SEARCH · Search PubMed

Results for “Longitudinal phenotype”

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.

SourceResearch connectionFrom yearThrough year

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

At least 163 records · Page 9Linked to original sources

PubMed2003

Using genetic admixture to explain racial differences in insulin-related phenotypes.

Documented differences in measures of insulin secretion and action between African Americans and European Americans may be due to either genetic or environmental factors. This study used genetic admixture (ADM), determined from approximately 20 ancestry informative markers, and a questionnaire designed to assess socioeconomic status (SES) to examine potential genetic and environmental contributions to minimal model-derived measures of insulin sensitivity (S(I)), fasting insulin, and the acute insulin response to glucose (AIR(g)) in 125 children residing in Birmingham, Alabama. The study was longitudinal in design and yielded multiple outcome measures on each subject. Mixed models analysis was used to determine if ADM and SES were independently related to S(I), fasting insulin, and AIR(g) after adjusting for confounding factors (pubertal status, adiposity, age) and for repeated testing of individuals. In this cohort, African ADM ranged from 0% (individuals with no markers reflecting African ancestry) to 100% (individuals with all 20 markers reflecting African ancestry). Results indicated that ADM was independently related to S(I) (P < 0.001) and fasting insulin (P < 0.01), with individuals having greater African ADM having a lower S(I) and a higher fasting insulin concentration. Both ADM (P < 0.001) and SES (P < 0.05) were independently related to AIR(g); children with greater African ADM or lower SES had a higher AIR(g), even after adjusting for S(I). These observations suggest that use of ADM can replace assignment of individuals to categorical racial groups; that lower S(I) and higher fasting insulin among African Americans compared with European Americans may have a genetic basis; and that higher AIR(g) among African Americans may be due to both genetic factors and to environmental factors that remain to be identified.

Adipose Tissue↗

PubMed1994

The influence of apolipoprotein E polymorphism on plasma concentrations of apolipoprotein B and A-I during the first year of life.

Apolipoprotein (apo)E polymorphism has been shown to be associated with different serum levels of cholesterol, apoB, and apoE. In clarifying the degree of influence of the apoE isoforms, investigations in an early stage of life are useful. The aim of the study was to investigate the plasma levels of apoB and apoA-I as structural proteins of low and high density lipoproteins, in relation to apoE phenotypes during the first year of life. Conclusions about the relationship between apoE phenotype and the development of the lipoprotein patterns can be drawn. The concentrations of apoB and apoA-I in capillary plasma as well as the apoE phenotype were estimated in 199 newborns (7 days old) and in follow-up investigations of a subgroup of 45 at 1, 4, 12, 24, and 52 weeks. The phenotype frequencies were as follows: 70% apoE 3/3, 16% apoE 3/4, 10% apoE 2/3, 2.5% apoE 2/2, and 1.5% apoE 4/2. The plasma concentrations of apoB and apoA-I in the newborns (7 days old) averaged 55% of the adult value and increased toward the end of the first year of life up to approximately 85%. The course of the plasma concentrations of apoB and apoA-I in relation to the apoE phenotype showed that, beginning at 24 weeks, the apoB levels were significantly lower for the phenotype E 2/2 and in tendency also for the phenotype E 2/3 in comparison with E 3/3. At the end of the first year of life, the apoB levels in infants with apoE phenotype 2/2 increased only by 50% and yielded 0.59 g/L.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I↗

PubMed2005

Patterns of antimicrobial resistance among commensal Escherichia coli isolated from integrated multi-site housing and worker cohorts of humans and swine.

