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At least 1,441 records · Page 80Linked to original sources

PubMed1991

Therapeutic benefit of captopril in salt-loaded stroke-prone spontaneously hypertensive rats is independent of hypotensive effect.

In the present study we examined whether the angiotensin I converting enzyme inhibitor, captopril, would protect stroke-prone spontaneously hypertensive rats (SHRSP) from stroke and renal pathology over a 26-week period. In the control group of six untreated SHRSP fed Stroke-Prone Rodent Diet and 1% NaCl drinking solution, all animals developed severe hypertension and stroke by 16.1 weeks of age. In eight salt-loaded SHRSP treated with oral captopril (50 mg/kg/day) beginning at 8.4 weeks of age, systolic blood pressure was slightly but temporarily suppressed and then continued to rise; by 12 weeks of age systolic blood pressure reached levels of severe hypertension, 240 +/- 8 mm Hg, and did not differ from that of untreated SHRSP. No deaths or brain lesions were noted in captopril-treated SHRSP despite severe hypertension maintained through 26 weeks of age when the study ended. Captopril treatment prevented increases in urinary protein excretion (14 +/- 2 v 63 +/- 16 mg/day at 11.7 weeks of age, P less than .01) and the severe brain, renal, and cardiac vascular lesions observed in untreated SHRSP. When maintained on Stroke-Prone Rodent Diet and saline, plasma renin activity of untreated SHRSP surviving until 14.5 weeks of age was markedly increased (29.1 +/- 9.4 ng Ang I/mL/h) compared with either untreated SHRSP (9.2 +/- 2.5 ng Ang I/mL/h, P less than .01) or Wistar-Kyoto rats (3.5 +/- 1.0 ng Ang I/mL/h, P less than .01) maintained on standard diet and water.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed2001

Induction of glutathione S-transferase activity and protein expression in brown bullhead (Ameiurus nebulosus) liver by ethoxyquin.

The inducibility of hepatic cytosolic glutathione S-transferases (GSTs) was examined in brown bullheads, a freshwater fish that is highly susceptible to hepatic neoplasia following exposure to carcinogen-contaminated sediments. Juvenile bullheads were fed a semi-purified antioxidant-free diet supplemented with ethoxyquin (0.5% w/w dissolved in 3% corn oil), a prototypical rodent GST-inducing agent, twice daily for 14 days. Control bullheads received the antioxidant-free diet supplemented with corn oil (3% w/w). A significant increase (1.6-fold, p < or = 0.01) in hepatic cytosolic GST activity toward 1-chloro-2,4-dinitrobenzene (CDNB) was observed in the ethoxyquin-treated bullheads relative to control fish. A trend toward increased GST-NBC activity was observed in the ethoxyquin-treated fish (1.2-fold, p = 0.06), whereas no treatment-related effects were observed on GST activities toward ethacrynic acid (ECA). In contrast, GST activity toward (+/-)-anti-benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide (BPDE) was repressed in affinity-purified cytosolic fractions prepared from ethoxyquin-treated bullheads relative to control bullheads. Silver staining and densitometric analysis of isoelectric-focused, affinity-purified GST proteins revealed increased expression of two basic GST-like isoforms in ethoxyquin-treated fish. In summary, exposure to ethoxyquin increases brown bullhead GST-CDNB catalytic activity and hepatic cationic GST protein expression. However, the increase in overall GST-CDNB activity by ethoxyquin is associated with repression of GST-BPDE activity, suggesting differential effects on hepatic bullhead GST isoforms by ethoxyquin. The potential repression of bullhead GST isoforms that conjugate the carcinogenic metabolites of PAH metabolism under conditions of environmental chemical exposure could be a contributing factor in the sensitivity of bullheads to pollutant-associated neoplasia.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed2000

Activated neutrophils induce nitric oxide production in Kupffer cells.

