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Biomedical subjects

L Holcomb

Publications and source records attributed to L Holcomb.

9 recordsLinked to original sources
PubMed2001

Fundamentalism, multiculturalism and problems of conducting research with populations in developing nations.

A growing number of nurse researchers travel globally to conduct research in poor and underserved populations in developing nations. These researchers, while well versed in research ethics, often find it difficult to apply traditional ethical standards to populations in developing countries. The problem of applying ethical standards across cultures is explained by a long-standing debate about the nature of ethical principles. Fundamentalism is the philosophical stance that ethical principles are universal, while the anthropologically-based 'multicultural' model claims the philosophical position that principles are culturally bound. The authors explicate the two philosophical stances and advocate a morally sensitive but moderate position of 'ethical multiculturalism' rather than favouring either of the above philosophical positions. The final section suggests ways to promote ethical multiculturalism while planning and conducting nursing research.

Cultural Diversity↗
PubMed2001

Assessing the female sexual assault survivor.

Because sexual assault survivors often seek treatment in primary care settings, clinicians must be prepared to evaluate these patients in a nonjudgmental manner. The initial evaluation includes a medical and assault history. During the physical examination, physical injuries are noted and forensic evidence is collected. Treatment includes prophylaxis for pregnancy and sexually transmitted infections and counseling referrals. This article focuses on care of the adult female sexual assault survivor. Psychosocial support, physical examination, collection of evidence, treatment, and documentation are discussed.

Contraceptives, Postcoital↗
PubMed1999

The Client Encounter Form: conceptual development, reliability analysis, and clinical applications.

This descriptive correlational study investigated the reliability of a new measure of client-nurse practitioner interaction, the Client Encounter Form (CEF), and used the CEF to describe the domains of client-nurse practitioner interaction that occurred during problem and preventative visits at a primary care clinic. The CEF is based on Cox's Interactional Model of Client Health Behavior. Data were collected from a convenience sample of 41 primary care clinic visits. Descriptive data on all clients and the patterns of use characterized by the CEF were collected using retrospective chart review (n = 60). Reliability testing showed the CEF has high interrater reliability; Cohen's Kappas for its dimensions ranged from 0.78-1.0. The CEF was also shown to be useable in a primary care clinic. Health information, affective support, goal setting, and technical procedures were consistently part of the nurse-client interactions in this sample, demonstrating they are part of the nurse practitioner model of care. Analysis revealed different patterns of interaction for preventative and problem-oriented visits. Preventative visits had higher levels of health promotion information, psychological affective support, and health promotion goal-setting behaviors. Problem visits included more information regarding the client's diagnosis, medications, and treatments, and more affective support related to the client's physical condition.

Adolescent↗
PubMed1998

Impaired spatial navigation learning in transgenic mice over-expressing heme oxygenase-1.

Transgenic mice expressing heme oxygenase-1 (HO-1) using the neuron-specific enolase promoter were impaired in learning the Morris water maze compared to nontransgenic littermates. The memory of the HO-1 mice for the location of the platform was similarly impaired when tested using a probe trial after 7 training blocks, but performance on visible platform trials was similar for both groups of mice. Importantly, both HO-1 and nontransgenic mice had normal sensorimotor function, and performed the same on a Y-maze alternation task, highlighting the specificity of memory deficit in the spatial navigation task. These results suggest that carbon monoxide, one product of HO-1 activity, interferes in the development of spatial navigation memory, and may play a role in normal memory function.

Animals↗
PubMed1998

Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes.

Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes. The mutant APP(K670N,M671L) transgenic line, Tg2576, shows markedly elevated amyloid beta-protein (A beta) levels at an early age and, by 9-12 months, develops extracellular AD-type A beta deposits in the cortex and hippocampus. Mutant PS1 transgenic mice do not show abnormal pathology, but do display subtly elevated levels of the highly amyloidogenic 42- or 43-amino acid peptide A beta42(43). Here we demonstrate that the doubly transgenic progeny from a cross between line Tg2576 and a mutant PS1M146L transgenic line develop large numbers of fibrillar A beta deposits in cerebral cortex and hippocampus far earlier than their singly transgenic Tg2576 littermates. In the period preceding overt A beta deposition, the doubly transgenic mice show a selective 41% increase in A beta42(43) in their brains. Thus, the development of AD-like pathology is substantially enhanced when a PS1 mutation, which causes a modest increase in A beta42(43), is introduced into Tg2576-derived mice. Remarkably, both doubly and singly transgenic mice showed reduced spontaneous alternation performance in a "Y" maze before substantial A beta deposition was apparent. This suggests that some aspects of the behavioral phenotype in these mice may be related to an event that precedes plaque formation.

