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PubMed2006

Exposure to a specific pulsed low-frequency magnetic field: a double-blind placebo-controlled study of effects on pain ratings in rheumatoid arthritis and fibromyalgia patients.

BACKGROUND: Specific pulsed electromagnetic fields (PEMFs) have been shown to induce analgesia (antinociception) in snails, rodents and healthy human volunteers. OBJECTIVE: The effect of specific PEMF exposure on pain and anxiety ratings was investigated in two patient populations. DESIGN: A double-blind, randomized, placebo-controlled parallel design was used. METHOD: The present study investigated the effects of an acute 30 min magnetic field exposure (less than or equal to 400 microTpk; less than 3 kHz) on pain (McGill Pain Questionnaire [MPQ], visual analogue scale [VAS]) and anxiety (VAS) ratings in female rheumatoid arthritis (RA) (n=13; mean age 52 years) and fibromyalgia (FM) patients (n=18; mean age 51 years) who received either the PEMF or sham exposure treatment. RESULTS: A repeated measures analysis revealed a significant pre-post-testing by condition interaction for the MPQ Pain Rating Index total for the RA patients, F(1,11)=5.09, P<0.05, estimate of effect size = 0.32, power = 0.54. A significant pre-post-effect for the same variable was present for the FM patients, F(1,15)=16.2, P<0.01, estimate of effect size = 0.52, power =0.96. Similar findings were found for MPQ subcomponents and the VAS (pain). There was no significant reduction in VAS anxiety ratings pre- to post-exposure for either the RA or FM patients. CONCLUSION: These findings provide some initial support for the use of PEMF exposure in reducing pain in chronic pain populations and warrants continued investigation into the use of PEMF exposure for short-term pain relief.

Adult↗

PubMed2006

Genetic investigation of the TSPYL1 gene in sudden infant death syndrome.

BACKGROUND: Sudden infant death syndrome (SIDS) constitutes the most frequent cause of death in the postperinatal period in Germany. Recently, a lethal phenotype characterized by sudden infant death with dysgenesis of the testes syndrome (SIDDT) was identified to be caused by loss of function mutations in the TSPYL1 gene. PURPOSE: The study's purpose was to reveal a possible role of TSPYL1 in SIDS. METHODS: DNA samples of 126 SIDS cases and 261 controls were investigated. RESULTS: We found five sequence variations, each of them causing an amino acid substitution. No Hardy Weinberg disequilibrium and no significant difference in allele frequencies between patients and controls were observed for any variation. In one female patient a p.F366L amino acid polymorphism was found heterozygous, which could not be displayed in controls. A pathogenic implication of this substitution, which is conserved in primates and rodents, cannot be ruled out completely. Because SIDDT is the result of homozygous TSPYL1 mutations, this heterozygous exchange cannot solely explain the sudden death in this child. The reported mutation associated with SIDDT (457_458insG) was not detectable in our cohort. CONCLUSION: No association of sequence variations in the TSPYL1 gene and SIDS has been found in a German cohort. Genetic analysis of TSPYL1 seems to be of limited significance in the differential diagnosis of SIDS without dysgenesis of the testes.

Aged↗

PubMed2005

Recognition of familiar individuals in golden hamsters: a new method and functional neuroanatomy.

The ability to recognize individuals is essential for many aspects of social interaction and social organization, yet we know relatively little about the neural mechanisms underlying this ability. Most laboratory studies of individual recognition in rodents have studied differential responses to familiar versus unfamiliar individuals rather than differential responses to equally well known individuals having different significance for the subject. In experiment 1, we use a new method for studying true individual recognition in which male hamsters first had different experiences with two stimulus males (exposures to one male across a wire-mesh barrier and fights with another male). One day later, losers of fights were tested in a Y-maze for reactions to one of the two familiar males. Subjects tested with the familiar winner avoided this stimulus male, but subjects tested with the familiar, neutral male were attracted to him. Immunohistochemistry for c-Fos and Egr-1 implicate several areas of the brain in individual recognition, particularly the anterior piriform cortex, the CA1 and CA3 regions of anterior dorsal hippocampus, anterior and posterior dentate gyrus, and perirhinal cortex. In experiment 2, temporary inactivation of the CA1 region of anterior dorsal hippocampus by microinfusion of lidocaine eliminated the avoidance of the familiar winner, but a saline control injection had no effect. These results are the first to use a rodent model to characterize neural circuits involved in the recognition of equally well known individuals and the corresponding emotional responses to them.

