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D Malo

Publications and source records attributed to D Malo.

66 records · Page 4Linked to original sources
PubMed1990

Decrease of blood pressure in spontaneously hypertensive mice by heat treatment.

Although the increased sensitivity of hypertensive animals to heat stress has been reported, the effect of chronic heat exposure has not been examined. The specific goal of the present investigation was to study the impact of chronic heat treatment on the blood pressure of spontaneously hypertensive mice. Chronic 40 degrees C heat exposure for 5 min daily progressively lowered basal blood pressure in hypertensive mice within 20 days, without any change in normal mice. In fact, after 35 days of chronic heat treatment, the basal blood pressure of hypertensive mice was indistinguishable from that of the normotensives. Repeated immobilization and prewarming as normal procedures for recording blood pressure contributed to the decrease in blood pressure by 10 to 12 mm Hg, but chronic heat by itself was significantly more potent in reducing it by an additional 20 mm Hg. After the discontinuation of chronic heat application, the basal blood pressure of hypertensive mice returned with time to the level registered in sham-handled hypertensive controls. These results demonstrate that, although acute heat is more detrimental to hypertensive mice, brief, chronic exposure to mild heat stress is beneficial in that it normalizes basal blood pressure.

Animals↗
PubMed1990

Immunogenetics of mycobacterial infections: mouse-human homologies.

In the mouse, innate resistance or susceptibility to infection with numerous mycobacteria is controlled by the Bcg host resistance locus located on the centromeric region of chromosome 1. The resistance/susceptibility phenotype is expressed by the mature tissue macrophage and Bcg has been identified as a locus that is involved in the regulation of macrophage activation and in the modulation of acquired immune responses to mycobacteria. Experiments aimed at the cloning of the Bcg gene via a "reverse genetics" approach have generated a detailed genetic map in the immediate vicinity of the locus, placing Bcg within the reach of long-range eukaryotic cloning techniques. The chromosomal segment around Bcg in the mouse is exactly conserved onto the long arm (q) of human chromosome 2. Linkage of genetic markers from human chromosome 2q with susceptibility to leprosy or tuberculosis would support both the existence of a susceptibility gene in humans and the contention that this susceptibility gene is a homologue of the mouse Bcg locus.

Animals↗
PubMed1990

Increased transcription of a major stress gene in spontaneously hypertensive mice.

Environmental stress factors, including temperature, modify the severity of hypertension, a genetic disease. Hypertensive animals and humans respond abnormally to heat exposure, and this abnormality is reflected at the cellular level by an increment in a major stress (heat-shock) gene expression. The present studies demonstrate that increased hsp70 gene expression is due to its heightened transcription rate. The genetic basis of environmental susceptibility to hypertension may thus involve an abnormal control of heat shock genes.

Amanitins↗
PubMed1990

Heat stress genes in hypertension.

Genetically hypertensive animals such as spontaneously hypertensive rats (SHR) and mice are more sensitive to thermal stress than normotensive controls. Genetic breeding experiments have demonstrated that the gene responsible for thermosensitivity segregates with an increase in blood pressure in the F2 generation and represents a genetic locus of hypertension. Due to a higher transcription rate of the heat shock protein 70 (hsp70) gene, which is a major heat stress gene, the accumulation of hsp messenger (m)RNA is increased in hypertension. Higher thermosensitivity and increased hsp mRNA accumulation are also observed in neonatal cardiomyocytes and cultured vascular smooth muscle cells from SHR, suggesting that these abnormalities are primary in character. This higher hsp70 transcription rate in hypertension could be due to an abnormality in the promoter region, to an interaction between heat stress trans-acting factor and heat stress element within the promoter of hsp70 or to an abnormal activation of heat stress trans-acting factor. A study using recombinant inbred animals has indicated that RT1 complex gene(s), a major histocompatibility complex in the rat, may be involved in the development of hypertension. These findings, together with the fact that hsp70 is located in the major histocompatibility complex, suggest that hsp70 gene or associated genes within the RT1 complex are responsible for environmental control of the expression of hypertension.

Animals↗
PubMed1989

Thermosensitivity, a possible new locus involved in genetic hypertension.

Spontaneously hypertensive mice have been characterized as more sensitive to environmental heat than normotensive mice. A breeding program was therefore initiated to examine the possible genetic link between thermosensitivity and hypertension. Crossbreeding of spontaneously hypertensive mice with randomly bred normotensive mice produced F1 hybrids, which were then intercrossed to create a F2 population. Thermosensitivity was measured with a noninvasive method. The rate of body temperature increase was significantly (p less than 0.001) higher in the hypertensive mice (1.74 +/- 0.04 degrees C/min) compared with normal controls (1.13 +/- 0.03 degrees C/min). The frequency distribution of the rate of body temperature increase among the progenies was consistent with the hypothesis that a single gene locus determines the observed difference in thermosensitivity between normal and hypertensive mice. The allele that determines the rate of body temperature increase in normal mice was dominant in relation to the allele contributed by hypertensive mice. In the F2 population, a bimodal distribution determined two phenotypes: less than 1.40 degrees C/min and greater than 1.40 degrees C/min. A significant difference (p less than 0.01) in blood pressure of 11 mm Hg was observed between these two phenotypes. In addition, a positive correlation (p less than 0.01) was noted between the rate of body temperature increase and blood pressure in the F2 progeny. We conclude that there is possibly a single locus controlling thermosensitivity, which exhibits additive-dominance inheritance. Alleles of this particular trait segregate in part with an increment in blood pressure. The results support the possibility that the increased thermosensitivity seen in hypertensive mice is associated with one of the genes that contributes to their high blood pressure.

