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PubMed2000

The contributions of emissions and spatial microenvironments to exposure to indoor air pollution from biomass combustion in Kenya.

Acute and chronic respiratory diseases, which are causally linked to exposure to indoor air pollution in developing countries, are the leading cause of global morbidity and mortality. Efforts to develop effective intervention strategies and detailed quantification of the exposure-response relationship for indoor particulate matter require accurate estimates of exposure. We used continuous monitoring of indoor air pollution and individual time-activity budget data to construct detailed profiles of exposure for 345 individuals in 55 households in rural Kenya. Data for analysis were from two hundred ten 14-hour days of continuous real-time monitoring of concentrations of particulate matter [less than/equal to] 10 microm in aerodynamic diameter and the location and activities of household members. These data were supplemented by data on the spatial dispersion of pollution and from interviews. Young and adult women had not only the highest absolute exposure to particulate matter (2, 795 and 4,898 microg/m(3) average daily exposure concentrations, respectively) but also the largest exposure relative to that of males in the same age group (2.5 and 4.8 times, respectively). Exposure during brief high-intensity emission episodes accounts for 31-61% of the total exposure of household members who take part in cooking and 0-11% for those who do not. Simple models that neglect the spatial distribution of pollution within the home, intense emission episodes, and activity patterns underestimate exposure by 3-71% for different demographic subgroups, resulting in inaccurate and biased estimations. Health and intervention impact studies should therefore consider in detail the critical role of exposure patterns, including the short periods of intense emission, to avoid spurious assessments of risks and benefits.

Adolescent↗
PubMedDate not supplied

Entrapment of enzyme in water-restricted microenvironment for enzyme-mediated catalysis under microemulsion-based organogels.

Nonaqueous enzymology has emerged as a major area of biotechnology research and development. Enzymes in organic solvents offer great potential for the biocatalysis of a wide range of chemical processes that cannot occur in water. One of the most commonly used methods for carrying out enzymatic conversions in organic solvents is enzymes solubilized in water-in-oil (w/o) microemulsions or water containing reverse micelles. In reverse micelles, enzyme molecules are solubilized in discrete hydrated micelles formed by surfactants within a continuous phase, i.e., nonpolar organic solvent. Under appropriate conditions, these solutions are homogeneous, thermodynamically stable, and optically transparent. However, there are very few examples of preparative-scale enzyme-catalyzed synthesis in water-in-oil microemulsion. One reason is that despite the advantages offered by microemulsion media, product isolation and enzyme reuse from such single-phase liquid medium is more complex than in competing methodologies in which the catalyst is present as a separate solid phase. Therefore, the approach simplifying product isolation, and enzyme reuse from microemulsion-based media, has been the use of a gelled microemulsion system, especially gelatin silica nanocomposite.

Enzymes↗
PubMedDate not supplied

Fluorescence spectroscopy of the tryptophan microenvironment in Carcinus aestuarii hemocyanin.

The steady-state and time-resolved fluorescence properties of the multitryptophan minimal subunit CaeSS2 from Carcinus aestuarii hemocyanin have been studied with the aim of probing the environment of the fluorophores within the protein matrix. Subunit a of Panulirus interruptus hemocyanin, whose X-ray structure is known, has been also studied. The results are compared with those collected with other two monomeric fractions (CaeSS1, CaeSS3) produced by dissociation of the native, oligomeric protein as well as with those of the hexameric aggregate. Three classes of tryptophan residues can be singled out by a combination of fluorescence quenching and lifetime measurements on the holo-Hc (the copper containing, oxygen binding form) and the apo-Hc (the copper-free derivative). One class of tryptophans is exposed to the protein surface. Some of these residues are proposed to be involved in the intersubunit interactions in CaeSS1 and CaeSS3 fractions whereas in CaeSS2 the protein matrix masks them. This suggests the occurrence of conformational rearrangements after detachment of the subunit from the native aggregate, which could explain the inability of CaeSS2 to reassociate. A second class of tryptophan has been correlatively assigned, by comparison with the results obtained with Panulirus interruptus hemocyanin, to residues in close proximity to the active site. The third class includes buried, active site-distant, residues.

