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At least 793 records · Page 44Linked to original sources
PubMed1999

A ketogenic diet increases the resistance to pentylenetetrazole-induced seizures in the rat.

PURPOSE: The purpose of this study was to test the hypothesis that a ketogenic diet would increase the resistance of rats to pentylenetetrazole (PTZ)-induced seizures and to understand the relation of ketonemia to seizure resistance. METHODS: A freely consumed, high-fat (ketogenic) diet was administered to male Sprague-Dawley rats for 5-10 weeks, while control animals were fed either rodent chow or a high-carbohydrate diet. Ketonemia was measured as plasma levels of beta-hydroxybutyric acid (beta-OHB). Seizures were induced by tail-vein infusion of pentylenetetrazole. RESULTS: The ketogenic diet produced a highly significant (p<0.01) increase in beta-OHB levels within 5 days. Induction of seizures by PTZ 35 days after animals were placed on their respective diets showed that ketogenic animals had a significantly (p<0.01) increased threshold for seizure induction compared with those fed an isocaloric diet of either high-carbohydrate or normal rodent chow. Ketogenic animals did not exhibit increased seizure severity relative to controls, despite receiving consistently higher doses of PTZ. CONCLUSIONS: The ketogenic diet resulted in an increased seizure threshold, confirming the hypothesis, and seizure threshold was found to be a direct function of the level of ketonemia.

3-Hydroxybutyric Acid↗
PubMed1997

Genetic control of telomerase and replicative senescence in human and rodent cells.

The ribonucleoprotein telomerase is detectable in most human cancer cells and immortalized cells but is absent or inactive in the vast majority of normal counterparts. Repression of telomerase activity in human somatic cells, which leads to telomere shortening and replicative senescence, may have evolved as a protective mechanism against immortalization, unfettered clonal evolution and cancer. Rodent cells in culture are far more susceptible to immortalization and malignant progression than human cells. This can be explained by our observation that normal diploid rodent (hamster) fibroblasts possess active telomerase throughout their proliferative life span, and therefore they do not require a telomerase activation step during immortalization. Monochromosome transfer techniques have enabled us to identify powerful telomerase repressive activity specifically associated with the introduction of a single copy of human chromosome 3 into human carcinoma cells. Fine-structure deletion analysis of non-repressed hybrids has permitted us to map the position of the candidate telomerase repressor gene to 3p21.1-3p21.3. A strategy for isolating the gene has been developed involving a combination of fine-structure deletion mapping and functional gene transfer approaches. The availability of cloned telomerase repressor genes will advance our understanding of telomerase regulation in the human soma and its disruption during human cancer development.

Animals↗
PubMed1994

Uptake and metabolism of albumin by rodent incisor enamel in vivo and postmortem: implications for control of mineralization by albumin.

The distribution of albumin throughout enamel development in the rat mandibular incisor was investigated using sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS PAGE) and Western blotting employing an anti-rat albumin antibody. Intact albumin was detectable at all stages of enamel development but was most evident during late secretion/transition. Its concentration was subsequently reduced during the maturation stage. Albumin degradation products appeared during the transition/early maturation stage indicating that albumin breakdown preceded its removal. As albumin inhibits apatite crystal growth, its degradation and removal may be a necessary prerequisite for normal enamel crystal growth, perhaps reflecting a general mechanism for removal of residual endogenous matrix or adventitious crystal growth inhibitors. Additional studies revealed that the maturation stage was particularly susceptible to albumin influx postmortem. Albumin could therefore form part of the natural crystal growth control process, which, if not removed, could hamper maturation and lead to white spot hypoplasias.

