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Control of plague in Taranto, Italy, 1945-1946; an account of a successful programme of rodent extermination.
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Interim guidance for minimizing risk for human lymphocytic choriomeningitis virus infection associated with rodents.
In May 2005, CDC received reports of four organ-transplant recipients with unknown illness. All were discovered to have been infected with lymphocytic choriomeningitis virus (LCMV) via a common organ donor. Epidemiologic investigation traced the source of the virus to a pet hamster purchased by the donor from a local pet store. LCMV testing of other rodents at the pet store revealed three other LCMV-infected rodents (two hamsters and a guinea pig), supplied by a single distributor (distributor A). Preliminary laboratory testing of hamsters from distributor A has identified an infection rate of approximately 3% among the animals sampled. The facility of distributor A is under quarantine until it can be documented as free of LCMV infection. This report provides background information on LCMV and interim guidance for the public on reducing risk for LCMV infection from pet rodents.
The effect of food restriction by time-scheduled feeding on the development of body-weight, lifespan and incidence of spontaneous tumours and diseases in male Han:SPRD rats.
Food consumption, development of body weight, lifespan and incidence of spontaneous diseases and tumours were investigated in 3 groups of 96 male Han:SPRD rats each maintained in a longevity study from weaning up to their natural death. All rats were fed a commercial cereal-based diet. One group received food ad libitum and was used as control group. Access to the diet was controlled in the other two groups by means of an automatic timer. The rats of one of the latter groups were fed nocturnally (4 x 42 min daily during the dark period) and those of the other adiurnally (4 x 42 min daily, each two times during dark and light period). Time-scheduled feeding caused an evident food restriction compared with the food consumption of the rats fed ad libitum. This food restriction, however, was significantly more pronounced in the younger animals during the first weeks after weaning than in the older rats. The body weight development corresponded to the feed intake. In animals subjected to food restriction the weight remained below that of rats fed ad libitum during all age periods. Furthermore, time-scheduled feeding caused an important increase of the mean life expectancy and a reduction in the incidences of chronic nephropathy and purulent and chronic forms of prostatitis. Only a slight effect of controlled feeding was observed on the incidence of alveolar lipoproteinosis. Time-scheduled feeding did not cause a reduction in the incidence of tumours, but it delayed their occurrence. The risk to develop various types of tumours during the third year of life was significantly higher in the ad libitum group than in the rats fed by a controlled regime. The automaton Han:CHRONOFEEDER, used in this study, has proved to be an appropriate, relatively inexpensive and easily installable feeding system for automatic control of food accessibility. It is suitable to implement controlled feeding and food restriction of rodents in longterm experiments.
The role of the renin-angiotensin system in blood pressure regulation in normotensive animals and man.
The role of the renin-angiotensin system in the control of blood pressure in normal rodents, primates and man has been evaluated using inhibitors which block the system at various stages. Renin plays a major role in the maintenance of blood pressure under volume depletion. In subjects with a normal salt intake, the contribution of the renin-angiotensin system in maintaining blood pressure levels can be evaluated using angiotensin converting enzyme (ACE) inhibitors. The contribution of the renin-angiotensin system can now be evaluated more closely following the development of new substances which block the renin-angiotensinogen reaction. Available data strongly suggest that renin contributes to the maintenance of blood pressure levels in subjects with a normal salt intake, although to a lesser degree than in subjects on a low sodium intake. The renin-angiotensin system plays a role in the regulation of blood pressure levels in normal experimental animals and man--its importance depending on the state of sodium balance.
Rodent models of focal ischemia.
Experimental models of focal ischemia have provided an unparalleled insight into the dynamic events that surround ischemic brain injury. The dichotomous capacity of existing rodent models of focal ischemia to provide a controlled environment to examine the pathogenesis of focal ischemia and to allow assessment of the efficacy of potential therapeutic intervention is reviewed. The established rodent model of permanent middle cerebral artery occlusion (electrocoagulation) is critically examined and set against the distinctive features of novel methods that have been developed to reduce invasive surgery and to examine the pathological consequences of reperfusing a previously ischemic area. Emphasis has been placed on the technical requirements of each model that affect outcome and reproducibility.
Angiotensin I-converting enzyme inhibition but not angiotensin II suppression alters angiotensin I-converting enzyme gene expression in vessels and epithelia.