Animals↗

PubMed1994

T-cell control of immunity to the asexual blood stages of the malaria parasite.

Both antibody-dependent and antibody-independent mechanisms are involved in immune protection against the asexual blood stages of the malaria parasite. It is well established that T cells play a crucial role in both induction and maintenance of this immunity. Of the two T-cell subsets (CD4+, CD8+) carrying alpha/beta T-cell receptors, the CD4+ T cells are of major importance for the development of blood stage immunity in both experimental and human malaria. In mice, CD4+ T cells comprise at least two functionally distinct cell types (TH1, TH2), distinguished on the basis of their lymphokine production. The balance between these subsets is critical for the outcome of an infection. In some rodent malarias, TH1 cells producing IFN-gamma and IL-2 are important for controlling infection in its early phases, while TH2 cells, producing i.a. IL-4 and IL-10, together with antibodies, are important for parasite clearance in later phases of infection. Distinct CD4+ T cells of either TH1 or TH2 type also have regulatory functions in human P. falciparum infection. In contrast to the CD4+ T cells, the role of CD8+ T cells in blood stage infection appears to be limited, but suppression of some CD4+ activities has been reported for both experimental and human malaria. As in other infections, peripheral T cells equipped with gamma/delta receptors are strongly upregulated in malaria and also respond to parasite antigens in vitro by proliferation and lymphokine production. However, the importance of the gamma/delta T cells for protection when compared with pathogenesis is presently unclear. Rapid advances made in recent years in the characterization and cloning of plasmodial antigens eliciting immune protection have made it possible to define some of the antigenic structures involved in T-cell immunity. This, together with an improved understanding of cellular mechanisms, provides some basis for the development of modern malaria vaccines.

Animals↗

PubMedDate not supplied

Analgesic nephropathy in rodents.

While it is clear that humans suffer from "classic" analgesic nephropathy, the causative agents and mechanisms are still not known. A review of the literature revealed that chronic acetaminophen exposure does not produce renal papillary necrosis in rodents or humans. In contrast, while chronic aspirin exposure to rodents results in renal papillary necrosis with renal morphological and functional changes similar to that described in humans, epidemiological studies do not implicate aspirin alone in human analgesic nephropathy. The difference in the effects of aspirin in humans and rats may be due to the inability of epidemiological studies to detect aspirin-induced analgesic nephropathy or more likely to the fact that species differences exist, with the rat being more sensitive than humans. With respect to combinations of aspirin and acetaminophen, with or without caffeine, there are minimal tightly controlled studies. In addition, there is little evidence of enhanced renal papillary necrosis in rodents treated with aspirin and acetaminophen combinations. In summary, it remains to be determined what chemical entities cause "classic" analgesic nephropathy in humans and the mechanisms of this toxicity such that preventative measures can be instituted. Elucidation of the mechanisms of analgesic nephropathy has been hampered due to the lack of animal models that closely mimic the human disease. Rodents do not appear to be an appropriate model.

Acetaminophen↗

PubMed1993

Prairie rattlesnakes (Crotalus viridis) respond to rodent blood with chemosensory searching.

In Experiment I, homogenized rodent tissue was applied to the lips of prairie rattlesnakes (Crotalus viridis). This treatment produced elevated rates of tongue flicking compared to controls that received water, but the elevations seen following stimulation with homogenate were not as large as those seen after snakes struck prey. In Experiment II, water, rodent blood, and integumentary cues were applied to the lips of rattlesnakes, and only blood resulted in elevated rates of tongue flicking. We conclude that blood is a critical component of the homogenate. It is hypothesized that detection of blood during predatory strikes may be a causal element in the triggering of strike-induced chemosensory searching, a typical component of rattlesnake predatory behavior.