Albumins↗
PubMed1999

Germ cell-specific cyclic adenosine 3',5'-monophosphate response element modulator expression in rodent and primate testis is maintained despite gonadotropin deficiency.

cAMP response element modulator (CREM) is an important component of the cAMP-mediated signaling pathway and is essential for differentiation of haploid male germ cells. In the rodent, testicular expression of CREM is believed to be controlled by FSH. We studied the expression pattern of CREM and gonadotropic control in the nonhuman primate and rodent testis. Adult cynomolgus monkeys (Macaca fascicularis) received daily either vehicle or the potent GnRH antagonist (ANT) cetrorelix for periods of 25 and 56 days. Rats were also exposed to vehicle or ANT for periods of 14 and 42 days. ANT treatment suppressed pituitary gonadotropin secretion, reduced testis size, and altered spermatogenesis. A rabbit polyclonal antibody raised against recombinant CREM tau and reacting with CREM alpha, -beta, -gamma, -tau1, and -tau2 at similar affinities was used for immunocytochemistry and Western blotting. CREM expression was seen in round spermatids, with highest levels during spermatogenic stages V-VII, but declined with progression of spermatid development in the primate. Similar observations were made for the rat testis. Thus, CREM expression was maximal at the onset of acrosome formation and was low or undetectable upon initiation of spermatid elongation in both species. A weak, but specific, CREM signal was seen in mid- to late pachytene spermatocytes and during meiotic division in both species. After ANT exposure, the germ cell- and stage-specific pattern of CREM expression was quantitatively retained at all time points and in both species. Northern and Western blot analysis confirmed the maintenance of testicular CREM expression despite 25 days of ANT treatment. A retrospective immunocytochemical analysis of rat testes 14 days posthypophysectomy revealed CREM signals in round spermatids. These findings demonstrate that the testicular expression of CREM is not entirely dependent on gonadotropic hormones but, rather, on the maturational stage of haploid round germ cells.

Animals↗
PubMed1983

Stage specificity in the mesenchyme requirement of rodent lung epithelium in vitro: a matter of growth control?

Epithelia from lung rudiments in which secondary bronchial buds are already established (14th and 13th gestational day for rat and mouse respectively) are able to undergo branching morphogenesis and cytodifferentiation in submandibular mesenchyme in vitro, whereas lung epithelium from one day younger foetuses rarely gives a morphogenetic response to submandibular mesenchyme and usually differentiates into primary (non-budding) bronchial epithelium. The failure of 13-day rat lung epithelium to respond to submandibular mesenchyme can be prevented by peeling off the submandibular mesenchyme from the lung epithelium after 2 1/2 days culture and replacing the same mesenchyme, or renewing it with fresh salivary mesenchyme ex vivo. Changes in the epithelial contour are visible by 10 h and buds form within 24 h; this is followed by branching morphogenesis in more than 66% of the samples. The number of cells in S-phase in the epithelium is doubled within 3 to 5 h after the operation and the number of mitotic cells (colchicine block) is increased during an 11 to 19 h period after the operation. Substituting stomach mesenchyme for submandibular mesenchyme after the operation failed to elicit morphogenesis or an increase in the number of S-phase cells in the epithelium. The proportion of epithelial cells in S-phase in unoperated recombinants does not differ from the proportion in the primary bronchial epithelium (non-budding) of homotypic lung recombinants, whereas the proportion of S-phase cells in operated recombinants approaches that found in the buds of homotypic lung recombinants. The distribution of S-phase cells in visibly responding recombinants 15 to 17 h after operation shows the same heterogeneity as in homotypic lung recombinants, newly formed buds having twice as many cells labelled with [3H]thymidine as the non-budding area. Cell cycle parameters of intact rat lung growing in vitro were estimated using the labelled mitoses method. Primary bronchial epithelium and bronchial buds both had a total cell cycle time of about 13 h and an S-phase of about 10 h. The growth fraction was 0.54 in the primary bronchus and 0.95 in the buds. It is suggested that, also in the recombinants, differences in the proportion of S-phase cells at any one time in morphogenetically active and inactive areas of the epithelium are due to differences in the growth fraction. It is concluded that an early event in the morphogenetic response of lung epithelium to submandibular mesenchyme after removing and restoring the mesenchyme is an increase in the size of the population of dividing cells and it is suggested that a high proportion of dividing cells in an epithelial population is a prerequisite for further interaction of epithelium and mesenchyme leading to branching morphogenesis.