The concentration of angiotensin-converting enzyme (ACE) increases during chronic treatment with ACE inhibitors for unknown reasons. We investigated whether alterations in ACE mRNA and ACE concentration occur in the different tissues during ACE inhibition and the role of angiotensins in these regulations by comparing ACE inhibitors with other blockers of the renin-angiotensin system. Enalapril, an ACE inhibitor, in the range of 0.3 to 10 mg/kg/day in rats induced dose- and time-dependant increases in plasma ACE up to two to three times control values. There were significant increases in the steady state ACE mRNA in the lung (32%), duodenum (64%) and aorta (324%) and 40% to 140% increases in membrane-bound enzyme concentration in these tissues and in the heart and kidney. The ACE content of purified duodenal brush border was increased by 80%, but the enzyme and its mRNA in the testis were not altered. The angiotensin II receptor antagonist losartan at several regimens of up to 30 mg/kg twice a day for 14 days produced no change in plasma ACE level or lung ACE mRNA. The human renin inhibitor ciprokiren was tested in guinea pigs, a species sensitive to this compound. Both enalapril and cilazapril induced 2-fold increases in plasma ACE, but ciprokiren (24 mg/kg/day for 12 days) had no effect. Enalapril treatment of BN/Kat rats (lacking circulating kininogens) caused a similar increase in ACE as in other rats. This study documents a general increase in ACE gene expression and enzyme concentration in tissues during ACE inhibition, with the exception of the testis, most probably reflecting an activation of the 5', so-called somatic promoter of the ACE gene. Angiotensins are not involved in this regulation and do not seem to control ACE gene expression in normal rodents.
Uncoupling protein-1 mRNA expression in obese human subjects: the role of sequence variations at the uncoupling protein-1 gene locus.
Uncoupling protein-1 (UCP-1) activity in brown adipose tissue increases thermogenesis, contributes to facultative energy expenditure in humans, and has been implicated in the pathogenesis of rodent obesity. To determine genetic factors controlling UCP-1 expression in humans, we measured intra- and extraperitoneal UCP-1 mRNA abundance levels by a competitive RT-PCR method and compared expression levels with common sequence variations in the beta3-adrenergic receptor gene and the distal UCP-1 gene promoter in obese human subjects. While median and average UCP-1 mRNA levels in both the intra- and extraperitoneal tissue were lower in subjects heterozygous for the Trp64Arg mutation in the beta3-adrenergic receptor gene, this difference was not statistically significant. However, a strong association of intraperitoneal UCP-1 mRNA abundance with the UCP-1 gene polymorphism at -3826 relative to the transcription start site was observed that explained 19.3% of the interindividual variability. The minor allele imparted a dose-dependent reduction on UCP gene expression. The importance of sequence variations at the UCP-1 gene locus as a common source of UCP-1 mRNA abundance variability was supported by allele-specific expression studies utilizing a newly identified polymorphism in exon 2 of the UCP-1 gene that predicts a substitution of alanine by threonine. In four subjects heterozygous for the -3826 polymorphism, the mRNA species transcribed from the wild-type allele accounted for 63+/-6% percent of total intraperitoneal mRNA abundance. In one subject homozygous for the minor promoter allele, wild-type mRNA was also more abundant than variant mRNA. Thus, the UCP-1 polymorphism at -3826 is probably only a marker for a frequent mutation causing reduced mRNA expression.
Rodent resistance to the anticoagulant rodenticides, with particular reference to Denmark.
Inherited resistance to anticoagulant rodenticides was discovered in populations of Rattus norvegicus about 14 years ago. Similar resistance has now been reported from several countries in north-western Europe and from the USA. In order to detect resistance and to control it effectively, basic data on the susceptibility of rat populations are required for each country, and trapping surveys should be made in any area where resistance is suspected. Acute poisons are needed to control resistant rats although the shift from anticoagulants to acute poisons is a retrograde step as far as efficiency is concerned, and increases the hazard of control operations to man and other animals. Resistance to anticoagulants in Mus musculus has been reported from England, and resistant mice are probably to be found in other countries also in view of the great individual variation in susceptibility of this species to these rodenticides.
Impairment of long-term potentiation and spatial memory in leptin receptor-deficient rodents.
Leptin is well known to be involved in the control of feeding, reproduction and neuroendocrine functions through its action on the hypothalamus. However, leptin receptors are found in brain regions other than the hypothalamus (including the hippocampus and cerebral cortex) suggesting extrahypothalamic functions. We investigated hippocampal long-term potentiation (LTP) and long-term depression (LTD), and the spatial-memory function in two leptin receptor-deficient rodents (Zucker rats and db/db mice). In brain slices, the CA1 hippocampal region of both strains showed impairments of LTP and LTD; leptin (10(-12) M) did not improve these impairments in either strain. These strains also showed lower basal levels of Ca(2+)/calmodulin-dependent protein kinase II activity in the CA1 region than the respective controls, and the levels did not respond to tetanic stimulation. These strains also showed impaired spatial memory in the Morris water-maze test (i.e. longer swim-path lengths during training sessions and less frequent crossings of the platform's original location in the probe test. From these results we suggest that the leptin receptor-deficient animals show impaired LTP in CA1 and poor spatial memory due, at least in part, to a deficiency in leptin receptors in the hippocampus.