Neutrophils (PMN) are proposed to contribute to hepatic dysfunction during sepsis. Transmigrating PMN have been demonstrated to adhere to and injure parenchymal cells (hepatocytes); however, the effect of sepsis-activated PMN on hepatic macrophages or Kupffer cells (KC) is poorly characterized. We hypothesize that PMN influence KC inflammatory mediator production, including nitric oxide. Rodent KC were co-cultured with PMN obtained from controls (Norm-PMN) or endotoxemic rats [lipopolysaccharide (LPS)-PMN] for 18 h. After an 18-h incubation, supernatants and cell lysates of the KC were analyzed for nitric oxide (NO) production. Co-cultures with LPS-PMN/KC demonstrated significantly increased production of nitrite and up-regulation of inducible nitric oxide synthase (iNOS) protein compared to KC alone or Norm-PMN/KC co-cultures. Immunohistochemistry revealed preferential iNOS protein staining in the cytoplasm of KC cultured with LPS-PMN compared to controls. Nitrite production in co-cultures of KC and LPS-PMN where cell contact was inhibited by a cell impermeable but diffusable membrane was significantly reduced. These data provide evidence that KC can be stimulated directly by activated PMN for production of NO. Further, they suggest another mechanism by which PMN modulate hepatic function during sepsis.

Animals↗

PubMed2006

Effects of type I interferons on Friend retrovirus infection.

The type I interferon (IFN) response plays an important role in the control of many viral infections. However, since there is no rodent animal model for human immunodeficiency virus, the antiviral effect of IFN-alpha and IFN-beta in retroviral infections is not well characterized. In the current study we have used the Friend virus (FV) model to determine the activity of type I interferons against a murine retrovirus. After FV infection of mice, IFN-alpha and IFN-beta could be measured between 12 and 48 h in the serum. The important role of type I IFN in the early immune defense against FV became evident when mice deficient in IFN type I receptor (IFNAR(-/-)) or IFN-beta (IFN-beta(-/-)) were infected. The levels of FV infection in plasma and in spleen were higher in both strains of knockout mice than in C57BL/6 wild-type mice. This difference was induced by an antiviral effect of IFN-alpha and IFN-beta and was most likely mediated by antiviral enzymes as well as by an effect of these IFNs on T-cell responses. Interestingly, the lack of IFNAR and IFN-beta enhanced viral loads during acute and chronic FV infection. Exogenous IFN-alpha could be used therapeutically to reduce FV replication during acute but not chronic infection. These findings indicate that type I IFN plays an important role in the immediate antiviral defense against Friend retrovirus infection.

Animals↗

PubMed2002

Natriuretic peptide-dependent lipolysis in fat cells is a primate specificity.

We have recently demonstrated that natriuretic peptides (NPs), which are known for regulation of blood pressure via membrane guanylyl cyclase (GC) receptors, are lipolytic in human adipose tissue. In this study, we compared the NP control of lipolysis in adipocytes from humans, nonhuman primates (macaques), rodents (rats, mice, hamsters), and nonrodent mammals (rabbits, dogs). Isolated adipocytes from these species were exposed to increasing concentrations of atrial NP (ANP) or isoproterenol (beta-adrenergic agonist). Although isoproterenol was lipolytic in all of the species, ANP only enhanced lipolysis in human and macaque adipocytes. In primate fat cells, NP-induced lipolysis involved a cGMP-dependent pathway. Binding studies and real-time quantitative PCR assays revealed that rat adipocytes expressed a higher density of NP receptors compared with humans but with a different subtype pattern of expression; type-A GC receptors predominate in human fat cells. This was also confirmed by the weak GC-activity stimulation and the reduced cGMP formation under ANP exposure in rat adipocytes compared with human fat cells. In conclusion, NP-induced lipolysis is a primate specificity, and adipocytes from ANP-nonresponsive species present a predominance of "clearance" receptors and very low expression of "biologically active" receptors.

Adipocytes↗

PubMedDate not supplied

Mesh implants in hernia repair. Inflammatory cell response in a rat model.

