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Chloroform, generally regarded as a non-genotoxic compound, is associated with the induction of liver and/or kidney tumors in laboratory mice and rats. In particular, chloroform produced renal tubule tumors in low incidence in male Osborne-Mendel rats when administered by corn-oil gavage or in the drinking water. There is a lack of data on intermediate endpoints that may be linked to renal cancer development in this strain of rat, in contrast to mice. Specifically, evidence linking chloroform-induced liver and kidney tumors in mice with cytotoxicity and regenerative cell proliferation is very strong, but weak in the rat. In the present study, kidney tissue from a carcinogenicity bioassay of chloroform in Osborne-Mendel rats was re-evaluated for histological evidence of compound-induced cytotoxicity and cell turnover. All rats treated with 1800 ppm (160 mg/kg/day, high-dose group) in the drinking water for 2 years and half the rats treated with 900 ppm (81 mg/kg/day) had mild to moderate changes in proximal convoluted tubules in the mid to deep cortex indicative of chronic cytotoxicity. Tubule alterations specifically associated with chronic chloroform exposure included cytoplasmic basophilia, cytoplasmic vacuolation, and nuclear crowding consistent with simple tubule hyperplasia. Occasional pyknotic cells, mitotic figures in proximal tubules, and prominent karyomegaly of the renal tubule epithelium were present. These alterations were not present in control groups or at the 200-ppm (19 mg/kg/day) or 400-ppm (38 mg/kg/day) dose levels. This new information adds substantially to the weight of evidence that the key events in chloroform-induced carcinogenicity in rat kidney include sustained cellular toxicity and chronic regenerative hyperplasia.
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BACKGROUND: Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) have important functions during skin development, repair and maintenance. MMP-2 and MMP-9 (gelatinase A and gelatinase B) are involved in regulating keratinocyte migration. OBJECTIVES: To analyse whether Apligraf, a bilayered tissue-engineered human skin equivalent (HSE), produces gelatinases and TIMPs and whether or not epidermal-dermal interactions regulate MMP activity. METHODS: The tissue distribution of MMP-2, MMP-9, TIMP-1, TIMP-2 and fibronectin was analysed by immunohistochemistry. Secreted MMP activity was quantified by a fluorimetric assay and gelatin zymography was used to monitor gelatinases in tissue culture supernatants. RESULTS: Apligraf expressed MMP-2 and MMP-9 and contained immunohistochemically detectable amounts of TIMP-1 and TIMP-2. The gelatinases were predominantly produced in the epidermis, whereas immunostaining of TIMP-1 and TIMP-2 was largely confined to the dermal component of the HSE. Fibronectin was expressed only in the dermis. Gelatin zymography demonstrated that intact Apligraf produced both MMP-2 and MMP-9, the latter predominantly in its latent form. Separation of the dermis from the epidermis resulted in an enhanced production and activation of MMP-9 by the epidermal layer, and secretion of latent and active MMP-2 by the dermal layer. Moreover, the incubation media of the separated epidermis demonstrated significantly stronger MMP activity than did intact Apligraf or its dermal component. CONCLUSIONS: These observations provide evidence that epidermal-dermal interactions suppress epidermal gelatinase activity. In addition, coexpression of TIMPs and fibronectin in the Apligraf dermis suggests that the product has the potential to counteract the imbalance between matrix production and degradation in chronic wounds and thus may support wound re-epithelialization.
The percent of code type agreement with the original MMPI is compared with the new MMPI-2, an earlier re-norming of the MMPI by Colligan, Osborne, Swenson, and Offord (1983), the MMPI-168, and test/retest comparisons of the MMPI with itself. Code type agreement ranges from lows of 31 to 41% for the test/retest comparability of the original MMPI with itself to 40 to 67% hit rates for the MMPI-2, the MMPI 1983 norms, and the MMPI-168. The effect of this on interpretation is discussed in the context of previous studies on the MMPI code types in relation to broadband diagnosis and comparisons of clinical accuracy of computerized reports that have utilized various MMPI versions.
Between 1996 and 2000, rates of cryptosporidiosis in North West England were significantly higher than overall in England and Wales, particularly during the first half of each year. In addition, during the second quarter of each year in this period, up to 40% of all cases recorded in England and Wales were from the North West Region. In 2001, cryptosporidiosis dramatically decreased throughout the United Kingdom and the springtime excess of cases formerly seen in the North West was no longer apparent. This changed epidemiology was due to a decline in cases of Cryptosporidium parvum (formerly genotype 2), associated with zoonotic transmission. Although the initial loss of a spring peak of infection corresponded with the outbreak of foot-and-mouth disease throughout the United Kingdom, its continued absence relates to major structural changes in the North West public water supply. This study highlights the far-reaching public health benefit of local working relationships in addressing re-occurring disease issues.
