Open Access Pub publishes peer-reviewed, free-to-read open-access articles. Showing
articles matching Personalized Medicine — open any to read the full text,
or download the PDF or XML.
Nov 2025 DOI 10.14302/issn.2326-0793.jpgr-25-5573
Advancements in proteomic and genomic technologies have transformed molecular biology by enabling comprehensive analysis of biological systems at the molecular level. This literature review explores the evolution, methodologies, and practical applications of key proteomic and genomic techniques. In proteomics, tools such as two-dimensional electrophoresis, mass spectrometry, Western blotting, Edman degradation, and functional protein microarrays have facilitated high-throughput protein identification, post-translational modification analysis, and biomarker discovery. Similarly, genomic methodologies like PCR, recombinant DNA technology, gel electrophoresis, and Southern blotting have revolutionized gene detection, manipulation, and expression profiling. The review also highlights the interdisciplinary impact of these technologies across clinical diagnostics, oncology, autoimmune disorders, infectious disease surveillance, cardiovascular research, and personalized nutrition. Integrative approaches combining proteomics and genomics are enabling the discovery of novel therapeutic targets, improving disease classification, and advancing precision medicine. Despite current limitations, such as the absence of amplification techniques for proteins and challenges in data interpretation, ongoing innovations promise to bridge these gaps. This synthesis underscores the pivotal role of molecular techniques in deepening our understanding of human biology and accelerating biomedical advancements for improved healthcare outcomes.
Dec 2025
The journey from personalized medicine to customized nutrition represents a significant paradigm shift in healthcare, emphasizing the holistic method for a person's or girl's well-being. in this transition, the know how of the unique genetic makeup , metabolic profile, and way of lifestyles elements of everybody will become paramount. customized medicinal drug has long centered on tailoring scientific remedies to the genetic and physiological traits of sufferers, optimizing efficacy, and minimizing detrimental effects. Now, custom-designed nutrients increase this idea further, recognizing that weight reduction plays an essential function in health and disease prevention. Key to this evolution is the mixing of advanced technology together with genomics, metabolomics, and microbiomics, allowing the suitable identification of dietary styles and nutritional requirements tailored to a person's particular desires. This summary explores the trajectory of this adventure, highlighting the pivotal characteristic of interdisciplinary collaboration among healthcare professionals, nutritionists, and researchers. With the useful resource of leveraging slicing facet generation and records-pushed strategies, personalized vitamins keep the promise of revolutionizing knowledge we method nutritional interventions, moving some distance from generalized guidelines towards targeted strategies tailored to all people's precise organic make up and way of life. expertise, traumatic conditions which include accessibility to this technology, ethical issues, and the desire for sturdy, proof-primarily based practices remain. In conclusion, the shift from customized treatments to personalized nutrient expertise is a transformative generation in healthcare, empowering people to take proactive management of their health through tailor made nutrition interventions. This summary underscores the importance of endured studies and collaboration in figuring out the entire functionality of personalized vitamins in selling health and well-being.