BACKGROUND: In the reinforcement of the abdominal wall with mesh implants, various complications including hernia recurrence, abdominal pain, seroma formation and infection are discussed to depend on the biocompatibility of the alloplastic prosthesis. Particularly macrophages, T-cells and mast cells have been shown to play a major role in the inflammatory response to biomaterials. To approach biocompatibility of surgical meshes we therefore examined the infiltrate of these cells as well as the proliferation rate in response to different clinically applied materials. MATERIALS AND METHODS: Three mesh materials (polypropylene: PP, Prolene; polyethylene terephthalate: PET, Mersilene, and polypropylene/polyglactin: PP + PG, Vypro) were compared after inlay implantation in a standardized rodent animal model. A suture-closed laparotomy served as control. After 7 and 90 days of implantation, histochemical analysis of the inflammatory response to all biomaterials was performed: macrophages (ED3), T-cells (CD3), proliferating cells (PCNA) and mast cells (Giemsa) were investigated. RESULTS: In all groups a persisting T-cell response was observed. Colonization of the interface with macrophages showed a pronounced reduction in the PP + PG-mesh group. Infiltration of mast cells at the tissue graft interface showed a time-dependent decrease in the PET- and PP + PG-mesh groups, whereas in contrast, index of mast cells increased in the PP-mesh group. At both time points, indices of proliferation were highest in the PP-mesh group. CONCLUSION: The present data confirm the development of a biomaterial-dependent chronic inflammatory response to surgical meshes with macrophages as the predominant cell type. Further research on the recruitment of inflammatory cells and in particular on the role of mast cells and their granular products should be encouraged.

Animals↗

PubMed1997

Detection and characterisation of anti-endomysial antibody in coeliac disease using human umbilical cord.

OBJECTIVES: To verify the effectiveness of human umbilical cord (HUC) in the detection of anti-endomysial antibodies (AEA) in coeliac disease and to characterize further these antibodies by studying tissue adsorption characteristics and antibody inhibition studies. METHODS: AEA were detected on HUC and primate oesophagus in a blind study, using sera from 46 patients with untreated coeliac disease and 108 controls. Tissue adsorption studies were performed using homogenized tissue from rodent liver, HUC, primate oesophagus and human liver. Sera were adsorbed with each of these homogenates and antibody was detected using HUC, primate oesophagus and rat kidney. In the inhibition experiments AEA was detected on HUC, and inhibition of binding was attempted by pre-incubating the sections with antibodies against collagen types I, III and IV. RESULTS: The sensitivity of AEA was 91% when detected on HUC, 89% when detected on primate oesophagus (93% and 91%, respectively, after exclusion of 1 patient with IgA deficiency). Specificity was 100% for both assays. Tissue adsorption studies showed identical results for AEA detected on both HUC or primate oesophagus, whereas antireticulin antibody was adsorbed only by rodent tissue. Blocking of the HUC with anticollagen antibodies did not prevent binding of AEA. CONCLUSIONS: HUC is an effective substrate for the detection of AEA and may be superior to primate oesophagus. The antibody detected by HUC shows identical tissue adsorption specificities to that detected on primate oesophagus.

Adolescent↗

PubMed2002

Assessment of tissue oxygen tension: comparison of dynamic fluorescence quenching and polarographic electrode technique.

INTRODUCTION AND METHODS: Dynamic fluorescence quenching is a technique that may overcome some of the limitations associated with measurement of tissue partial oxygen tension (PO2). We compared this technique with a polarographic Eppendorf needle electrode method using a saline tonometer in which the PO2 could be controlled. We also tested the fluorescence quenching system in a rodent model of skeletal muscle ischemiahypoxia. RESULTS: Both systems measured PO2 accurately in the tonometer, and there was excellent correlation between them (r(2) = 0.99). The polarographic system exhibited proportional bias that was not evident with the fluorescence method. In vivo, the fluorescence quenching technique provided a readily recordable signal that varied as expected. DISCUSSION: Measurement of tissue PO2 using fluorescence quenching is at least as accurate as measurement using the Eppendorf needle electrode in vitro, and may prove useful in vivo for assessment of tissue oxygenation.

Animals↗

PubMed2002

Nuclear organization in differentiating oligodendrocytes.

