against Brugia malayi microfilariae induced by a monoclonal antibody which promotes killing by macrophages and recognizes surface antigen(s).

Several monoclonal antibodies were produced following the immunization of mice with infective larvae of Brugia malayi. One of these gives a positive fluorescence reaction on the surface of B. malayi microfilariae and this particular monoclonal antibody (IgM isotype) was able to mediate mouse peritoneal macrophage adherence to, and killing of, B. malayi microfilariae in vitro. Adherence and killing were enhanced by fresh normal mouse serum, suggesting a role for complement. When the same monoclonal antibody was passively transferred to mice harbouring microfilariae in their circulation, a complete clearance of microfilariae was observed in 70% of the animals. This monoclonal antibody was able to recognize antigenic determinants (of 110,000 MW) present on the surface of B. malayi microfilariae by radioimmunoprecipitation.

Animals↗

The use of monoclonal antibodies in studies of filarial parasite antigens.

The strength of the hybridoma technology in providing probes for the study of parasite immunology is obvious. The use of monoclonal antibodies should greatly expedite the task of the identification and the isolation of antigens which are relevant to host protection, of immunodiagnosis and of immunopathology. We have produced a series of monoclonal antibodies against Brugia malayi which causes lymphatic filariasis in man. One of these monoclonal antibodies (IgM isotype) can detect circulating antigens in the sera of individuals and of laboratory animals infected with B. malayi by radioimmunoprecipitation-PEG assay. This monoclonal antibody can bind to the relevant epitope of the circulating antigen or to the antigenic determinants of the immune complexes that remained exposed in the complex. A few monoclonal antibodies raised against B. malayi were selected, one of which gave positive fluorescence reaction on the surface of microfilariae. This particular monoclonal antibody showed such biological activities as conferring resistance to circulating microfilariae and inducing cell-mediated killing of microfilariae in vitro. The same monoclonal antibody was able to identify antigenic determinants (of mol. wt, 110 Kd) on the surface of B. malayi microfilariae which may be involved in effector mechanisms related to the development of transmission inhibiting immunity in lymphatic filariasis.

Animals↗

Detection of IgE in the sera of rodents: comparison of the applicability of ELISA and RIA.

RIA and ELISA were compared for their ability to detect IgE in different rodent species. With a sheep anti-rat IgE antibody good correlation (P less than 0.001) between the 2 assay methods for IgE was found in rats. RIA failed to detect the IgE of Mastomys natalensis while ELISA proved to be a suitable test. However, both tests failed to measure IgE in sera of Nile rats.

Animals↗

Filaricidal effects of cyclosporin-A against Dipetalonema viteae in Mastomys natalensis.

Outbred male Mastomys natalensis were injected subcutaneously with 100 infective larvae of Dipetalonema viteae obtained from Ornithodorus tartakovskyi. Groups of five animals were treated with 30 mg/kg of the immunosuppressive drug Cyclosporin-A daily for five days (experimental) or Miglyol 812 (control). One group served as untreated controls. Contrary to expectations, 60% of the animals were completely protected against D. viteae and the remainder were partially protected. The mechanism remains unknown.

Animals↗

Neutrophil-mediated killing of Dipetalonema viteae microfilariae: simultaneous presence of IgE, IgG antibodies and complement is required.

Neutrophils from the peripheral washings of normal rats in the presence of sera obtained from rats immune to circulating microfilariae adhered to and killed the microfilariae of Dipetalonema viteae in vitro within 16-24 hr. No significant adherence or cytotoxicity was mediated by sera collected from animals with a high microfilaraemia or from normal rats. Ultrastructural studies show that neutrophils, which are bigger than microfilariae, can easily internalize the small larvae resulting in the disintegration of the parasite. Immunoadsorption and inhibition experiments showed that the adherence-promoting activity resides both in IgG and IgE classes of antibody. However, the mere participation of these two antibodies is not sufficient to effect neutrophil adherence towards microfilariae, the presence of complement is also required. Samples of fresh immune rat serum (fIRS) depleted in alternative pathway components of complement by treatment with zymosan A failed to mediate cell adherence to the parasite. fIRS inactivated for the classical pathway of complement by the chelating agent EGTA partially retains its activity in mediating cytotoxicity to microfilariae. The striking antigenic specificity of D. viteae antibodies was shown by their ability to mediate cytotoxicity only to D. viteae but not towards Brugia malayi microfilariae.

Animals↗

Onchocerca volvulus: detection of circulating antigen by monoclonal antibodies in human onchocerciasis.

A monoclonal antibody of the IgM class recognizing Onchocerca volvulus circulating antigen (COA) was obtained. This monoclonal antibody was used in a radioimmunoprecipitation-PEG assay (RIPEGA) to detect circulating antigen in onchocerciasis patients' sera. COA could be detected in 63 (80%) of the 79 African patient sera tested, and in 126 (76%) of the 164 Indian (Venezuela) sera studied. There was no direct correlation between the presence of COA detected in the patient serum and the level of microfilarodermia. The RIPEGA using this monoclonal antibody detected COA in 91% of children under 10 years old, whereas the microfilarodermia in this group was positive in only 52% of the cases. The specificity of this test is improved compared to the results obtained with polyclonal antibodies. Immunofluorescence studies suggest that the COA might be located in the microfilaria cuticle.

Adolescent↗

A variant of toxic shock syndrome. Clinical, microbiologic, and autopsy findings in a fatal case.

A 16-year-old boy had toxic shock syndrome (TSS); Staphylococcus aureus bacteremia developed 11 hours prior to his death, which was three days after onset of the illness. The isoelectric focusing pattern of the staphylococcal isolate differed from both non-TSS and classic TSS S aureus isolates. Anatomic findings suggest three pathogenetic mechanisms: (1) immune complex-associated pulmonary microangiitis and vasculitis in the skin and skeletal muscle; (2) parenchymal cell "microvesicular" fatty metamorphosis in the liver, myocardium, renal tubules, and pancreas, and (3) pancarditis.

Adolescent↗

Transplacental transfer of rodent microfilariae induces antigen-specific tolerance in rats.

Microfilariae are the smallest form in the life-cycle of filarial nematode parasites. They are released by the adult female worms and migrate through the blood and extracellular fluids where they can be transmitted by vectors. A few reports have indicated the possibility of the transmission of microfilarial infection from mother to offspring. We have infected rats with adult females of the rodent filaria, Dipetalonema viteae, and report here that the transfer to D. viteae microfilaria does indeed occur through the placenta. Exposure to specific antigens early in development can readily induce immune tolerance. We observed that a state of reversible immune unresponsiveness occurred in rats as a result of pre- and post-natal exposure to microfilariae and this was associated with impairment of T-cell responses. The induction of tolerance allowed D. viteae infective larvae to reach maturity in the Fischer rat which is otherwise innately resistant to this practice.

Animals↗