We examined antimicrobial resistance (AR) phenotypes among commensal Escherichia coli isolated from fecal matter of humans and swine housed in a semi-closed and uniquely integrated multi-site farrow-to-plate operation. Aggregate cohorts of humans consisted of (1) "control" groups of consumers, (2) groups of swine workers, and (3) groups of slaughter-plant workers. Analyses of cross-sectional AR data from 472 human and 376 swine isolates are presented. AR phenotypes among these isolates were compared by (1) host species, (2) facility location, (3) facility type, (4) housing (human) or production (swine) cohort, and (5) sample collection period and time of day. There were significant (p < 0.05) differences in isolates among host-species with swine uniformly at greater risk for (1) AR to four specific antimicrobials (kanamycin, streptomycin, sulfamethoxazole, tetracycline), and (2) multiple resistance phenotypes (p < 0.0001). Facility type and unit location were more often associated with AR differences among swine isolates than among human isolates. Swine production group was significantly associated with AR prevalence (p < 0.05) for nine antimicrobials; in general, purchased boars, suckling piglets, weaned piglets, and lactating sows were at higher risk of AR. There was no significant (p > 0.05) association of human occupational/consumer cohort with AR prevalence. Several unique AR phenotypes were detected in each of the human- and swine-intake groups. These data establish baseline characteristics for an on-going 3-year longitudinal study designed to further characterize AR phenotype and genotype in this population. Host-, facility-, and cohort-specific data demonstrate that sufficient prevalence differences exist to permit the future quantification of AR transmission, should it occur. Based on these cross-sectional data, occupational exposure to either swine-rearing or swine-slaughter facilities does not appear to be associated with the prevalence of phenotypic resistance among the commensal fecal E. coli isolated from this integrated system.

Animal Husbandry↗

PubMed2000

Spatially regulated differentiation of endometrial vascular smooth muscle cells.

Angiogenesis within the human endometrium involves the development of arterioles and elaboration of a capillary network. It was postulated that maturation of these arterioles involves a spatially regulated process of vascular smooth muscle cell (VSMC) differentiation. The endometrial vascular tree was therefore examined immunohistochemically for evidence of longitudinal and radial gradients of VSMC phenotype. Twenty-three hysterectomy specimens and 15 first trimester decidual tissues were studied. Five cytoskeletal markers (alpha and gamma-smooth muscle (sm) actin, sm myosin, desmin, vimentin), three endothelial markers (CD31, CD34, factor VIII related antigen) and two steroid receptors (oestrogen and progesterone) were detected immunohistochemically. alpha-sm actin was present throughout the wall of basal arterial segments and extended longitudinally towards the endometrial surface. Sm myosin expression was more restricted longitudinally and radially within in the vascular tree. The expression of gamma-sm actin was even more restricted than myosin. In first trimester decidua, however, gamma-sm actin was widely distributed within the wall of spiral arteries that were not invaded by trophoblast. Oestrogen and progesterone receptors were present in peri-vascular stromal cells but absent from vascular smooth muscle and endothelium. Endometrial VSMC differentiation involves a progressive increase in cytoskeletal complexity and occurs in a spatially regulated fashion.

Actins↗

PubMed1998

Neuropeptide tyrosine-like immunoreactivity (NPY-LI) in ganglion neurons in the adrenal gland of the flat snake (Waglerophis merremii).

In previous morphological and histochemical studies on the adrenal gland of the flat snake, no data demonstrating the existence of ganglion neurons has been reported. The aim of this paper was therefore to establish the presence of ganglion neurons in the adrenal gland of the flat snake Waglerophis merremii and, further to study their chemical phenotype using immunohistochemistry. Our results showed the presence of cells which were immunolabelled with the neuronal marker neurofilament 10 and were thus identified as large ganglion neurons. These cells were localized in the dorsal ribbon of the gland, suggesting a noradrenergic phenotype, exhibited long processes with a longitudinal direction and co-expressed neuropeptide tyrosine- (NPY) and tyrosine hydroxylase-like immunoreactivities (-LI). In addition, NPY-immunoreactive (-IR) fibers were recognized with a wide distribution throughout the gland whereas vasoactive intestinal polypeptide (VIP)-IR fibers were only observed between clusters of cortical and adrenergic chromaffin cells. No cells containing VIP-LI were detected within the gland. Based on their histochemical phenotype, ganglion cells containing NPY and TH could correspond to ganglion neurons type I of the rat. The possible absence of type II ganglion neurons in the adrenal gland of the snake is discussed.

Adrenal Medulla↗

PubMed1998

Association of apolipoprotein E phenotype with plasma lipoproteins in African-American and white young adults. The CARDIA Study. Coronary Artery Risk Development in Young Adults.