Many studies have suggested that the 3D organization of chromatin and proteins within the nucleus contributes to the regulation of gene expression. We tested multiple aspects of this nuclear organization model within a primary cell culture system. Oligodendrocyte lineage cells were examined to facilitate analysis of nuclear organization relative to a highly expressed tissue-specific gene, proteolipid protein (PLP), which exhibits transcriptional upregulation during differentiation from the immature progenitor stage to the mature oligodendrocyte stage. Oligodendrocyte lineage cells were isolated from brains of neonatal male rodents, and differentiation from oligodendrocyte progenitors to mature oligodendrocytes was controlled with culture conditions. Genomic in situ hybridization was used to detect the single copy of the X-linked PLP gene within each interphase nucleus. The PLP gene was not randomly distributed within the nucleus, but was consistently associated with the nuclear periphery in both progenitors and differentiated oligodendrocytes. PLP and a second simultaneously upregulated gene, the myelin basic protein (MBP) gene, were spatially separated in both progenitors and differentiated oligodendrocytes. Increased transcriptional activity of the PLP gene in differentiated oligodendrocytes corresponded with local accumulation of SC35 splicing factors. Differentiation did not alter the frequency of association of the PLP gene with domains of myelin transcription factor 1 (Myt1), which binds the PLP promoter. In addition to our specific findings related to the PLP gene, these data obtained from primary oligodendrocyte lineage cells support a nuclear organization model in which (1). nuclear proteins and genes can exhibit specific patterns of distribution within nuclei, and (2). activation of tissue-specific genes is associated with changes in local protein distribution rather than spatial clustering of coordinately regulated genes. This nuclear organization may be critical for complex nucleic-acid-protein interactions controlling normal cell development, and may be an important factor in aberrant regulation of cell differentiation and gene expression in transformed cells.

Active Transport, Cell Nucleus↗

PubMed2004

From genomes to vaccines via the proteome.

An effective vaccine against schistosomiasis mansoni would be a valuable control tool and the high levels of protection elicited in rodents and primates by radiation-attenuated cercariae provide proof of principle. A major obstacle to vaccine development is the difficulty of identifying the antigens that mediate protection, not least because of the size of the genome at 280Mb DNA encoding 14,000 to 20,000 genes. The technologies collectively called proteomics, including 2D electrophoresis, liquid chromatography and mass spectrometry, now permit any protein to be identified provided there is extensive DNA data, and preferably a genome sequence. Applied to soluble (cytosolic) proteins from schistosomes, proteomics reveals the great similarity in composition between life cycle stages, with several WHO vaccine candidates amongst the most abundant constituents. The proteomic approach has been successfully applied to identify the secretions used by cercaria to penetrate host skin, the gut secretions of adult worms and the proteins exposed on the tegument surface. Soluble proteins can also be separated by 2D electrophoresis before western blotting to identify the full range of antigenic targets present in a parasite preparation. The next step is to discover which target proteins represent the weak points in the worm's defences.

Animals↗

PubMed2004

Feeding patterns of Triatoma longipennis Usinger (Hemiptera, Reduviidae) in peridomestic habitats of a rural community in Jalisco State, Mexico.

We analyzed triatomine blood feeding patterns to evaluate the role of peridomiciles in Trypanosoma cruzi transmission at the rural village of Tepehuaje de Morelos at Jalisco State, Mexico (1999). A total of 206 bugs were collected in 11 out of 26 households (42.3%). Nymphs predominated in the collections (64.9% of the total). Except for one Triatoma barberi female, a species that belongs to the protracta species complex, all adults were Triatoma longipennis, a species of the phyllosoma complex. Triatomines were exclusively present in peridomestic sites mainly piles of tiles and bricks, and none were found indoors. Overall infection rate was 56.6% and no significant differences (P > 0.05) were observed between nymphs and adults or males and females. Identified blood meals were chicken (29.4%), opossum (20.9%), pig (24.5%), murid (20.9%), dog (3.5%), and armadillo (0.7%). No gut content reacted against anti-human, anti-bovine, anti-rabbit, and anti-cat sera. In contrast to fifth nymphs and adults, 87% of the small nymphs fed on one host, indicating that they are less mobile than other stages. Most fifth nymphs and adults fed on domestic hosts, while small nymphs mainly fed on opossum and murid. Infection blood-meal indexes were around 50% for single meals on opossum and murid, stressing their importance as trypanosome donors. Peridomiciles in Tepehuaje could be regarded as interaction sites among domestic and wild and synanthropic mammals and triatomines, which would facilitate circulation of the same T. cruzi strains between domestic and sylvatic cycles. Stone-made walls and building materials, which hold synanthropic rodents and opossums, should be considered as targets for vector control measures.