Animals↗
PubMed1999

Design, construction, and validation of a large capacity rodent magnetic field exposure laboratory.

A magnetic field exposure laboratory has been constructed to support National Toxicology Program studies for the evaluation of the toxicity and carcinogenicity of pure, linearly polarized, 60 Hz magnetic fields in rodents. This dual corridor, controlled access facility can support the simultaneous exposure of 1200 rats and 1200 mice. The facility contains fully redundant electrical and environmental control systems and was constructed using non-metallic materials to maintain low levels of background (ambient), stray, and cross-talk magnetic fields. The exposure module design provides for large uniform exposure volumes with good control of stray and cross-talk fields, while allowing the use of roll-around cage racks for simplified animal husbandry. Stray fields and cross-talk have been further reduced by the inclusion of "steering coils" in each exposure module. Ambient 60 Hz fields (less cross-talk) in all exposure rooms are <0.1 microT (1 mG), and static magnetic fields have been mapped extensively. Magnetic field strength, waveform, temperature, relative humidity, light intensity, noise level, vibration, and air flow in all animal holding areas are tightly regulated, and are monitored continuously during all studies. Field uniformity in the animal exposure volumes is better than -/+l0%; a systematic program of cage, rack, and room rotation controls for possible positional effects within the exposure system. Magnetic fields are turned on and off over multiple cycles to prevent the induction of transients associated with abrupt field level changes. Total harmonic distortion is <3% at all field strengths. The facility has been used to study magnetic field bioeffects in rodent model systems in experiments ranging in duration from 8 weeks to 2 years.

Air Movements↗
PubMed1993

Autoreactivity in patients with Behçet's disease.

Behçet's disease (BD) has features consistent with an immunopathogenic mechanism. We tested 23 patients with BD and 139 normal controls for autoantibodies to nuclear, cardiolipin and smooth muscle antigens using indirect immunofluorescence, immunodiffusion, Western blots and an enzyme immunosorbent assay. Serum immunoglobulin G, M and A levels were measured by standard radial immunodiffusion techniques. The prevalence of the following autoantibodies was raised in patients with BD compared with the control group: ANA on rodent (P < 0.05) and human (P < 0.01) substrates and smooth muscle antibody (P < 0.001). Anticardiolipin antibody was detected in one patient (GPL 23.1 U). Antibodies to the ribonucleoproteins Ro, La, Sm and RNP were not found. Levels of serum immunoglobulins G, M and A were elevated in BD compared with the controls and this was significant for immunoglobulin M (P < 0.05) and A (P < 0.001). These findings support the concept of a polyclonal B cell activation in BD.

Adult↗
PubMedDate not supplied

Long-term studies of hantavirus reservoir populations in the southwestern United States: rationale, potential, and methods.

Hantaviruses are rodent-borne zoonotic agents that cause hemorrhagic fever with renal syndrome in Asia and Europe and hantavirus pulmonary syndrome (HPS) in North and South America. The epidemiology of human diseases caused by these viruses is tied to the ecology of the rodent hosts, and effective control and prevention relies on a through understanding of host ecology. After the 1993 HPS outbreak in the southwestern United States, the Centers for Disease Control and Prevention initiated long-term studies of the temporal dynamics of hantavirus infection in host populations. These studies, which used mark-recapture techniques on 24 trapping webs at nine sites in the southwestern United States, were designed to monitor changes in reservoir population densities and in the prevalence and incidence of infection; quantify environmental factors associated with these changes; and when linked to surveillance databases for HPS, lead to predictive models of human risk to be used in the design and implementation of control and prevention measures for human hantavirus disease.

Animals↗
PubMed1981

Comparative effect of the three rodenticides warfarin, difenacoum and brodifacoum on eight rodent species in short feeding periods.

Short laboratory feeding tests were carried out with the anticoagulants warfarin, difenacoum, and brodifacoum on a number of European rodent species: Clethrionomys glareolus, Microtus agrestis, M. arvalis, Apodemus flavicollis, A. sylvaticus, Mus musculus, Rattus rattus and R. norvegicus. It was found that the toxicity to all species was highest with brodifacoum and lowest with warfarin, and that only 0.005% brodifacoum would give a complete mortality in most species after one day's feeding. The potential of this compound for the control of microtine field rodents is suggested.

