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At least 199 records · Page 11Linked to original sources
PubMed1996

Emerging & re-emerging bacterial pathogens in India.

In spite of major successes against infectious diseases in the 20th century, new infectious diseases have emerged and old ones re-emerged in recent decades in different parts of the world. A brief survey of emerging and re-emerging bacterial diseases of public health importance in India is presented in this paper. Plague re-appeared in two outbreaks in Maharashtra and Gujarat in 1994, indicating a breakdown of the public health measures that had prevented its occurrence for several decades. Leptospirosis appears to be on the increase in Kerala, Tamilnadu and the Andamans during the last 2 decades, probably due to increased farming and inadequate rodent control. It is suggested that melioidosis due to the soil organism Burkholderia pseudomallei may be prevalent in many parts of India, but is under-diagnosed and under-reported. Since 1991, a completely new choleragenic Vibrio cholerae, designated 0139 has emerged in southern India and spread to other parts of India and to neighbouring countries, setting in motion the 8th cholera pandemic. Animal anthrax is very common in many parts of India, but human anthrax is recognised in only certain limited locations. In the Chittoor and North Arcot districts, its prevalence had increased in recent years. Since 1990, a multi-drug resistant variety of typhoid fever had been prevalent in many parts of India, caused by Salmonella typhi resistant to chloramphenicol, ampicillin and trimethoprim-sulphamethoxazole. Nosocomial methicillin-resistant Staphylococcus aureus infection seems to be widely prevalent in hospitals in many regions in India, and its prevalence seems to be on the rise. These pathogens pose new threats to public health, and call for appropriate responses. Microbiological expertise and epidemiological surveillance are deficient in the health care and public health systems in India; therefore even infections and diseases that have been under control elsewhere remain prevalent in the country, but are also under-diagnosed and under-reported. Without improving microbiological expertise and application as well as epidemiological skills and practices, emerging and re-emerging diseases may not be recognised, identified or intercepted in their early stages.

Animals↗
PubMed1998

[Epidemiology and epizootiology of plague: the major role of the surveillance of reservoir populations of wild rodents in the control of permanent foci].

Plague is a bacterial infection, due to Yersinia pestis. It is essentially a zoonosis of rodents, communicable from rodent to rodent and from rodent to man by flea bite. From the first human case, acquired from rodents, interhuman transmission occurs by means of flea bite (bubonic plague) or is airborne (primary pulmonary plague). Long term implantation of plague amongst wild rodents populations after the third pandemic (1894 to present), created inveterate foci in all continents, except Europe. Those wild rodents settlements in arid biotopes, preserved from human activities, represent the main reservoir of plague. Their determination is mandatory for the surveillance of epizootics and the prevention of epidemics.

Animals↗
PubMedDate not supplied

Perturbation of rodent hepatocyte growth control by nongenotoxic hepatocarcinogens: mechanisms and lack of relevance for human health (review).

During the development of new industrial and pharmaceutical chemicals, it is necessary to determine whether they are potential carcinogens. However, there are no short-term tests available for nongenotoxic carcinogens that do not damage DNA yet cause tumours in rodent bioassays. The peroxisome proliferators (PPs) constitute a diverse class of nongenotoxic carcinogens that include chemicals of therapeutic, industrial and environmental importance such as hypolipidaemic fibrate drugs, clingwrap/medical tubing plasticizers and certain pesticides and solvents. PPs induce DNA synthesis and suppress apoptosis in rat and mouse hepatocytes, leading to tumour formation. In addition to altering hepatocyte growth and survival, PPs cause peroxisome proliferation and the induction of enzymes of the beta-oxidation pathway. PPs mediate their biological responses in rodents via activation of the nuclear hormone receptor PPARalpha (peroxisome proliferator activated receptor alpha) which regulates expression of the genes associated with response to PPs. The mechanisms through which normally quiescent hepatocytes are recruited into the cell cycle currently remain obscure. However, it is probable that expression of hepatic cytokines by hepatic macrophages (Kupffer cells) may be involved. In common with other classes of nongenotoxic carcinogen, there are remarkable species differences in response to PPs; humans respond to the fibrate hypolipidaemic PPs via a reduction in serum cholesterol but appear refractory to the adverse effects of PPs such as hepatic peroxisome proliferation, DNA synthesis and tumour formation. The molecular basis of the observed species differences in response to PPs is unclear at present, but recent data support a quantitative hypothesis wherein PPARalpha expression levels are sufficient in humans to mediate hypolipidaemia, but too low for transcriptional regulation of the full battery of genes associated with the adverse effects seen in rodents such as peroxisome proliferation, liver enlargement and tumours. A more detailed understanding of the mechanisms through which these chemicals cause tumours in rodents and how humans may differ will assist in extrapolation of rodent data to human risk assessment.