Alzheimer Disease↗
PubMed1996

Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1.

Mutations in the genes encoding amyloid-beta precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) are known to cause early-onset, autosomal dominant Alzheimer's disease. Studies of plasma and fibroblasts from subjects with these mutations have established that they all alter amyloid beta-protein (beta APP) processing, which normally leads to the secretion of amyloid-beta protein (relative molecular mass 4,000; M(r) 4K; approximately 90% A beta1-40, approximately 10% A beta1-42(43)), so that the extracellular concentration of A beta42(43) is increased. This increase in A beta42(43) is believed to be the critical change that initiates Alzheimer's disease pathogenesis because A beta42(43) is deposited early and selectively in the senile plaques that are observed in the brains of patients with all forms of the disease. To establish that the presenilin mutations increase the amount of A beta42(43) in the brain and to test whether presenilin mutations act as true (gain of function) dominants, we have now constructed mice expressing wild-type and mutant presenilin genes. Analysis of these mice showed that overexpression of mutant, but not wild-type, PS1 selectively increases brain A beta42(43). These results indicate that the presenilin mutations probably cause Alzheimer's disease through a gain of deleterious function that increases the amount of A beta42(43) in the brain.

Amyloid beta-Peptides↗
PubMed1987

Relationship of basic research in toxicology to environmental standard setting: the case of polybrominated biphenyls in Michigan.

The accidental contamination of dairy cattle feed in Michigan in 1973-74 with polybrominated biphenyls (PBB) led to the contamination of cattle and people consuming their products. This led to an extensive animal and product monitoring and disposal program conducted by the Michigan Department of Agriculture and the Department of Natural Resources. It also led to several studies of the people of Michigan, extensive research on the chemicals, and an unprecedented establishment by the Legislature of a Toxic Substance Control Commission. Only a few relatively minor components of the PBB mixture that contaminated Michigan are metabolized and another group of minor components seem responsible for the toxicity, which, similar to that caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), includes induction of microsomal enzymes, liver hypertrophy, thymic involution, porphyria, anorexia and chloracne. PBB were found to produce the "dioxin-like" toxicity with roughly 0.01% the potency of TCDD. Both non-toxic as well as toxic congeners were found to be tumor promotors. To date it is impossible to unequivocally conclude that any human health effects can be attributed to PBB. The Toxic Substance Control Commission was established as an independent oversight body with responsibility to gather information, investigate, coordinate and make recommendations concerning toxic substances and the handling of toxic substances incidents. The Commission has declared two toxic substances emergencies and made several recommendations for regulating and solving toxic substances problems but its major activities have evolved towards a role as an environmental ombudsman.

Animals↗
PubMedDate not supplied

Stomatococcus mucilaginosus bacteremias. Typical case presentations, simplified diagnostic criteria, and a literature review.

Even though Stomatococcus mucilaginosus is considered indigenous oral-pharyngeal flora, cited literature and case reports indicate that it can be the cause of infectious conditions. Tested strains were isolated from blood, the oral region, and wound sources. The organism was routinely misidentified or not identified by conventional or commercial systems (Vitek, STAPH-Trac). Four antimicrobial diagnostic disks for example, bacitracin (0.04 units; Taxo A), furazolidone (100 micrograms), novobiocin (5 micrograms), and polymyxin B (300 units), were evaluated as possible addition to previously applied biochemical characteristics that differentiate between S. mucilaginosus, Micrococcus sp., and coagulase-negative staphylococci. Consistent antimicrobial susceptibility patterns among our isolates to the diagnostic disks produced applicable characteristics for discriminating S. mucilaginosus from similar microorganisms. However, therapeutic choices of antimicrobial agents should be guided by individual organism susceptibility test results because of variable, often resistant patterns to beta-lactams, aminoglycosides, macrolides, new fluoroquinolones, and sulfonamides.

Adult↗