Animals↗
PubMed2005

Abnormalities of neurogenesis in the R6/2 mouse model of Huntington's disease are attributable to the in vivo microenvironment.

Huntington's disease (HD) is an autosomal dominant neurodegenerative condition characterized by movement disorders, psychiatric disturbance, and cognitive decline. There are no treatments to halt or reverse the disease. Mammalian neurogenesis persists into adulthood in the subventricular zone (SVZ) and dentate gyrus (DG) of the hippocampus. In 2001, our laboratory published the hypothesis that neurogenesis is impaired in neurodegenerative diseases and that this may contribute to disease progression. Since then, it has been shown that neurogenesis is reduced in the DG of transgenic HD mice but increased in the SVZ of HD patients. We sought to characterize neurogenesis further. We found that, in the DG of the transgenic R6/2 mouse model of HD, newborn cell proliferation and morphology, but not differentiation or survival, was compromised. In R6/2 mice, neurogenesis failed to upregulate in the DG in response to seizures. Basal SVZ neurogenesis was similar between R6/2 mice and their wild-type littermates. There was no difference in the in vitro growth of adult neural precursor cells (NPCs) between genotypes. These results suggest that abnormal neurogenesis in the R6/2 mouse is not attributable to an intrinsic impairment of the NPC itself but is attributable to the environment in which the cell is located.

Aging↗
PubMed1987

The thyroid microenvironment in autoimmune thyroid disease: effects of TSH and lymphokines on thyroid lymphocytes and thyroid cells.

Thyroid lymphocytes synthesize thyroid autoantibodies in close proximity to thyroid cells and consequently soluble mediators such as TSH and interleukins (IL) 1 and 2 may have unforeseen effects on lymphocytes and thyrocytes, respectively. Investigations of thyroid autoantibody synthesis by thyroid lymphocytes in vitro showed that TSH did not affect microsomal (Mic) antibody production, but thyroglobulin (Tg) antibody synthesis was decreased, probably as a result of complexing between Tg antibody and Tg secreted by small numbers of thyrocytes in the cell suspension. IL-1 and IL-2 partially mimicked the inhibitory effects on spontaneous autoantibody synthesis induced by Pokeweed mitogen (PWM) in cultures of thyroid lymphocytes. This inhibition may require a number of soluble mediators released by T cells in response to the mitogen; however, depletion studies indicated that the cell type responsible for PWM inhibition is unlikely to be a suppressor T cell and may be an NK cell. IL-1 and IL-2 had little effect on the viability of thyrocyte monolayers in an 18 h assay, but antibody dependent cells cytotoxicity (ADCC) using blood lymphocytes and thyroid autoantibody positive sera was demonstrated; further, the cytotoxicity appeared to be due to Mic antibodies. It is possible that IL-1 and/or IL-2 (as well as other cytokines) may affect thyroid cells after longer periods of exposure, either by altering them functionally or by direct damage. However, assuming that NK cells are present in sufficient numbers in the gland, ADCC could play a major role in the development of hypothyroidism in Hashimoto's disease.

Cells, Cultured↗
PubMed1989

Gossypol-induced modifications in the microenvironment of rat epididymal spermatozoa.

Gossypol acetic acid (20, 25 or 30 mg/kg/day orally for 5 weeks) decreased epididymal weight in adult Sprague-Dawley rats but the epididymal concentrations of proteins, lactate dehydrogenase and acid phosphatase were unchanged. The concentrations of carnitine, inositol and potassium in epididymal fluid were decreased in a dose-related manner. These modifications were not due to disturbances of Leydig and Sertoli cell functions which were normal. We suggest that the reduction in epididymal secretion results from a decrease in the number of spermatozoa rather than from a direct action of gossypol on the epididymal epithelium.

Animals↗
PubMed2005

Selective apoptotic behaviour of bovine herpesvirus 1 in an epithelial-like microenvironment.