Animals↗

PubMed2002

Expression and localization of Indian hedgehog (Ihh) and parathyroid hormone related protein (PTHrP) in the human growth plate during pubertal development.

Indian Hedgehog (Ihh) has been reported to control the rate of cartilage differentiation during skeletal morphogenesis in rodents through a negative feedback loop involving parathyroid hormone related protein (PTHrP). The role of Ihh and PTHrP in the regulation of human epiphyseal chondrocytes is unknown. The aim of the current study was to examine the expression and localization of Ihh and PTHrP in the human growth plate at various pubertal stages. Growth plate biopsies were obtained from patients subjected to epiphyseal surgery and the expression of Ihh and PTHrP was detected by immunohistochemistry. We show that Ihh and PTHrP are expressed mainly in early hypertrophic chondrocytes in the human growth plate. The levels of expression of Ihh and PTHrP are higher in early stages of puberty than later. Our results suggest that Ihh and PTHrP are present in the human growth plate and that Ihh and PTHrP may be involved in the regulation of pubertal growth in humans.

Adolescent↗

PubMed2001

Fas-mediated apoptosis causes elimination of virus-specific cytotoxic T cells in the virus-infected liver.

Immunity to allogeneic MHC Ags is weak in rodent livers, raising questions as to the mechanisms that might control responses in this organ. Infection with an adenovirus vector reveals that T cell-mediated immunity to nonself-Ags in the liver is self-limiting. Virus-induced liver injury decreases and coincides with disappearance of virus-specific CTL, concomitant to an increase of apoptotic T cells early after infection. But whereas death in CD4 cells is independent of Fas, perforin, and TNF-alpha, that of CD8 cells requires Fas and not perforin or TNF-alpha pathways. Fas ligand is expressed on liver-infiltrating cells, pointing to death by fratricide that causes almost complete disappearance of virus-specific CTL 4 wk after infection. CTL elimination is virus dose dependent, and high doses induced high alanine aminotransferase values, elevated expression of Fas ligand on CD8 cells, and increased CD8 cell migration into the infected liver.

Adenoviridae Infections↗

PubMed2000

Developmental and tissue-specific regulation of parathyroid hormone (PTH)/PTH-related peptide receptor gene expression.

Parathyoid hormone (PTH) and PTH-related peptide (PTHrP) signal through a common PTH/PTHrP receptor (PTHR1). PTH is secreted by the parathyroids and functions in an endocrine manner to regulate extracellular fluid calcium concentrations, largely by interacting with receptors expressed in kidney and bone. PTHrP, on the other hand, is widely expressed and acts by autocrine or paracrine signaling to modulate a range of physiological and developmental responses. PTH1R1 signaling is required both in the adult and during development, and ablation of PTHR1 gene expression results in an embryonic lethal phenotype in both mice and humans. Consequently, the PTHR1 is widely expressed, and transcription of its gene is tissue specific and developmentally regulated. This review focuses on our current knowledge of the mechanisms controlling expression of the PTHR1 gene in humans and in rodents, both during development and in the adult. We also compare the conserved and distinct aspects of PTHR1 gene regulation in the two systems and their bearing on signaling by PTH and PTHrP.

Animals↗

PubMedDate not supplied

[Morbidity and prophylaxis of hemorrhagic fever with renal syndrome in the Republic of Bashkortostan].