Retinal degeneration in a rodent model of Smith-Lemli-Opitz syndrome: electrophysiologic, biochemical, and morphologic features.
OBJECTIVE: To assess the electrophysiologic, histologic, and biochemical features of an animal model of Smith-Lemli-Opitz syndrome (SLOS). METHODS: Sprague-Dawley rats were treated with AY9944, a selective inhibitor of 3beta-hydroxysterol-Delta(7)-reductase (the affected enzyme in SLOS). Dark- and light-adapted electroretinograms were obtained from treated and control animals. From each animal, 1 retina was analyzed by microscopy, and the contralateral retina plus serum samples were analyzed for sterol composition. The main outcome measures were rod and cone electroretinographic amplitudes and implicit times, outer nuclear layer (ONL) thickness, rod outer segment length, pyknotic ONL nucleus counts, and the 7-dehydrocholesterol/cholesterol mole ratio in the retina and serum. RESULTS: By 10 weeks' postnatal age, rod and cone electroretinographic wave amplitudes in AY9944-treated animals were significantly reduced and implicit times were significantly increased relative to controls. Maximal rod photoresponse and gain values were reduced approximately 2-fold in treated animals relative to controls. The ONL thickness and average rod outer segment length were reduced by approximately 18% and 33%, respectively, and ONL pyknotic nucleus counts were approximately 4.5-fold greater in treated animals relative to controls. The retinal pigment epithelium of treated animals contained massive amounts of membranous/lipid inclusions not routinely observed in controls. The 7-dehydrocholesterol/cholesterol mole ratios in treated retinas and serum samples were approximately 5:1 and 9:1, respectively, whereas the ratios in control tissues were essentially zero. CONCLUSIONS: This rodent model exhibits the key biochemical hallmarks associated with SLOS and displays electrophysiologic deficits comparable to or greater than those observed in the human disease. Clinical Relevance These results predict retinal degeneration in patients with SLOS, particularly those with the more severe (type II) form of the disease, and may be more broadly relevant to other inborn errors of cholesterol biosynthesis. This animal model may also be of use in evaluating therapeutic treatments for SLOS and in understanding the slow phototransduction kinetics observed in patients with SLOS.
High prevalence of hantavirus antibodies in bank voles (Clethrionomys glareolus) captured in the vicinity of households afflicted with nephropathia epidemica.
Puumala virus, the causative agent of nephropathia epidemica (NE), occurs endemically in Europe and is spread mainly by the bank vole (Clethrionomys glareolus). In the vicinity of each of four households afflicted with NE, we studied rodents with regard to population density and prevalence of Puumala virus-specific antibodies. For each case area, a control area was randomly selected 10 km away, without regard to the presence of human settlement. During 6,000 trap nights, 328 rodents were caught, of which 299 were C. glareolus. The mean rodent densities of case and control areas were 6.6 and 3.7 animals per 100 trap nights (P < 0.001). The prevalence of serum antibodies was 15.9% in case areas compared with 5.6% in control areas (P < 0.05). In three of the case areas, where NE had occurred 3-10 weeks before trapping, the rodent density and seroprevalence were much higher than in the fourth area, where NE occurred 38 weeks before trapping. In conclusion, C. glareolus seropositive for Puumala virus occurred more frequently near households afflicted with NE than in control areas 10 km away.
Rhythmic whisking by rat: retraction as well as protraction of the vibrissae is under active muscular control.
The rhythmic motor activity of the vibrissae that rodents use for the tactile localization of objects provides a model system for understanding patterned motor activity in mammals. The muscles that drive this whisking are only partially fixed relative to bony attachments and thus shift their position along with the movement. As a means to characterize the pattern of muscular dynamics during different patterns of whisking, we recorded electromyogram (EMG) activity from the muscles that propel individual follicles, as well as EMG activity from a muscle group that moves the mystacial pad. The dominant pattern of whisking in our behavioral paradigm, referred to as exploratory whisking, consisted of large amplitude sweeps in the frequency range of 5-15 Hz. The frequency remained remarkably constant within a bout of whisking but changed values between bouts. The extrinsic musculature, which shifts the surface of the pad backwards, was found to be activated in approximate antiphase to that of the intrinsic muscles, which rotate individual vibrissae forward. Thus retraction of the vibrissae was driven by a backward shift in the attachment point of the follicles to the mystacial pad. In a less frequent pattern of whisking, referred to as foveal whisking, the vibrissae are thrust forward and palpate objects with low-amplitude movements that are in the higher frequency range of 15-25 Hz. Protraction of the vibrissae remains driven by the intrinsic muscles, while retraction in this pattern is largely passive. Interestingly, a mechanical argument suggests that activation of the extrinsic muscles during foveal whisking is not expected to affect the angle of the vibrissae. As a means to establish if the phasic control of the intrinsic versus extrinsic muscles depended on sensory feedback, we characterized whisking before and after bilateral transections of the infraorbital branch of the trigeminal sensory nerve. The loss of sensory feedback had no net effect on the antiphase relation between activation of the intrinsic versus extrinsic muscles over the full frequency range for exploratory whisking. These data point to the existence of a dual-phase central pattern generator that drives the vibrissae.