Animals↗
PubMed1988

Genetic and molecular characteristics of thermosensitivity in hypertension.

Acute heat exposure is more lethal to spontaneously hypertensive mice (SHM) than to normal mice, whereas chronic heat treatment appears to be more beneficial in SHM, in that it normalizes blood pressure. By genetic breeding experiments, we demonstrated that the gene responsible for thermosensitivity segregates with an increment of blood pressure in the F2-generation and represents a genetic locus of hypertension. The molecular response to heat characterized by the induction of heat stress genes is abnormal in hypertension. There is an earlier accumulation and decline of heat-stress proteins (HSP70) and their messenger (m) RNA following heat exposure in tissues obtained from hypertensive mice. Our results indicate that thermosensitivity is genetically linked with hypertension and characterized by an abnormality in the synthesis of stress proteins as well as in the expression of their mRNA following heat exposure, which implies that a genetic defect is present in response to environmental stress in spontaneous hypertension.

Animals↗
PubMed1986

Effects of bolus injection of epinephrine and norepinephrine on systolic time intervals in stress-resistant and stress-susceptible pigs.

Systolic time intervals were measured in 15 stress-susceptible (SS) pigs to derive regression equations to determine to what extent their ventricular functions differed from those of stress-resistant (SR) pigs. Regression analysis revealed that the RR interval was the variable that was significantly (P less than 0.01) related to electromechanical systole and left ventricular ejection time. The preejection period (PEP) was independent of the RR interval. A normal increase of all systolic time intervals with age, independent of the RR interval, was also observed in SR and SS pigs. The 55-kg SS pigs had a higher noradrenergic tone than did 15-kg and 90-kg SS pigs, because their mean arterial blood pressure was higher and because their index values for electromechanical systole and their PEP were shorter than those of SR pigs of the same body weights. The cardiovascular responses to biogenic amines were also different according to the degree of development and stress susceptibility. Changes in mean arterial pressure and PEP were not as pronounced after injections of epinephrine and norepinephrine (10(-8) mol/kg of body weight) were given. Subsequently, a decrease in cardiovascular responses to epinephrine and norepinephrine injections in 90-kg SS pigs were recorded. These results indicate that 55-kg SS pigs have a higher level of circulating catecholamines and that the myocardium becomes less sensitive to epinephrine and norepinephrine after it is chronically exposed to these amines.

Animals↗
PubMed1985

Management of acute flexor tendon injury in the hand.

In this report, we have attempted to review the current state of the art with regard to the treatment of partial flexor tendon injuries, the strength of the flexor tendons and its relationship to complete tendon lacerations, and the importance of passive joint motion to improve tendon excursion. At this time, it appears that most partial flexor tendon injuries are best treated by nonsurgical repair and an early active assisted or passive range-of-motion exercise program for a period of 3 to 4 weeks. Protecting the hand up to a total of 10 to 12 weeks seems reasonable based on studies of tendon strength. Surgical intervention is necessary to prevent complications of triggering, entrapment, or rupture, which generally occur with lacerations of greater than 60%. We would reserve the repair of partial flexor tendon injuries to lacerations where tendon rupture, triggering, or entrapment would be expected. After flexor tendon repair, knowledge of the strength of tendons and the need for passive mobilization are important. There is not sufficient strength within the flexor tendon repair site to allow for active mobilization sooner than 17 days. Probably only with a lateral trap stitch similar to that described by Becker or with extremely well supervised and trusted patients can active motion be started this early. There is insufficient intrinsic tendon strength to consider active motion (without assistance) earlier than 3 1/2 to 4 weeks. Passive range of motion using the Kleinert-Atasoy or Durand technique before this period is important in not only increasing tendon gliding (or excursion) but also being a stimulus to improve flexor tendon healing strength.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Comparative genomics and host resistance against infectious diseases.

The large size and complexity of the human genome have limited the identification and functional characterization of components of the innate immune system that play a critical role in front-line defense against invading microorganisms. However, advances in genome analysis (including the development of comprehensive sets of informative genetic markers, improved physical mapping methods, and novel techniques for transcript identification) have reduced the obstacles to discovery of novel host resistance genes. Study of the genomic organization and content of widely divergent vertebrate species has shown a remarkable degree of evolutionary conservation and enables meaningful cross-species comparison and analysis of newly discovered genes. Application of comparative genomics to host resistance will rapidly expand our understanding of human immune defense by facilitating the translation of knowledge acquired through the study of model organisms. We review the rationale and resources for comparative genomic analysis and describe three examples of host resistance genes successfully identified by this approach.

Agammaglobulinemia↗
PubMedDate not supplied

[The McGill model and local community service centers. A fetching combination].

How can the use of a specific conceptual model help nurses provide care that is best suited to their clients' real needs? The McGill model, for example, seems to be appropriate to community health applications, for it concentrates on health promotion and brings together all the elements underlying a family-development view of care. The authors of this article describe the basics of the McGill model, in terms of the four concepts of the nursing metaparadigm (health, the person, the environment and nursing (and discuss a concrete example of a health situation.

Canada↗