Animals↗

PubMedDate not supplied

Regeneration of skeletal and cardiac muscle in mammals: do nonprimate models resemble human pathology?

Most of the available information regarding the regenerative potential and compensatory remodeling of mammalian tissues has been obtained from nonprimate animals, mainly rodent experimental models. The increasing use of transgenic mice for studies of the mechanisms controlling organogenesis and regeneration also requires a clear understanding of their applicability as experimental models for studies of similar processes in humans and other mammals. Application of modern cell biology methods to studies of regenerative processes has provided new insights into similarity and differences in cellular responses to injury in the tissues of different mammalian species. During more than 200-million years of progressive divergent evolution of mammals, cellular mechanisms of tissue regeneration and compensatory remodeling evolved together with increasingly adaptive functional specialization and structural complexity of mammalian tissues and organs. Rodents represent a phylogenetically ancient order of mammals that has conservatively retained a number of morphofunctional characteristics of early representatives of this class, which include enhanced regenerative capacity of tissues. A comparative analysis of regenerative processes in skeletal and cardiac muscle, as well as in several other mammalian tissues, shows that time courses and intensities of regeneration in response to the same type of injury vary even within taxonomically related species (e.g., rat, mouse, and hamster). The warm bloodedness of mammals facilitated the development of more complex mechanisms of metabolic, immune, and neurohumoral regulation, which resulted in a stronger dependence of regenerative processes on vascularization and innervation. For this reason, interspecies modifications of regenerative responses are limited by the capacity of the animal to resorb rapidly the foci of necrosis and to revascularize and reinnervate the volume of the regenerating tissue. These differences, among other factors, result in significantly lower rates of reparative regeneration in mammals possessing larger body sizes than rodents. A review of these data strongly indicates that the phylogenetic age and biological differences between different species should be taken into account before extrapolation of regenerative properties of nonprimate tissues on the regenerative responses in the primates.

Animals↗

PubMed1994

Acute toxic and teratogenic effects of cyclic imides in rodents.

Four structurally different cyclic imides or related derivatives (o-(N-phthalimido)acetophenone (1), 2,3-dihydrophthalazine-1,4-dione (2), N-(4-methylphenyl)diphenamide (3), and 4,6-dihydro-5H-dibenz[c,e]azepine (4) were examined for acute toxicity in mice at multiple doses, for long term toxicity at a single dose in rats, and for deleterious effects on fertility and pup development in rodents. No deleterious effects were observed when mice were administered agents at 20, 50, and 100 mg/kg/day for seven days. All other measured characteristics and values were normal for the four compounds. The principle effect of the compounds was to reduce the percent pregnancies in treated mice compared to the controls. Compound 2 afforded the greatest reduction of pregnancy (54%) at 100 mg/kg/day. Compounds 3 and 4 caused a minor reduction in pregnancy (12-20%). The compounds did not appear to cause measureable teratogenic effects; pups of treated rodents thrived and survived as well as controls. There were no effects on murine male fertility when compounds were administered at 20, 50, and 100 mg/kg/day for six weeks.

Animals↗

PubMed1993

Overexpression of mouse D-type cyclins accelerates G1 phase in rodent fibroblasts.

Mammalian D-type cyclins are growth factor-regulated, delayed early response genes that are presumed to control progression through the G1 phase of the cell cycle by governing the activity of cyclin-dependent kinases (cdks). Overexpression of mouse cyclin D1 in serum-stimulated mouse NIH-3T3 and rat-2 fibroblasts increased their rates of G0 to S- and G1- to S-phase transit by several hours, leading to an equivalent contraction of their mean cell generation times. Although such cells remained contact inhibited and anchorage dependent, they manifested a reduced serum requirement for growth and were smaller in size than their normal counterparts. Ectopic expression of cyclin D2 in rodent fibroblasts, either alone or together with exogenous cdk4, shortened their G0- to S-phase interval and reduced their serum dependency, but cyclin D2 alone did not alter cell size significantly. When cells were microinjected during the G1 interval with a monoclonal antibody specifically reactive to cyclin D1, parental rodent fibroblasts and derivatives overexpressing this cyclin were inhibited from entering S phase, but cells injected near the G1/S phase transition were refractory to antibody-induced growth suppression. Thus, cyclin D1, and most likely D2, are rate limiting for G1 progression.