Apolipoprotein E phenotype (APOE phenotype) has been demonstrated to be a genetic determinant of cardiovascular disease. This atherogenicity may be a reflection of the association of APOE phenotype and plasma lipoprotein concentrations. The Coronary Artery Risk Development in Young Adults (CARDIA) Study affords the opportunity to assess the frequency of apolipoprotein E alleles in population-based samples of African Americans and whites in the United States and to compare the associations of APOE phenotype with lipoprotein and apoprotein concentrations. Data from 3,485 African-American and white men and women between the ages of 25 and 37 years who attended the fourth CARDIA Study examination in 1992-1993 were used in this analysis. African-American men and women had significantly higher frequencies of E2 and E4 phenotype and thus higher frequencies of *epsilon2 and *epsilon4 alleles (p < 0.005). Men and women of both races with APOE4 phenotype generally had higher low density lipoprotein cholesterol, apolipoprotein B, and lipoprotein(a) concentrations and lower high density lipoprotein cholesterol concentration, and individuals with APOE3 phenotype had the lowest triglyceride concentration. Major differences between African Americans and whites were observed in the distribution of APOE phenotypes and *epsilon alleles, but APOE phenotype was associated with similar differences in lipoprotein and apoprotein concentrations in both races. The data suggest that APOE phenotype may be a risk factor for cardiovascular disease in both African Americans and whites because it is associated similarly with an adverse lipoprotein profile.

Adolescent↗

PubMed2003

The genetics of cross-sectional and longitudinal body mass index.

There has been a lack of consistency in detecting chromosomal loci that are linked to obesity-related traits. This may be due, in part, to the phenotype definition. Many studies use a one-time, single measurement as a phenotype while one's weight often fluctuates considerably throughout adulthood. Longitudinal data from the Framingham Heart Study were used to derive alternative phenotypes that may lead to more consistent findings. Body mass index (BMI), a measurement for obesity, is known to increase with age and then plateau or decline slightly; the decline phase may represent a threshold or survivor effect. We propose to use the weight gain phase of BMI to derive phenotypes useful for linkage analysis of obesity. Two phenotypes considered in the present study are the average of and the slope of the BMI measurements in the gain phase (gain mean and gain slope). For comparison, we also considered the average of all BMI measurements available (overall mean). Linkage analysis using the gain mean phenotype exhibited two markers with LOD scores greater than 3, with the largest score of 3.52 on chromosome 4 at ATA2A03. In contrast, no LOD scores greater than 3 were observed when overall mean was used. The gain slope produced weak evidence for linkage on chromosome 4 with a multipoint LOD score of 1.77 at GATA8A05. Our analysis shows how omitting the decline phase of BMI in the definition of obesity phenotypes can result in evidence for linkage which might have been otherwise overlooked.

Adolescent↗

PubMed2003

Variance components linkage analysis for adjusted systolic blood pressure in the Framingham Heart Study.

We performed variance components linkage analysis in nuclear families from the Framingham Heart Study on nine phenotypes derived from systolic blood pressure (SBP). The phenotypes were the maximum and mean SBP, and SBP at age 40, each analyzed either uncorrected, or corrected using two subsets of epidemiological/clinical factors. Evidence for linkage to chromosome 8p was detected with all phenotypes except the uncorrected maximum SBP, suggesting this region harbors a gene contributing to variation in SBP.

Adult↗

PubMed2005

Human immunosenescence: is it infectious?

Morbidity and mortality due to infectious disease is greater in the elderly than in the young, at least partly because of age-associated decreased immune competence, which renders individuals more susceptible to pathogens. This susceptibility is particularly evident for novel infectious agents such as in severe acute respiratory syndrome but is also all too apparent for common pathogens such as influenza. Many years ago, it was noted that the elderly possessed oligoclonal expansions of T cells, especially of CD8(+) cells. At the same time, it was established that cytomegalovirus (CMV) seropositivity was associated with many of the same phenotypic and functional alterations to T-cell immunity that were being reported as biomarkers associated with aging. It was discovered that CMV was the prime driving force behind most of the oligoclonal expansions and altered phenotypes and functions of CD8 cells. Independently, longitudinal studies of a free-living population of the very old in Sweden over the past decade have led to the emerging concept of an 'immune risk phenotype' (IRP), predicting mortality, which was itself found to be associated with CMV seropositivity. These findings support our hypothesis that the manner in which CMV and the host immune system interact is critical in determining the IRP and hence is predictive of mortality. In this sense, then, we suggest that immunosenescence is contagious.

Aging↗

PubMed2000

Genotype and phenotype of cytochrome P450 2D6 in human immunodeficiency virus-positive patients and patients with acquired immunodeficiency syndrome.

