Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “complex diseases”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed2006

Linkage analysis for complex diseases using variance component analysis: SOLAR.

Variance component linkage analysis has become one of the most popular tools for the analysis of poly genic phenotypes. In particular for cardiovascular disease, such as coronary artery disease and myocardial infarction, variance component analysis holds some unique advantages. This analysis approach is versatile, affording the user the ability to incorporate the interplay between risk factors, genetic susceptibility, the effect of environmental factors, or the joint analysis of multiple phenotypes in the analysis. In this chapter, we present as an introduction the statistical background of variance component analysis as implemented in the genetic analysis package SOLAR.

Analysis of Variance↗
PubMed2006

Nanotechnology: intelligent design to treat complex disease.

The purpose of this expert review is to discuss the impact of nanotechnology in the treatment of the major health threats including cancer, infections, metabolic diseases, autoimmune diseases, and inflammations. Indeed, during the past 30 years, the explosive growth of nanotechnology has burst into challenging innovations in pharmacology, the main input being the ability to perform temporal and spatial site-specific delivery. This has led to some marketed compounds through the last decade. Although the introduction of nanotechnology obviously permitted to step over numerous milestones toward the development of the "magic bullet" proposed a century ago by the immunologist Paul Ehrlich, there are, however, unresolved delivery problems to be still addressed. These scientific and technological locks are discussed along this review together with an analysis of the current situation concerning the industrial development.

Animals↗
PubMed1979

Eosinophilic gastroenteritis--a complex disease entity.

Although usually regarded as merely a manifestation of a simple food allergy, eosinophilic gastroenteritis remains a poorly understood disorder. Characterized by peripheral eosinophilia, eosinophilic infiltration of the bowel wall to a variable depth and gastrointestinal complaints, the disease responds inconsistently to simple food withdrawal programs. Immunoglobulin E (IgE) antibodies to specific food substances have been found in a few patients leading to a postulated pathophysiologic mechanism involving tissue mast cells, release of slow-reacting substance of anaphylaxis (SRS-A) and chemotaxis of eosinophils. Oral steroids appear, in uncontrolled trials, to ameliorate the disease.

Adult↗
PubMed2005

Ethical issues associated with conducting genetic family studies of complex disease.

PURPOSE: To examine subjects' recognition of the risks and ethical issues associated with enrollment in genetic family studies (GFS) and explore how this recognition affects their informed and voluntary participation. METHODS: A cross-sectional study design including both quantitative and qualitative data was employed. Structured interviews using the Contextual Assessment Approach Questionnaire (CAA-Q) were conducted with 246 Mexican American (MA) participants. To gain in-depth understanding of questionnaire responses, semi-structured interviews with 30 participants were conducted. All participants were interviewed before their enrollment in the Family Investigation of Nephropathy and Diabetes (FIND). RESULTS: Subjects' average age was 56 years; 62% were females. Seventy-eight percent of participants were not formally educated beyond high school and 72% reported an annual household income of < or =20,000 dollars. Eighty-five percent agreed to provide researchers with information on relatives' ages, gender, and education. Sixty-five percent of participants were willing to provide identifiable information such as names, addresses, and phone numbers of relatives. Sixty-three percent of participants indicated that there were direct benefits (i.e., supporting research) to disclosing relatives' information. Seventy-six percent stated that there were no risks associated with participation in GFS (e.g., discrimination or confidentiality of genetic information) compared with 10% who said that there were such risks. While discussing potential risks, subjects did not consider these to influence their decision to participate. CONCLUSIONS: Subjects enrolled in GFS did not recognize and tended to underestimate the social and cultural risks associated with their participation in GFS. If subjects do not fully comprehend the risks, this raises questions concerning their ability to provide informed consent and to voluntarily participate. We propose a subject-centered approach that views enrollment as an active process in which subjects and recruiters give and receive information on risks and ethical issues related to participation, which enhances protection of the rights and welfare of subjects participating in GFS.

Adult↗
PubMed2004

Axonal damage in multiple sclerosis: a complex issue in a complex disease.

Multiple sclerosis is no longer considered to simply be an autoimmune demyelinating disease. Axonal destruction is another central pathological feature and a contributor to the accumulating disability of disease progression. The mechanism underlying axonal pathology has not been fully clarified but does not appear to be a simple one. The relationship between axonal damage and other components of the pathological features such as demyelination, inflammation and remyelination are under intense investigation. Experimental data suggest that therapeutic interventions such as the induction of rapid remyelination may lead to the protection of axons. In addition to immunomodulation, future strategies for neuroprotection may be of great importance.

Adjuvants, Immunologic↗
PubMed2006

X-linked premature ovarian failure: a complex disease.

Involvement of the X chromosome in premature ovarian failure was demonstrated by the relatively frequent chromosomal rearrangements in patients, but the requirement of two X chromosomes for ovarian function was quite unexplained until recently. Review of the data on chromosomal rearrangements suggests that several genes along the X chromosomes contribute to ovarian function. In most instances, no single X chromosome gene has a causative role in premature ovarian failure, and the phenotype is likely to derive from the additive effect of X-linked and non-X-linked factors. Recent data on a small group of balanced X-autosome translocations showed that X-linked premature ovarian failure might also be caused by a different mechanism, namely position effect of the X chromosome on non-X-linked genes, and suggest a peculiar organization of the X chromosome during oogenesis.

Animals↗