3T3 Cells↗

PubMed1992

Alcohol consumption and the etiology of colorectal cancer: a review of the scientific evidence from 1957 to 1991.

The relationship between alcohol consumption and colorectal cancer in humans has been examined in 52 major studies in the past 35 years. An association was found in five of the seven correlational studies. An elevated risk was found in about half of the 31 case-control studies and, of these, in 9 of the 10 studies using community controls but in only 5 of the 17 studies using hospital controls (p = 0.008), suggesting that the absence of association when hospital controls are used is due to a high prevalence of alcohol consumption/alcohol-related illness in the hospital controls. Of the 14 cohort studies, an association with alcohol was found in 10, while in 3 of the 4 cohort studies in which an association was not found the alcohol data obtained were somewhat restricted. A positive dose-response effect was found in two of three cohort studies and in all four case-control studies with community controls in which this effect was examined. In both case-control and cohort studies, the association was found for females and males and for colon and rectal cancer. When the type of alcohol consumed was examined separately, beer was the principal type of at-risk alcoholic beverage, with much less risk for spirits and least risk for wine. Statistically significant elevations of risk were more often found in males than in females and slightly more frequently for rectal than for colon cancer and were related almost entirely to beer, rather than to wine or spirit, consumption. The alcohol risk was independent of the dietary risk in those studies that controlled for this factor. There was some confirmatory evidence for alcohol augmentation in rodent models of chemically induced carcinogenesis in six of nine studies. The hypotheses of alcohol as a direct and specific colorectal carcinogen include increased mucosal cell proliferation, the activation of intestinal procarcinogens, and the role of unabsorbed carcinogens, particularly in beer. Also, five of six other human studies showed an association between alcohol/beer consumption and adenomatous polyps, consistent with the hypothesis that alcohol stimulates the colorectal mucosa. General or indirect carcinogenic effects of alcohol include immunodepression, activation of liver procarcinogens, and changes in bile composition, as well as nitrosamine content of alcoholic beverages and increased tissue nitrosamine levels. With alcohol/beer consumption, the overall conclusion on present evidence is that alcohol, particularly beer consumption, is an etiologic factor for colon and rectal cancer for females and males.(ABSTRACT TRUNCATED AT 400 WORDS)

Alcohol Drinking↗

PubMed2000

Dopamine release and uptake dynamics within nonhuman primate striatum in vitro.

The putamen of the human striatum is a heterogeneous nucleus that contains the primary site of loss of dopamine (DA) in Parkinson's disease (PD). Furthermore, different functional domains of the putamen are heterogeneously susceptible to DA loss, and yet the dynamic regulation of extracellular DA concentration ([DA](o)) and comparison between domains has not been explored in the primate brain. In these studies, DA was measured in real time using fast-scan cyclic voltammetry at a carbon-fiber microelectrode in vitro in striatal sections from the common marmoset (Callithrix jacchus). [DA](o) released by a single stimulus pulse varied threefold along a ventromedial-dorsolateral axis. DA uptake was via the DA transporter (GBR12909 sensitive, desipramine insensitive). On the basis of data modeling with simulations of Michaelis-Menten kinetics, rate maximum, V(max), varied with region: both [DA](o) and V(max) were greatest in regions most vulnerable in PD. These differences were reflected in part by regional variation in DA content. [DA](o), V(max), and regional variation were two- to threefold greater than in rodent caudatoputamen. In addition, steady-state [DA](o) at physiological firing rates in primate striatum was controlled by depolarization frequency, uptake, and presynaptic autoreceptors. Furthermore, regulation of [DA](o) by these mechanisms differed significantly between limbic- and motor-associated domains. These data indicate interspecies heterogeneity in striatal DA dynamics that must be considered when extrapolating behavioral and drug responses from rodent to the primate brain. Moreover, the heterogeneity demonstrated within the primate putamen in the availability and dynamic regulation of DA may be central to understanding DA function in health, cocaine abuse, and disease.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1995