OBJECTIVE: To examine the distribution of the cytochrome P450 (CYP) CYP2D6 phenotype and its relation to genotype, concomitant medication, and disease state in human immunodeficiency virus (HIV)-positive patients. DESIGN: A cross sectional study with a longitudinal component compared individual genotypes for CYP2D6 to the CYP2D6 phenotype. METHODS: Sixty-one predominately male Caucasian, HIV-positive patients were recruited and CYP2D6 genotypes [extensive metabolizer (EM) or poor metabolizer (PM)] determined by polymerase chain reaction (PCR)-based amplification, followed by restriction fragment-length analysis. The patients were also phenotyped using dextromethorphan (DM) to determine their respective enzyme activity and assigned either a CYP2D6 EM or PM phenotype. Complete medical and treatment histories were compiled. A total of 44 patients were tested longitudinally. RESULTS: Fifty-nine patients (97%) possessed an EM genotype, consistent with previously observed distributions in demographically similar populations. In healthy seronegative populations, genotype and phenotype have been shown to be essentially interchangeable measures of CYP2D6 activity. In this cohort, 2 of the 59 patients with an EM genotype expressed a PM phenotype. In addition, 4 EM patients were less extensive DM metabolizers than any of the patients receiving medication known to inhibit CYP2D6. This apparent shift toward the PM phenotype from the EM genotype was associated with the presence of active illness. CONCLUSION: Changes may occur in HIV-positive patients such that their CYP2D6 activity approaches that of PMs, despite having an EM genotype. Neither active disease nor drug interactions alone explain the shift.

Acquired Immunodeficiency Syndrome↗

PubMed2003

Numerous, small, darkly pigmented melanocytic nevi: the cheetah phenotype.

BACKGROUND: The presence of multiple atypical nevi or numerous melanocytic nevi increases the risk for the development of cutaneous melanoma. OBJECTIVE: We sought to describe a distinct clinical phenotype characterized by numerous (>100), small (< or =4 mm), darkly pigmented melanocytic nevi that are uniform in color. METHODS: Biopsy specimens from 6 patients (3 men and 3 women; age range, 44 to 81 years) with this clinical phenotype were reviewed and compared with a database of melanocytic lesions analyzed by the Yale Dermatopathology Laboratory (YDL) in the year 2000. RESULTS: Of the 6 patients, 4 had multiple primary melanomas develop (n = 2-4), ranging from in situ to 1.0 mm in depth. The other 2 patients each had 1 nevus with severe cytologic atypia. When compared with the YDL database, our patients were more likely to have the following pigmented lesions: junctional melanocytic nevi, junctional lentiginous nevi, junctional nevi with cytologic atypia, and simple lentigines (P <.001). CONCLUSIONS: The longitudinal evaluation of patients with this phenotype can be challenging because similar-appearing pigmented lesions (small and uniformly dark-brown to black) had a range of histologic diagnoses from simple lentigo to junctional lentiginous nevus to thin melanoma.

Adult↗

PubMed1998

Analysis of pol gene heterogeneity, viral quasispecies, and drug resistance in individuals infected with group O strains of human immunodeficiency virus type 1.

Nucleotide sequences of the reverse transcriptase (RT) coding region have been compared in four new human immunodeficiency virus type 1 (HIV-1) group O isolates. Phylogenetic analysis of this pol region highlights a cluster of these four HIV-1 group O sequences with seven other group O isolates (5% intracluster nucleotide sequence diversity) similar to clusters classified as subtypes in HIV-1 group M (an average of 4.9% intrasubtype sequence diversity). Based on these analyses, this group O cluster has been designated subtype A-O. A longitudinal study of a heterosexual couple infected with group O (ESP1 and ESP2) allowed a detailed analysis of RT sequences (amino acids 28 to 219). Directed evolution and a slightly higher mutation frequency was observed in the RT sequences of patient ESP2, treated with antiretroviral drugs, than that from the untreated patient ESP1. Antiretroviral treatment also selected for specific substitutions, M184V and T215Y in the RT coding region, conferring resistance to 3'-dideoxy-3'-thiacytidine and zidovudine, respectively. A Gly98 to Glu RT substitution identified in the treated patient suggests a possible reversion of a nonnucleoside RT inhibitor-resistant phenotype. Using RT clones from this longitudinal study, both heteroduplex tracking assay and cloning-sequencing techniques were employed for an extensive genetic analysis of pol gene quasispecies. Amino acid substitutions (i.e., Phe-77 to Leu, Lys-101 to Glu, and Val-106 to Iso) associated with antiretroviral resistance were identified in RT clones from HIV-1 group O-infected patients not subjected to drug therapy or treated with unrelated drugs. Finally, phylogenetic relationships between RT clones of the treated ESP2 patient and those of the untreated ESP1 patient show how drug pressure can direct evolution of viral pol gene quasispecies independently of direct drug-resistant substitutions.