Animals↗
PubMed1993

FRAR course on laboratory approaches to aging. Genetic quality control in laboratory rodents.

Laboratory rodents are widely used in gerontological research. Many different strains are available, and superficially there is little to distinguish them (many are albino), although they may differ markedly in life span and pattern of spontaneous disease, as well as for a whole range of biochemical, immunological, behavioural and physiological characteristics. As experience has shown that strains can easily become muddled, some form of genetic quality control is essential. There is no single method of genetic quality control which can be recommended for all occasions. Methods based on identification of Mendelian genetic markers, such as biochemical and immunological polymorphisms can be sensitive, but may be expensive and require considerable expertise. Methods based on simultaneous study of several markers, such as skin grafting and polyvalent strain-specific antisera, may be cheaper but less flexible. DNA fingerprinting and the use of microsatellite markers appear to be the methods of choice in the future, though these are still expensive and require considerable expertise.

Animals↗
PubMed1993

FRAR course on laboratory approaches to aging. Microbiological effects and quality control in laboratory rodents.

Numerous viruses, mycoplasmas, bacteria and parasites have been associated with infectious diseases in laboratory animals. It is clear that pathogenic agents causing overt disease represent a serious hazard to research results in both short- as well as long-term studies. However, these organisms may contaminate colonies without causing any clinical or pathological symptom. This makes research less reliable because of the more subtle effects of the silent infections, especially in long-term studies as in aging research. The establishment of animal colonies that were free from these (micro-) organisms has increased substantially the value of animals used in biomedical research. Characterization of the health status and microbiological monitoring of the animals in experiments are particularly important. This paper reviews many of the major considerations in the efforts to maintain animals free of unwanted organisms, including quality and sources of animals, transportation and quarantine, maintenance during experimentation, microbiological characterization and monitoring of animals and environment.

Animal Husbandry↗
PubMed1991

The effect of unsaturated and saturated dietary lipids on the pattern of daily torpor and the fatty acid composition of tissues and membranes of the deer mouse Peromyscus maniculatus.

Dietary lipids strongly influence the pattern of torpor and the body lipid composition of mammalian hibernators. The object of the present study was to investigate whether these diet-induced physiological and biochemical changes also occur in species that show shallow, daily torpor. Deer mice, Peromyscus maniculatus, were fed with rodent chow (control diet) or rodent chow with either 10% sunflower seed oil (unsaturated diet) or 10% sheep fat (saturated diet). Animals on the unsaturated diet showed a greater occurrence of torpor (80-100% vs 26-43%), longer torpor bouts (4.5 vs 2.25 h), a lower metabolic rate during torpor (0.96 vs 2.25 ml O2.g-1.h-1), and a smaller loss of body mass during withdrawal of food (2.35 vs 3.90 g) than animals on the saturated diet; controls were intermediate. These diet-induced physiological changes were associated with significant alterations in the fatty acid composition of depot fat, leg muscle and brain total lipids, and heart mitochondrial phospholipids. Significant differences in the total unsaturated fatty acid (UFA) content between animals on saturated and unsaturated diet were observed in depot fat (55.7% vs 81.1%) and leg muscle (56.4% vs 72.1%). Major compositional differences between diet groups also occurred in the concentration of n6 and/or n3 fatty acids of brain and heart mitochondria. The study suggests that dietary lipids may play an important role in the seasonal adjustment of physiology in heterothermic mammals.

Adipose Tissue↗
PubMed1996

Monitoring weight drop velocity and foam stiffness as an aid to quality control of a rodent model of impact acceleration neurotrauma.

Since the publication by Marmarou of a new rodent model of head injury, an increasing number of centres are adopting the model for use in a variety of paradigms. We report on two simple methods we have applied which allows us to monitor weight drop velocity and foam stiffness, both of which are critical factors for producing repeatable closed head injury with this model. We hope the application of these methods will assist in the standardisation of this model between centres.

Animals↗
PubMed1992

Ecoepidemiology of leishmaniases in Syria. 3. Leishmania major infection in Psammomys obesus provides clues to life history of the rodent and possible control measures.