4-Hydroxycoumarins↗
PubMed2003

Repeated fasting/refeeding elevates plasma leptin without increasing fat mass in rats.

It is known that repeated fasting and refeeding increase capacity of fat storage in adipose tissue as an adaptive response to fasting. However, the amount of weight gain in fasted/refed animals falls behind the control level in most rodent studies. Leptin, an adipocyte-derived hormone that impacts on energy homeostasis, may be up-regulated by repeated cycles of fasting and refeeding. In this study, we investigated the adaptive response of leptin to repeated cycles of 1-day fasting and 1-day refeeding for 42 days in rats. The repeated fasting and refeeding (RFR) rats gained less body weight than the controls. Daily food intake of the RFR rats was decreased after Day 16 and remained suppressed. Circulating leptin levels of the RFR rats were significantly elevated at Day 35 compared with the controls and at Day 44 compared with the controls and pair-fed (PF) rats. Leptin mRNA levels of these rats were also significantly increased in retroperitoneal white adipose tissue (RT-WAT) compared with the controls and PF rats. Moreover, hypothalamic proopiomelanocortic (POMC) gene expression was augmented in the RFR rats compared with the controls and PF rats. However, there was no statistical difference in percent visceral fat mass among the experimental groups. Lipoprotein lipase (LPL) mRNA levels of RFR rats were significantly increased in RT-WAT compared with the controls and PF rats. These data indicated that leptin was up-regulated in response to chronic repeated fasting and refeeding cycles without a concomitant increase in adiposity, and the augmented leptin levels were associated with an increase in POMC gene expression, reduced food intake, and diminished body weight gain.

Adaptation, Physiological↗
PubMed2026

Auditory brainstem response in the identification of cochlear synaptopathy in aged rodents: a systematic review with meta-analysis.

PURPOSE: This systematic review and meta-analysis evaluated the diagnostic performance of auditory brainstem response (ABR) for identifying age-related cochlear synaptopathies in rodents. METHOD: Following PRISMA guidelines, searches were conducted in PubMed/MEDLINE, Cochrane Library, Scopus, Embase, Web of Science, SciELO, LILACS, and gray literature. Studies evaluating CS in naturally aged rodents using short-latency auditory evoked potentials (AEPs) were included. Study selection, data extraction, risk-of-bias (JBI Critical Appraisal Checklist for Analytical Cross-Sectional Studies), and certainty of the evidence (GRADE&#xae; system) assessment were conducted independently by two reviewers. Meta-analyses were performed using a random-effects model, with standardized mean differences and 95% confidence intervals. ABR wave I amplitudes were analyzed for click (80 and 90&#xa0;dB SPL) and tone-burst stimuli stratified by frequency. RESULTS: Among 3,008 identified records, 12 studies were included in the review and five in the meta-analysis. All included studies used ABR measures to investigate CS, with wave I amplitude being the most frequently evaluated biomarker. Meta-analysis demonstrated a significant reduction in ABR wave I amplitude in aged rodents compared with young controls for both click- and tone-burst-evoked responses. Tone-burst ABR showed no significant differences among the evaluated frequencies. These findings should be interpreted with caution due to the limited number of studies and the methodological heterogeneity, which may have reduced statistical power and comparability. CONCLUSIONS: The evidence supports ABR wave I amplitude as a sensitive electrophysiological marker of age-related CS in rodents. Nevertheless, further studies with standardized protocols are needed to strengthen its diagnostic utility and improve comparability across studies.

Animals↗
PubMedDate not supplied

Validation of a motor activity system by a robotically controlled vehicle and using standard reference compounds.