Regulatory aspects of placental iron transfer--a comparative study.
Receptor-mediated endocytosis is generally assumed to be the process by which the haemochorial placenta takes up iron from transferrin. The involvement of an additional nonendocytic process cannot, however, be excluded. It appears from a study of iron transport mechanisms and of the maturation of the transfer process that placental ferritin is involved in the transfer of iron from mother to fetus. The metabolic relationship between the ferritin pool and the placental transfer pool remains to be elucidated. There is no evidence for short-term regulation of placental transfer capacity in response to changes in the maternal iron supply or to changes in the trophoblastic iron content. This cannot yet be said of fetal feedback control of placental iron uptake because the experiments performed so far do not permit conclusions on this point. The capacity for iron uptake and transfer seems to increase in accordance with the ontogenetically determined placental growth pattern. This does not exclude long-range adaptive modifications of the transfer capacity in response to early maternal or fetal disturbances. The results obtained from studying placental maturation suggest that a possible long-term regulatory interaction between growing placenta and fetus may occur. Clinical evidence so far is inconclusive. The relatively moderate reductions in the fetal iron stores which are generally associated with severe iron-deficient pregnancies might be seen as an argument in favour of long-term placental control. The marked impact of pregnancy on maternal iron metabolism in rodents, as compared to other mammals, is possibly met by means of direct placental control of mucosal iron uptake. In primates, mucosal iron uptake during pregnancy seems to be governed by factors related to systemic iron deficiency only.
An improved technique for visually controlled pinealectomy in the rat.
An improved method for pinealectomizing rats and other small laboratory rodents is described which avoids bleeding and allows excision of the organ under exact visual control. After removing a small piece of the skull dorsal to the confluence of the transverse and dorsal sagittal sinuses, the latter is ligated and cut. The underlying pineal gland is then exposed and may be excised reliably without damage to the gland tissue or to adjacent brain structures. Intra- and post-operative complications are extremely rare.
[Zoonotic risk of rodents in livestock production].
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Female gender attenuates cytokine and chemokine expression and leukocyte recruitment in experimental rodent abdominal aortic aneurysms.
Female gender appears to be protective in the development of abdominal aortic aneurysms (AAAs). This study sought to identify gender differences in cytokine and chemokine expression in an experimental rodent AAA model. Male and female rodent aortas were perfused with either saline (control) or elastase to induce AAA formation. Aortic diameter was determined and aortic tissue was harvested on postperfusion days 4 and 7. Cytokine and chemokine gene expression was examined using focused gene arrays. Immunohistochemistry was used to quantify aortic leukocyte infiltration. Data were analyzed by Student's t-tests and ANOVA. Elastase-perfused female rodents developed significantly smaller aneurysms compared to males by day 7 (93 +/- 10% vs. 201 +/- 25%, P = 0.003). Elastase-perfused female aortas exhibited a fivefold decrease in expression of the BMP family and ligands of the TNF superfamily compared to males. In addition, the expression of members of the TGF beta and VEGF families were three to fourfold lower in female elastase-perfused aortas compared to males. Multiple members of the interleukin, CC chemokine receptor, and CC ligand families were detectable in only the male elastase-perfused aortas. Female elastase-perfused aortas demonstrated a corollary twofold lower neutrophil count (females: 17.5 +/- 1.1 PMN/HPF; males: 41 +/- 5.2 neutrophils/HPF, P = 0.01) and a 1.5-fold lower macrophage count (females: 12 +/- 1.1 macrophages/HPF; males: 17.5 +/- 1.1 macrophages/HPF, P = 0.003) compared to male elastase-perfused aortas. This study documents decreased expression of multiple cytokines and chemokines and diminished leukocyte trafficking in female rat aortas compared to male aortas following elastase perfusion. These genes may contribute to the gender disparity seen in AAA formation.