Collections of Psammomys obesus from near Damascus, Syria in May 1990 and November 1991 contained animals of all ages. Both series had a high prevalence of Leishmania major infection. Lesions were small in November and large in May. Assuming the two collections were representative of typical years, it is inferred that the breeding season is between October and May: there is high winter mortality of animals born early in the breeding season, but high survival of their parents, and there is high mortality in summer of animals aged between 17 and around 20 months. Transmission in summer is, therefore, between old adults shortly before their death and young adults born in late winter or spring. Juvenile animals are not exposed to the infection. If these findings are confirmed it should be relatively easy to break this tenuous cycle.

Animals↗
PubMed1999

A new methodology for controlled particle inhalation by small rodents.

In order to investigate the deposition, retention, and clearance mechanisms implicated in particle inhalation under standardized conditions, we developed a continuous negative-pressure ventilation system, whereby the breathing pattern in small rodents could be controlled during exposure to aerosols. Using an on-line open-flow set-up, 19 anesthetized, intubated, and paralyzed Syrian golden hamsters, individually contained within a whole-body box, were artificially ventilated under the said continuous negative-pressure conditions, 1 of 5 different combinations of breathing frequency and tidal volume being established. The animals were then exposed to aerosols containing 6-micron diameter polystyrene spheres, and the deposition of particles in the conducting airways was monitored photometrically. During exposure, the level of respiration (mean lung inflation) was stabilized by means of a negative-pressure vent. Breathing frequency and tidal volume, as well as the compliance of the system, remained virtually unchanged during the course of a single experiment, and in each case, a reproducible deposition of particles was achieved. Our findings indicate that tidal volume, but not breathing frequency, has a marked influence on the particle deposition ratio. Breathing frequency exerts opposing and counterbalancing effects on this latter parameter by enhancing the impaction of particles on the one hand, and by decreasing sedimentation on the other.

Administration, Inhalation↗
PubMed2007

Hypertonic saline solution increases the expression of heat shock protein 70 and improves lung inflammation early after reperfusion in a rodent model of controlled hemorrhage.

Hypertonic saline solution (HS solution, NaCl 7.5%) has shown to restore hemodynamic parameters in hemorrhagic shock and to decrease the inflammation triggered by ischemia-reperfusion injury (I-R). Therefore, our objective was to investigate the effects of HS solution on the mechanisms involved in I-R, in an experimental model of controlled hemorrhagic shock. Wistar rats (280-350 g) were submitted to controlled bleeding, keeping the mean arterial pressure around 40 mmHg, for 1 h. After that, rats were randomized and treated with HS solution (4 mL/kg) or normal saline (34 mL/kg). There were no differences in hemodynamic parameters between both groups for at least 2 h after shock. No difference either was observed in reactive oxygen species generation (measured indirectly by malondialdehyde concentration) or cytokines (interleukins 6 and 10) production (measured by enzyme-linked immunosorbent assay). Quantitative analysis of lung tissue showed a smaller neutrophil infiltration in animals that received HS solution. Moreover, the animals in the HS group showed an increased expression of heat shock protein 70. Therefore, we concluded that treatment of hemorrhagic shock with HS solution can decrease pulmonary inflammation and increase cellular protection by up-regulating heat shock protein 70 expression.

Animals↗
PubMed2004

Endothelin-1 regulates cardiac sympathetic innervation in the rodent heart by controlling nerve growth factor expression.

The cardiac sympathetic nerve plays an important role in regulating cardiac function, and nerve growth factor (NGF) contributes to its development and maintenance. However, little is known about the molecular mechanisms that regulate NGF expression and sympathetic innervation of the heart. In an effort to identify regulators of NGF in cardiomyocytes, we found that endothelin-1 specifically upregulated NGF expression in primary cultured cardiomyocytes. Endothelin-1-induced NGF augmentation was mediated by the endothelin-A receptor, Gibetagamma, PKC, the Src family, EGFR, extracellular signal-regulated kinase, p38MAPK, activator protein-1, and the CCAAT/enhancer-binding protein delta element. Either conditioned medium or coculture with endothelin-1-stimulated cardiomyocytes caused NGF-mediated PC12 cell differentiation. NGF expression, cardiac sympathetic innervation, and norepinephrine concentration were specifically reduced in endothelin-1-deficient mouse hearts, but not in angiotensinogen-deficient mice. In endothelin-1-deficient mice the sympathetic stellate ganglia exhibited excess apoptosis and displayed loss of neurons at the late embryonic stage. Furthermore, cardiac-specific overexpression of NGF in endothelin-1-deficient mice overcame the reduced sympathetic innervation and loss of stellate ganglia neurons. These findings indicate that endothelin-1 regulates NGF expression in cardiomyocytes and plays a critical role in sympathetic innervation of the heart.

Animals↗