INTRODUCTION: A series of experiments were undertaken to evaluate the accuracy, precision, specificity, and sensitivity of an automated, infrared photo beam-based open field motor activity system, the MotorMonitor v. 4.01, Hamilton-Kinder, LLC, for use in a good laboratory practices (GLP) Safety Pharmacology laboratory. METHODS: This evaluation consisted of two phases: (1) system validation, employing known inputs using the EM-100 Controller Photo Beam Validation System, a robotically controlled vehicle representing a rodent and (2) biologic validation, employing groups of rats treated with the standard pharmacologic agents diazepam or D-amphetamine. The MotorMonitor's parameters that described the open-field activity of a subject were: basic movements, total distance, fine movements, x/y horizontal ambulations, rearing, and total rest time. These measurements were evaluated over a number of zones within each enclosure. RESULTS: System validation with the EM-100 Controller Photo Beam Validation System showed that all the parameters accurately and precisely measured what they were intended to measure, with the exception of fine movements and x/y ambulations. Biologic validation using the central nervous system depressant diazepam at 1, 2, or 5 mg/kg, i.p. produced the expected dose-dependent reduction in rat motor activity. In contrast, the central nervous system stimulant D-amphetamine produced the expected increases in rat motor activity at 0.1 and 1 mg/kg, i.p, demonstrating the specificity and sensitivity of the system. DISCUSSION: Taken together, these studies of the accuracy, precision, specificity, and sensitivity show the importance of both system and biologic validation in the evaluation of an automated open field motor activity system for use in a GLP compliant laboratory.

Amphetamine↗
PubMed1994

The effect of hyperthermic treatment on electroencephalographic recovery after interruption of respiration in rats.

Electroencephalography (EEG) was utilized for investigating the effect of hyperthermia followed by apneic hypoxia in rats. They were heated whole-bodily to 41 degrees C for 15 min under the control of an artificial rodent ventilator, after drug-induced generalized paralysis. A transcutaneous oxygen saturation monitor was applied to detect the hypoxic condition. EEG was monitored with bipolar needle electrodes. The 72-kDa heat-shock protein (HSP72) in brain was analyzed by sodium dodecyl sulfate-polyacrylamide electrophoresis, followed by immunostaining with an anti-HSP72 antibody. There was no difference in the time interval from onset of apneic hypoxia to flat EEG between the hyperthermic and control groups, but cortical electrical activity appeared earlier in the hyperthermia group than the control group, after 90 s of ventilation interruption. The cardiac function did not change in the two groups. The HSP72 synthesis significantly increased in the brain of the rats with hyperthermic treatment.

Animals↗
PubMed2004

Nutritional iron deprivation attenuates kainate-induced neurotoxicity in rats: implications for involvement of iron in neurodegeneration.

There is evidence suggesting that oxidative stress contributes to kainate neurotoxicity. Since iron promotes oxidative stress, the present study explores how change in nutritional iron content modulates kainate-induced neurotoxicity. Rats received an iron-deficient diet (ID) from 22 days of age for 4 weeks. One control group received the same diet supplemented with iron and another control group received standard rodent diet. Cellular damage after subcutaneous kainate (10 mg/kg) was assessed by silver impregnation and gliosis by staining microglia. ID reduced cellular damage in piriform and entorhinal cortex, in thalamus, and in hippocampal layers CA1-3. ID also attenuated gliosis, except in the hippocampal CA1 layer. Given involvement of zinc in hippocampal neurotransmission and in oxidative stress, we tested for a possible interaction of nutritional iron with nutritional zinc. Rats were made iron-deficient and then assigned to supplementation with iron, zinc, or iron + zinc. Controls were continued on ID diet. After 2 weeks, rats were treated with kainate. Iron supplementation abolished the protective effect of ID in piriform and entorhinal cortex. In hippocampal CA1 and dorsal thalamus, neither iron nor zinc supplementation alone abolished the protective effect of ID against cellular damage. Iron + zinc supplementation abolished ID protection in dorsal thalamus, but not in reuniens nucleus. Kainate-induced gliosis in CA1 remained unaffected by nutritional treatments. Thus, in piriform and entorhinal cortex, nutritional iron has a major impact on cellular damage and gliosis. In hippocampal CA1, gliosis may associate with synaptic plasticity not modulated by nutritional iron, while cellular damage is sensitive to nutritional iron and zinc.