Adolescent↗

PubMed2005

Apolipoprotein A-II polymorphism and visceral adiposity in African-American and white women.

To determine the association between the -265 T to C substitution in the apolipoprotein A-II (APOA-II) gene and levels of visceral adipose tissue (VAT) in a group of premenopausal African-American and white women, we genotyped 237 women (115 African-American and 122 white) for this polymorphism. Body composition was assessed by DXA, and VAT was determined from a single computed tomography scan. In addition to VAT, we examined the association between the polymorphism and other phenotypes (total body fat, total abdominal adipose tissue, and subcutaneous abdominal adipose tissue). The mutant C allele in the APOA-II gene was less frequent in African-American compared with white women, 23% vs. 36%, respectively (p < 0.01). VAT was significantly higher in carriers of the C allele compared with noncarriers after adjustment for total body fat (p < 0.05). When separate analyses by ethnic group were conducted, the association between the polymorphism and VAT was observed in white (p < 0.05) but not African-American (p = 0.57) women. There was no association between the polymorphism and the other phenotypes. These results indicate a significant association between the T265C APOA-II polymorphism and levels of VAT in premenopausal women. This association is present in white but not African-American women.

Absorptiometry, Photon↗

PubMed2005

Do long-term HDL-C declines associated with a first birth vary by apo E phenotype? The Coronary Artery Risk Development in Young Adults (CARDIA) study.

BACKGROUND: High-density lipoprotein cholesterol (HDL-C) levels in premenopausal and postmenopausal women are differentially affected by exogenous sex hormones depending on their apolipoprotein E (apo E) genotype. Because endogenous sex hormones markedly increase during pregnancy, we examined whether HDL-C declines after a first birth varied by apo E polymorphisms. METHODS: In 1147 nulliparas (416 black, 731 white), fasting blood samples (nonpregnant) were drawn at baseline and at follow-up years 5, 7, and 10. Time-dependent pregnancy groups included 0 pregnancies (P0), 1+ short pregnancy (P1+), 1 birth (B1), 2 or more births (B2+). ApoE groups by alleles identified with a phenotype method included E4 (4/3 and 4/4), E3 (3/3), and E2 (2/2 and 3/2). Differences in adjusted mean HDL-C changes among pregnancy groups and ApoE groups were examined using repeated measures multiple linear regression. RESULTS: HDL-C declines associated with parity (one or more births) depended on ApoE group (ApoE*Pregnancy Interaction; p < 0.002). For B1 and B2+ vs. P0, HDL-C declines were -2.4 to -2.7 mg/dl in E4 and -3.4 to -4.1 mg/dl in E3. In E2, HDL-C declines were -6.6 mg/dl for one birth, and -11.5 mg/dl for two or more births, each relative to the 0 pregnancies (P0) group (linear trend, p < 0.001). CONCLUSIONS: The degree to which childbearing adversely affects long-term HDL-C declines varies by apo E phenotype, based on a method that accurately classifies genotype. Our findings show that 2/2 and 3/2 genotypes are associated with larger parity-related HDL-C declines than 3/3, 4/3, and 4/4 genotypes.

Adult↗

PubMed2007

Genetics of parentally reported asthma, eczema and rhinitis in 5-yr-old twins.

The aim of the present study was to examine the genetic and environmental contributions to the individual differences in susceptibility to asthma, eczema and rhinitis in childhood and their role in the association among these conditions. Information on asthma, eczema and rhinitis was obtained by parental report. Parents were asked whether a physician had ever diagnosed the condition. Complete data were available for 8,633 5-yr-old twin pairs born between 1986 and 1998. The frequency of parentally reported asthma, eczema and rhinitis was 8.7, 16.8 and 4.4%, respectively, and was higher in males than females. Genetic factors accounted for approximately 90% of the variance in the susceptibility to asthma, eczema and rhinitis. The magnitude of genetic factors did not differ between males and females. The remaining part of the variance was explained by environmental factors not shared by family members. The phenotypic correlations between parentally reported asthma, eczema and rhinitis were moderate and mainly mediated by the same genetic factors. The high heritability and the limited influence of shared environmental factors may point to gene x environment interactions. Future research should focus on this type of interaction processes.