Reduction by lifarizine of the neuronal damage induced by cerebral ischaemia in rodents.

1. The objective of this study was to evaluate the broad neurocytoprotective potential of the novel sodium-calcium ion channel modulator, lifarizine (RS-87476), in two rodent 72 h survival models of forebrain ischaemia. 2. Under fluothane anaesthesia, rats were subjected to 10 min four vessel occlusion and gerbils to either (i) 5 or (ii) 10 min bilateral carotid artery occlusion. 3. Rats were dosed parenterally solely post-ischaemia (reperfusion) in a series of five studies covering a range of intra-arterial/intraperitoneal (i.a./i.p.) combination doses from 2/10, 5/20, 20/100, 50/200 and 100/500 micrograms kg-1, where the initial loading dose was injected i.a. at 5 min. An i.p. dose was given at 15 min and repeated twice daily. In a sixth study, treatment at 50/200 micrograms kg-1 was deferred for 1 h. 4. Gerbils were treated (i) 15 min pre-ischaemia with either (a) 250, (b) 500 micrograms kg-1 i.p., or (c) 5 mg kg-1 by gavage (p.o.) for 3 days then at 1 h pre-ischaemia. Animals treated as (ii) received 500 micrograms kg-1 i.p. 15 min pre-ischaemia. The above doses were repeated twice daily for 3 days post-ischaemia for the respective groups. 5. In rats, the protective effect of lifarizine was regionally and cumulatively assessed in six brain regions (anterior and posterior neocortex, hippocampal CA1 subfield, thalamus, striatum, cerebellar Purkinje cells-brain stem) at each dose level. Cumulative (total) means +/-s.e.mean neurohistopathological scores(0-4) of 1.16+/-0.09 (n=5), 1.02+/-0.10 (n=5), 0.93+/-0.06 (n=6), 0.79+/-0.09 (n=9) and 0.45+/-0.16(n = 7), respectively, were obtained for the above treatment groups compared to the control (2.01 +/- 0.17,n = 16) group (P<0.0035). The score for the 1 h deferred treatment group was also significant at 0.77 +/- 0.10, n =5 (P< 0.0035). The normal group without ischaemia showed a score of 0.52 +/- 0.09 (n = 6).6. In gerbils, (i) percentage delayed neuronal death (DND) of hippocampal pyramidal cells in the CA1subfield was prevented at 250 (a) and 500 microg kg-' i.p. (b) (27.2+/- 14.6, n=6 and 26.9+/- 10.4%, n= 10 respectively, P<0.02) compared to controls (78.3+/-8.5%, n= 12) and by 5 mg kg-1 p.o. (c) (2.9+/-0.8%,n =l1, P <0.002). Mean +/- s.e.mean total brain scores (0-4) for each of 4 different features denoting cerebral 'oedema' were lower for normal brains (1.60 +/-0.34, n =6) and reduced in animals dosed at 250(a) (3.00+/-0.79, n=6) and 500 microg kg-1 i.p. (b) (3.75 0.36, n= 10) compared to controls (6.58+/-1.00,n = 12) (P< 0.02 -0.03). There was a linear relationship (r = 0.97) between the 'oedema' scores and percentage CA1 DND. Percentage CA1 DND in response to 10 min ischaemia (ii) was reduced(53.0+/-21.0%, n=6, P<0.05) compared to controls (100.0+/-0.0%, n=7).7 The significant neuroprotection shown by lifarizine in rodents substantiates findings in other species.These observations, together with its effect on ion channels and efficacy at extremely low doses offers novelty and suggests a broad spectrum of activity in ischaemia.