Animals↗
PubMed1998

Evidence that a novel type of progestational phase control occurs in the corn mouse, a South American murid rodent.

Most Muridae display a short luteal phase that becomes functional as a consequence of the prolactin release induced by the stimulation of copulation and/or lactation. The corn mouse also shows a short luteal phase, and we wanted to know whether copulation and/or lactation would release prolactin and maintain progesterone secretion in this species. Females in postpartum estrus were either allowed to copulate with an intact male or not, and either to lactate their young or not. Afterward, plasma progesterone was elevated over the baseline level only in females that had copulated and were bearing growing embryos (whether or not they were lactating), while prolactin was elevated only in lactating females. In another experiment, endometrial scratching induced decidualization both in females that had copulated with a vasectomized male and in those that had not copulated; sham operations had no effect in either case. Progesterone levels were elevated in decidualized animals as compared with their sham-operated controls. Results indicate that the initiation of the progestational phase in the corn mouse is not dependent on prolactin release. A short luteal phase during which nidation may occur has not yet been described in any other mammal.

Animals↗
PubMed1998

Cortical bone responses to 2G hypergravity in growing rats.

BACKGROUND: Rat cortical bone adaptation to chronic hypergravity (2G) was studied using young growing male Wistar rats (60 d). METHODS: Animals (10 rats) were subjected to chronic hypergravity (14 d) in order to understand the plastic nature of bone under a constant hypergravity stress using a special rodent habitat that was attached to a 12-ft. radius centrifuge. Also, an equal number of stationary controls were housed in a rodent vivarium containing identical cages that were used for centrifugation. After 14 d of centrifugation, femur bones were excised and prepared for morphological and biochemical measurements. RESULTS: Results showed that 2G had significantly shortened the femurs (3%) and reduced the cortical bone area (13%). In particular, hypergravity induced significant reductions in the thicknesses of cortical bone at the anterior (13%) and medial regions (15%) of the mid-diaphysis. However, femoral bone density, collagen and calcium concentrations were unaltered. The content of mature, stable bone collagen cross-links hydroxylysylpyridinoline (HP), lysylpyridinoline (LP), were significantly greater in bones from centrifuged animals. CONCLUSION: Our findings suggest that short term exposure to 2G does not enhance bone formation or induce changes in cortical bone composition, or alter specific gravity. These data also suggest that bone maturation as reflected by collagen cross-linking is upregulated. However, it is undetermined at this time whether the enhanced content of mature bone collagen in the centrifuged rats is a result of either an increased rate of cross-linking or reduction in the degradation of "older collagen."

Adaptation, Physiological↗
PubMed1999

Repair of an osseous facial critical-size defect using augmented fibrin sealant.

OBJECTIVE: Osseous defects of the head and neck are a common challenge for the otolaryngologist. To develop improved reconstructive options, osteoconductive engineering experiments are being conducted. A nasal critical-size defect (CSD) model has previously been described in which less than 7% bone healing is observed over 6 months. An implant containing fibrin sealant with and without osteoprogenitor cells is evaluated in this model. STUDY DESIGN: Randomized controlled trial using a rodent model. METHODS: A nasal CSD was surgically created in 18 male retired breeder Sprague-Dawley rats. Six animals were not implanted with any material, six received fibrin sealant consisting of fibrin (25 mg/mL) and thrombin (1000 U/mL), and six were implanted with fibrin sealant and rat calvarial osteoprogenitor cells (1.8 x 10(6) cells/mL). Thirty days later, the animals were examined at necropsy by planimetry, histological analysis of new bone growth, and radiodensitometric analysis of bone thickness. RESULTS: A thin layer of bone covered the defect in all of the treated animals. A statistically significant increase in bone density (P < .05) between fibrin sealant plus osteoprogenitor cells and each of the other groups was shown using radiodensitometric analysis. Histological analysis also confirmed this difference. CONCLUSION: Osteoprogenitor cells contained within fibrin sealant result in a greater augmentation of bone regeneration than controls or fibrin sealant alone.

Animals↗