Schizophrenia, like other "pathological" conditions, has not been systematically included in the general study of consciousness. By focusing on aspects of chronic schizophrenia, we attempt to survey one way of remedying this omission. Some basic components of Edmund Husserl's phenomenology of human experience (intentionality, constitution, and unbuilding) are explicated in detail, and these components are then employed in an account of exemplary aspects of chronic schizophrenia. We maintain that in schizophrenic experience some very basic constituents of reality--constituents so basic we call them "ontological"--are lost so that the patient must try to explicitly re-constitute those ontological features of the world. Using Husserl's concepts such experiences are described as a weakening of "automatic mental life" so that much of the world that is normally taken-for-granted cannot continue to be so. This requires the patient to actively busy him or herself with re-laying the ontological foundations of reality.
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Effects of starvation and re-feeding on adipocyte glycerolipid formation were investigated in young (age 48-55 days) and old rats (age 83-94 days). Adipocyte homogenates were used to assay glycerophosphate acyltransferase and Mg2+-dependent phosphatidase phosphohydrolase. Glycerophosphate acyltransferase was measured in the presence of [14C]glycerol 3-phosphate, palmitate, ATP, CoA and Mg2+. The release of inorganic phosphate from aqueous dispersed phosphatidase was taken as a measure of phosphatidate phosphohydrolase activity. Young rats starved for 48-72 h showed a 2-fold decline in the glycerophosphate acyltransferse activity. Older rats did not show any change in the glycerophosphate acyltransferase activity during 96 h starvation. Re-feeding of starved rats with chow for 48 h caused significant increases in the glycerophosphate acyltransferase activity. These changes were mainly limited to N-ethylmaleimide-sensitive glycerophosphate acyltransferase activity. These changes were mainly limited to N-ethylmaleimide-sensitive glycerophosphate acyltransferase. Phosphatidate phosphohydrolase activity decreased significantly (2-fold) during starvation in both young and old rats. Phosphatidate phosphohydrolase activity was regained completely after re-feeding of starved rats. Initial changes in the glycerophosphate acyltransferase and phosphatidate phosphohydrolase activities were very slow. Most notable increases in the glycerophosphate acyltransferase and phosphatidate phosphohydrolase activities were observed between 24 and 48 h after initiation of a re-feeding schedule. Mean adipocyte size decreased during starvation of rats for 72 h. Although considerable increases in the activities of both glycerophosphate acyltransferase and phosphatidate phosphohydrolase were apparent by re-feeding of starved rats for 48 h, mean adipocyte size did not change during this period. Thus, enzyme changes which occurred after re-feeding were independent of the adipocyte size. To separate the effects of age from the cell size on adipocyte glycerolipid formation during starvation and re-feeding periods, adipocytes from older rats were subjected to filtration through a nylon screen to obtain adipocytes of similar sizes. These studies suggest that the age of the animal significantly influences the effects of starvation and re-feeding on adipocyte glycerolipid formation.
This is an analysis of tumor margins of 108 patients who underwent a limited resection for infiltrating breast cancer, prior to starting radiation therapy. This represented the initial resection (IR) in 75 patients, and a re-excision (RE) after biopsy elsewhere in 33 patients. All specimens were processed by the India ink method prior to frozen and paraffin section analysis. Overall, the incidence of involved margins was 28% for the IR group, and 15% for the RE group. No correlation was found with the axillary node status, or with the type of prior surgery in the RE group. The data suggest a correlation between increasing tumor size and margin involvement. Further surgery in the IR group with involved margins yielded negative margins in all cases; the finding of residual carcinoma was correlated with the type of secondary surgery, that is, further re-excision or mastectomy.
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Psychophysical studies extending over a thirty-year period have repeatedly demonstrated that visual stimuli presented close to the onset of a saccadic eye movement are mislocalised both spatially and temporally. When post-saccadic visual references are available, this spatial distortion is best characterised by a compression of visual space toward the target of the saccadic eye movement. An important but unresolved issue, concerns the specificity of saccade-dependent visual mislocalisation phenomena. We investigated this by examining whether saccade-dependent spatial and temporal mislocalisation are observed in an individual (A.I.) who cannot make any form of eye movement (opthalamoplegia), but compensates when reading or scanning visual scenes by making saccadic head movements. We demonstrate that saccade-dependent spatial and temporal mislocalisation are absent in subject A.I. and suggest that spatiotemporal mislocalisation may be specific to rapid forms of movement, such as ocular saccades, that necessitate predictive re-mapping to maintain space constancy.
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The HIV/AIDS epidemic has caught millions of people in its path worldwide during the first 13 years since it surfaced; half a million Americans have been diagnosed with AIDS, and hundreds of thousands more are in earlier stages of HIV disease. Yet the sense of urgency one would expect should attend such awful numbers is strangely absent, prompting the bitter query "Whatever happened to AIDS?" This paper discusses the present status of progress with respect to the epidemic and explores some of the reasons that might partially explain both the inherent difficulties of research and the inappropriate public sense of quiescence. It then puts forward some suggested areas of research endeavor and/or public policy that could re-energize the flagging public response to this massive health disaster.