Animals↗

PubMed1997

Localization of dopamine receptors and associated mRNA in transplants of human fetal striatal tissue in rodents with experimental Huntington's disease.

Huntington's Disease (HD) is characterized by deficits in motor and cognitive functions. This neurodegenerative disease shows an extensive loss of medium-sized spiny projection neurons (GABAergic) within the neostriatum. With the loss of these neurons, there is a concomitant loss of associated receptors, such as those for GABA, glutamate, and dopamine. In the present study, we have addressed the question of whether dopamine receptors are re-established in the lesioned rodent striatum following the transplantation of human striatal cells. Human striatal cell suspension or saline (transplant controls) was injected into the striatum of rats previously lesioned with quinolinic acid (QA). Three nine months following transplantation, the animals were sacrificed and the brains were processed for receptor autoradiography and in situ hybridization of dopamine D1 and D2 receptor subtypes. Our results demonstrate that animals transplanted with human striatal cells show a significant increase in D1 receptors following transplantation when compared to the lesion area in control animals, while D1 receptor mRNA remains unchanged. In contrast to D1 receptor binding, D2 receptor levels are not increased in the lesioned and transplanted area of the striatum when compared to controls; however, D2 receptor mRNA levels are significantly increased. These results demonstrate that at the times the animals were examined, D1 and D2 receptors were differentially regulated. Our results further indicate that human striatal primordium will survive following transplantation and will express D1 receptors and D2 receptor mRNA that are depleted in the QA lesioned rodent striatum. This study compliments and extends previous findings on human striatal cell transplantation in rodent models of HD.

Animals↗

PubMed1991

Comparative effects of hypoxia on behavioral thermoregulation in rats, hamsters, and mice.

Recent studies using reptiles and other ectothermic species have shown that hypoxia lowers the set point for the control of body temperature. This is characterized by a preference for cooler ambient (Ta) and deep body temperatures (Tb) when placed in a temperature gradient. To elucidate the presence of this effect in mammals, the selected Ta and Tb of three rodent species (mouse, hamster, and rat) were measured while subjected to graded hypoxia in a temperature gradient. Individual animals were placed in the gradient for 30 min. Oxygen content of air entering the gradient was then reduced to a constant level for a period of 60 min by dilution with nitrogen. Tb was significantly reduced in all species at %O2 levels of 5.5-10%. Selected Ta was significantly reduced in the mouse at %O2 levels of 5.5 and 7.3%. Selected Ta of the hamster and rat were reduced slightly at %O2 levels of 5.8 and 7.4%, respectively; however, the effect was not statistically significant. To clarify the effects of hypoxia in these two species, the sample size of rat and hamster was increased to strengthen statistical analysis, and the animals were exposed for 60 min to %O2 levels of 7.4 and 6.7%, respectively. Both species exhibited a significant reduction in selected Ta during hypoxia concomitant with hypothermia. These data support the hypothesis that hypoxia lowers the set point for the control of body temperature in rodents.

Animals↗

PubMedDate not supplied

[Morphophysiologic status of the rodent thyroid gland in the case of alimentary obesity].

The studies were carried out on rodents with different ecology, suffering from alimentary obesity. Their weight was 1.3-1.5 that of control animals. Prolonged (3 months) maintaining of the animals in conditions of obesity led to sharp decrease in inclusion of 131I into thyroid parenchyma, synthesis and excretion of SB 131I into blood. Microscopy study of thyroid gland revealed an inhibition of hormone synthesis, as indicated by flattened epithelium, dense colloid in follicles, and other hypofunctional features. Obesity decreases the quantity of food consumed by the animals and their reproductive abilities. Comparison of data obtained on rodents with different ecology revealed that maximal inhibition of thyroid function at obesity was observed in yellow gopher as compared to rat and gerbil.