Apoptosis seems to play an important role in the pathogenic profile of bovine herpesvirus 1 (BHV-1) infection. Nitric oxide (NO) is also important as a signal molecule. In this study, apoptosis was selectively induced in HEp-2 cells in the early stage [1-3 h postinfection (PI)] of BHV-1 multiplication, and this apoptotic process was realised through the caspase-8, and partially through the caspase-3, pathway. BHV-1 infection inhibited staurosporine- (SS-) induced apoptosis only if the SS was added at 6 h PI. The results of this study showed that the 'NO-apoptosis' relation was realised through the caspase-8 pathway ('outer membrane receptor' pathway) at a later stage of infection in apoptosis induced by BHV-1 + SS. Our previous report (Yazici et al., 2004) and this study together showed that BHV-1 might induce and inhibit cell-type-specific pathways of apoptosis.

Apoptosis↗
PubMed2005

Dynamic contrast-enhanced and diffusion MRI show rapid and dramatic changes in tumor microenvironment in response to inhibition of HIF-1alpha using PX-478.

PX-478 is a new agent known to inhibit the hypoxia-responsive transcription factor, HIF-1alpha, in experimental tumors. The current study was undertaken in preparation for clinical trials to determine which noninvasive imaging endpoint(s) is sensitive to this drug's actions. Dynamic contrast-enhanced (DCE) and diffusion-weighted (DW) magnetic resonance imaging (MRI) were used to monitor acute effects on tumor hemodynamics and cellularity, respectively. Mice bearing human xenografts were treated either with PX-478 or vehicle, and imaged over time. DW imaging was performed at three b values to generate apparent diffusion coefficient of water (ADCw) maps. For DCE-MRI, a macromolecular contrast reagent, BSA-Gd-DTPA, was used to determine vascular permeability and vascular volume fractions. PX-478 induced a dramatic reduction in tumor blood vessel permeability within 2 hours after treatment, which returned to baseline by 48 hours. The anti-VEGF antibody, Avastin, reduced both the permeability and vascular volume. PX-478 had no effect on the perfusion behavior of a drug-resistant tumor system, A-549. Tumor cellularity, estimated from ADCw, was significantly decreased 24 and 36 hours after treatment. This is the earliest significant response of ADC to therapy yet reported. Based on these preclinical findings, both of these imaging endpoints will be included in the clinical trial of PX-478.

Animals↗
PubMed2006

Effects of aging and niche microenvironment on spermatogonial stem cell self-renewal.

Aging is evident in most tissues and organ systems, but the mechanisms of aging are difficult to identify and poorly understood. Here, we test the hypothesis that aging results in uncorrected defects in stem cell and/or niche function, which lead to system failure. We used the spermatogonial stem cell (SSC) transplantation assay to determine the effect of aging on testis stem cell/niche function in mice. Between 12 and 24 months of age, male mice experienced a declining level of fertility associated with decreased testis weight, level of spermatogenesis, and total stem cell content. However, when stem cells were consecutively passaged at 3-month intervals to testes of young males, these stem cells continued to produce spermatogenesis for more than 3 years. Thus, SSC self-renewal continues long past the normal life span of the animal when the stem cell is continually maintained in a young niche/microenvironment. Moreover, these data suggest that infertility in old males results from deterioration of the SSC niche and failure to support an appropriate balance between stem cell self-renewal and differentiation.

Aging↗
PubMed1999

Survival signals within the tumour microenvironment suppress drug-induced apoptosis: lessons learned from B lymphomas.

The suppression of apoptosis is one mechanism by which tumours become drug resitant. Extracellular signals from the germinal centre (GC) of secondary lymphoid tissue can rescue B cells from physiological- and chemotherapy-induced apoptosis. Such survival signals include CD40 receptor ligation, interleukin-4 (IL-4) receptor stimulation and the interaction of the integrin ligand VCAM-1 with its receptor. The GC environment was modelled in vitro by providing B lymphoma cells with these survival signals. JLP119 B lymphoma cells underwent apoptosis after exposure to the topisomerase II inhibitor etoposide and this was dramatically reduced when the cells were cultured in the GC system. CD40 receptor ligation resulted in increased levels of Bcl-XL. Etoposide diminished the binding between Bax and Bcl-XL but this was restored by IL-4 and VCAM-1 triggered signals. These data demonstrate combined effects of three microenvironmental signals on the Bcl-2 family and illustrate the potential importance of such signalling pathways in drug resistance of tumour cells.

Animals↗