The brief retrospective analysis of morbidity, epizootological data and preventive measures with respect to haemorrhagic fever with renal syndrome (HFRS) during the whole period of its registration on the territory of the Republic of Bashkortostan along with the structure of HFRS morbidity during epidemic seasons of 1998 and 1999 is presented. The main causes of decreased HFRS morbidity in 1998, its rise in 1999 as well as prognosis for the year 2000 were detected. The level of HFRS morbidity among the population was found to be directly related to the number of rodents and their infection rate. The basic strategy of epidemic control interventions has been proposed.

Animals↗

PubMed1992

Isolation and subcellular fractionation analysis of acini from rabbit lacrimal glands.

The rabbit has been a useful model for in vivo studies of the pharmacologic control of lacrimal gland fluid secretion. However, by contrast with rodent exorbital lacrimal glands, the rabbit lacrimal gland has not been subjected to detailed cellular, subcellular, or biochemical analyses. Procedures were developed to isolate rabbit lacrimal acini by collagenase digestion and mechanical dispersion. The preparations exhibited good morphology, and trypan blue exclusion rates generally exceeded 90%. The isolated acini responded to carbachol by releasing protein and increasing Na+ unidirectional influx rates. The presence of muscarinic cholinergic and beta-adrenergic receptors was indicated by specific binding of the muscarinic cholinergic antagonist, 3H-N-methylscopolamine (3H-NMS; dissociation constant, Kd, 0.55 nmol/l), and the beta-adrenergic antagonist, 3H-CGP12177 (Kd, 0.34 nmol/l). The maximal binding values measured in crude membrane preparations were 79 fmol/mg for 3H-NMS and 40 fmol/mg for 3H-CGP12177. Subcellular fractionation analyses showed various membrane populations, including a series of Golgi-derived populations admixed with a major endoplasmic reticulum-derived population, a population that may represent the basal-lateral plasma membranes, and a series of populations with characteristics suggesting they are involved in the assembly or recycling of basal-lateral membrane constituents. The authors believe the ability to isolate and analyze acinar preparations from the rabbit lacrimal gland will facilitate various studies of acinar cell biochemistry and physiology that would be impractical with the relatively smaller amounts of material that can be obtained from rat or mouse exorbital lacrimal glands.

Animals↗

PubMed1992

Design strategies, results and evaluations of long-term chemical carcinogenesis studies.

Long-term toxicology and chemical carcinogenesis experiments typically involve both sexes of two species of rodents divided randomly into sets of 50-60 animals per control and exposure groups. Ordinarily three exposure concentrations are gradated down from a top level likely to show some chemically associated toxicity, but which should not compromise the normal well-being or growth and survival patterns of the animals unduly. Duration of exposure is generally two years. Single, intermittent, or varied exposures are used to mimic specific occupational or environmental situations. Exposures are started prior to conception, during gestation and lactation, or at specified times thereafter. Extensive gross observations and microscopic pathology are performed on each animal, and incidences of neoplastic and nonneoplastic lesions are evaluated in age-adjusted statistical comparisons. The collated findings are then interpreted, evaluated, and presented for scientific peer review in public meetings, the aim being to identify qualitatively those environmental and occupational exposures that may likely induce cancer in humans.

Animals↗

PubMed2003

Discrete gene loci regulate neurodegeneration, lymphocyte infiltration, and major histocompatibility complex class II expression in the CNS.

Neurodegeneration and inflammation are fundamental aspects of many neurological diseases. A genome-wide scan of the response to ventral root avulsion (VRA) in a rat F2 cross discloses specific gene regions that regulate these processes. Two gene loci displayed linkage to neurodegeneration and T cell infiltration, respectively, and a single locus displayed extreme linkage to VRA-induced major histocompatibility complex class II expression on microglia. The demonstration that polymorphic genes in different loci control neurodegeneration and CNS inflammation has implications for various experimental rodent nervous system paradigms and potentially for genetically regulated susceptibility to a variety of human CNS diseases.

Animals↗