Animals↗

PubMed2005

Wild fauna as a probable animal reservoir for Trypanosoma brucei gambiense in Cameroon.

In order to study the existence of a wild animal reservoir for Trypanosoma brucei gambiense in South Cameroon, blood was collected from wild animals in three human African trypanosomiasis foci and from a nonendemic control area. The 1142 wild animals sampled belonged to 36 different species pertaining to eight orders (407 primates, 347 artiodactyls, 265 rodents, 54 pangolins, 53 carnivores, 11 saurians and crocodilians, and five hyraxes). QBC and KIVI tests detected trypanosomes on 1.7% (13/762) and 18.4% (43/234) of animals examined, respectively. Using specific primers, T. brucei non-gambiense group 1 DNA was detected on 56 animals (4.9%). This infection rate was 5.3% in the endemic zone and 3.8% in the control zone. Of the 832 animals of the endemic zone, PCR revealed T. b. gambiense group 1 DNA in 18 (2.2%). These hosts included two rodents, two artiodactyls, two carnivores and two primates. T. b. gambiense group 1 was absent from animals from the nonendemic zone. A decrease in the prevalence of T. b. gambiense group 1 was observed in wild animals from the Bipindi sleeping sickness focus after a medical survey and vector control in this area. The epidemiological implications of these findings remain to be determined with further investigations.

Animals↗

PubMed1989

Dissociation of hypothalamic effects on ultrasound production and copulation.

Two studies were conducted to compare the brain mechanisms for copulation with those controlling other sexual behaviors, such as the ultrasonic calls that help hamsters and other rodents attract potential mates. Specifically, male and female golden hamsters were castrated and hormone-primed prior to being observed for rates of ultrasound production and levels of sex-typical copulatory behavior (mounts, intromissions and ejaculations in males; lordosis in females). Such tests were conducted before and after subjects received sham operations or bilateral lesions of the preoptic area (POA), anterior hypothalamus (AH) or ventromedial hypothalamus (VMN). The results confirmed previous work in showing the POA lesions decrease rates of intromission, ejaculation and ultrasound production, while VMH lesions decrease lordosis duration. More surprising was the tendency of VMN lesions to increase rates of ultrasonic calling by both males and females. For males, these effects identify differences between the neural circuits controlling copulatory and noncopulatory sexual behaviors. For females, they suggest a mechanism for the behavioral incompatibility of ultrasound production and lordosis. In particular, they raise the possibility that the suspension of ultrasonic calling that normally accompanies lordosis reflects an increase in VMN activity that simultaneously provokes lordosis and inhibits vocalization.

Animals↗

PubMed2003

Interruption of the blood-stage cycle of the malaria parasite, Plasmodium chabaudi, by protein tyrosine kinase inhibitors.

Malaria is a devastating disease caused by a unicellular protozoan, Plasmodium, which affects 3.7 million people every year. Resistance of the parasite to classical treatments such as chloroquine requires the development of new drugs. To gain insight into the mechanisms that control Plasmodium cell cycle, we have examined the effects of kinase inhibitors on the blood-stage cycle of the rodent malaria parasite, Plasmodium chabaudi. In vitro incubation of red blood cells for 17 h at 37 degrees C with the inhibitors led to a decrease in the percent of infected cells, compared to control treatment, as follows: genistein (200 microM - 75%), staurosporine (1 microM - 58%), R03 (1 microM - 75%), and tyrphostins B44 (100 microM - 66%) and B46 (100 microM - 68%). All these treatments were shown to retard or prevent maturation of the intraerythrocytic parasites. The diverse concentration ranges at which these inhibitors exert their effects give a clue as to the types of signals that initiate the transitions between the different developmental stages of the parasite. The present data support our hypothesis that the maturation of the intraerythrocytic cycle of malaria parasites requires phosphorylation. In this respect, we have recently reported a high Ca2+ microenvironment surrounding the parasite within red blood cells. Several kinase activities are modulated by Ca2+. The molecular identification of the targets of these kinases could provide new strategies against malaria.

Animals↗