Asthma↗

PubMed1991

Phenotypic profiles of language-impaired children based on genetic/family history.

Although etiological influences in developmental language impairment (dysphasia) are not well defined, a significant increase of family aggregation for the disorder has been reported. We report data from a large cohort of language-impaired (LI) children participating in the San Diego longitudinal study in which we examined whether children with or without positive family histories show different phenotypic profiles. Due to the longitudinal design of the study, questions pertaining to change over time are also addressed. Second, a subgroup of the most impaired children were reevaluated to obtain additional information pertaining to family history and phenotypic outcome. Approximately 70% of the LI children met criteria for inclusion as family history positive, with fathers reporting a history of language or learning problems one and a half to two times as frequently as mothers. LI children with or without a positive family history were not significantly different on language skills or IQ. However, subjects having a positive family history for developmental language/learning problems were significantly lower in socioeconomic status and were rated by parents and teachers as having more attention-related behavior problems than their family history negative counterparts. Similarly, family history positive LI children performed more poorly on standardized academic tests as well as on tests of auditory processing and attention.

Child↗

PubMed1989

Development of antibodies to HIV-1 is associated with an increase in circulating CD3+CD4-CD8- lymphocytes.

This study investigated whether seroconversion with respect to human immunodeficiency virus, type 1 (HIV-1) was associated with an increase in lymphocytes expressing the CD3+CD4-CD8- phenotype. Proportions and absolute numbers of CD3+, CD4+, and CD8+ lymphocytes were determined prospectively over a 2.5-year period on 4954 homosexual and/or bisexual men participating in the Multicenter AIDS Cohort Study. Of the 4808 men whose serostatus at entry could be verified, 1745 were seropositive (SP) for antibodies to HIV-1 at entry into study, 2795 were uniformly seronegative (SN) for HIV-1 for 30 months, and 268 were seroconverters (SC) with respect to HIV-1 during this period. For each of six semiannual evaluations, proportions and numbers of CD3+CD4-CD8- lymphocytes (calculated as CD3- (CD4 + CD8] were both significantly greater in the SP group than in the SN group (P less than 0.001). Mean CD3+CD4-CD8- levels in the SC group were indistinguishable from those in the SN group before seroconversion, but by 3-9 months after seroconversion the SC group demonstrated absolute numbers of CD3+CD4-CD8- lymphocytes which were significantly increased (P less than 0.001) compared to the SN group using linear regression methods with adjustment for correlation of measurements within an individual over time. An additional significant increase occurred by 21-27 months after seroconversion (P = 0.006). These results are consistent with an association of HIV-1 seroconversion with an increase in circulating T lymphocytes expressing the CD3+CD4-CD8- phenotype (double negative T cells), a decrease in CD3-CD4-CD8+ natural killer cells, or both. An increase in double negative T cells could reflect a host defense mechanism against HIV-1 or effects of HIV-1 on T cell development.

Antigens, Differentiation, T-Lymphocyte↗

PubMed2026

Bridging genotype, phenotype, and clinical insight: the role of multi-omics in cardiovascular disease.

INTRODUCTION: It is increasingly evident that the multifactorial nature of cardiovascular disease requires the combination of different omics approaches for improving our mechanistic understanding, identifying novel drug targets, and developing accurate diagnostic, predictive, and prognostic biomarker panels. AREAS COVERED: We review the current state and the potential of multi-omics in cardiovascular disease, with a specific focus on plasma-, spatial-, and single-cell approaches. We discuss lipidomics as a genotype‑to‑phenotype bridge, the utility of remote longitudinal monitoring via microsampling/dried blood spots, and emerging clinical‑trial integrations of multi-omics approaches. We outline critical gaps in standardization and how to overcome these, pre‑analytical challenges and constraints that are often neglected, and data‑integration methods spanning from canonical correlation analysis to modern machine learning approaches. EXPERT OPINION: Multi‑omics can shape cardiovascular care by identifying drug targets in diseased tissue and by yielding small, usable biomarker panels.

Humans↗