Jun 2020 DOI 10.14302/issn.2691-8862.jvat-20-3417
Background Decreased antioxidant ability is one of the worsening conditions in AIDS.We aimed to evaluate total antioxidant ability among others, and their variation in HIV infected patients following their CD4+T cells count and viral load, in a context of new ART scarcity in most LMICs. Material and Methods We conducted a cross sectional study on 167 individuals (76 controls, 33 treatments naïve and 58 HIV-1 infected patients on ART). We assessed their plasma total antioxidant ability (FRAP), malondialdehyde (MDA) and thiol (SH) groups using standard spectrophotometric methods, then we calculated lipid peroxidation index (LPI). Statistical analysis was performed using GraphPad Prism 6. Data were analyzed by two-tailed unpaired t-test for two groups’ comparison and ANOVA for more than two groups. Pearson correlation between CD4+T cells count, viral load and the above markers was determined; P ≤ 0.05 was considered statistically significant. Results The following controls/naïve/treated subjects’ values for FRAP(mM) (1.907±0.074/1.77±0.05/1.695±0.03); MDA(μΜ) (0.781±0.081/1.115±0.118/ 1.342±0.109); SH (μΜ) (2.747±0.130/1.582±0.197/1.498 ±0.140)and LPI (0.43±0.61/ 0.61±0.7/2.59±0.83) were all obtained with P ≤ 0.05. The FRAP increased only with 3TC+TDF+EFV and 3TC+ABC+NVP cART while MDA decrease significantly with the later(p=0.027). MDA and LPI significantly increased in heavily treated patients with p<0.0014 and p=0.0001 respectively. overall, the patients showed an increase of viral loads following a decrease of CD4+T cells (r= -0.803, p=0.016) but 3TC+TDF+EFV seem to better manage the both. The only significant correlation was established between SH groups and CD4+Tcells count (r=0.447; p=0.0006); Conclusion Our study showed that thiol groups may be protective againstCD4+Tcells count depletion and that the cART 3TC+TDF+EFV, 3TC+ABC+NVP may be helpful in fighting against free radical generation and particularly 3TC+TDF+EFV as controlling CD4+Tcells count and viral load in long term treated patients. The study particularly showed the implication of cART in increasing lipid peroxidation index following the treatment duration in heavily treated patients, which aggravated their conditions in an area where drug options are limited, calling for new drugs availability and personalized medicine.
Sep 2019 DOI 10.14302/issn.2572-5424.jgm-19-3024
Background The objective of this review is to unify the various genetic defects along with elaborating metabolic pathways in Familial Combined Hyperlipidemia(FCHL) and also to differentiate the phenotype of FCHL from metabolic syndrome. Methods PubMed and Cochrane’s library was searched for keyword “Familial combined hyperlipidemia” and latter with “Familial combined hyperlipidemia genes” to finally shortlist 23 articles. Further search with key words “molecular pathogenesis of familial combined hyperlipidemia” and “metabolic syndrome and familial combined hyperlipidemia” was carried out for finding molecular defects in FCHL, non-molecular findings distinguishing FCHL from metabolic syndrome and overlapping features between FCHL and metabolic syndrome. Results Major culprit regions identified included Chromosome-1q21-q24(USF1 and FOXA2) , Ch-11q (APOA5), Ch-16q24, Ch-20q12-q13.1, Ch.4q32.3 (rs6829588), and Ch-19q13.32 containing PVRL-2 gene (Also known as Nectin-2). The genetic and metabolic pathways linked to FCHL may involve: 1-Defective clearance of Apo-B containing lipoproteins, 2-Overproduction of Apo-B containing lipoprotein i.e., VLDL and 3-Adipose tissue dysfunction. FCHL phenotype showed close resemblance with metabolic syndrome clinical and biochemical features with slight differences. Conclusion The reviewed data suggested that FCHL phenotype is the resultant end outcome from multiple molecular defects and thus underlying genetic defect identification in the index case is important for personalized medicine and incoming gene therapy. Further research is warranted to explore specific genetic defects.
Feb 2018
The possibility of tailoring treatment on specific characteristics of patients – i.e. personalized medicine – has received attention in the field of rheumatic diseases since biological DMARDs targeting a unique pathway have become available. However the idea of personalized rheumatology has advanced slowly, at different paces in different disease groups, and it is only now surfacing in the recommendations for assessment and treatment of rheumatoid arthritis (RA). Many of the difficulties encountered stem from the recognition that many rheumatic diseases are not a single entity but encompass different subsets identified on the basis of genetic traits, cellular and molecular characterization both in blood and in tissues, laboratory markers and clinical manifestations (most notably in SLE). These differences suggest a multiplicity of pathogenetic triggers, whose various combination results in slightly or very diverse presentations. Developments in companion diagnostics and the identification of distinct subsets within complex syndromes are going to allow the definition of predictive biomarkers able to reduce poor treatment outcome, thus ensuring that we are treating “the right patient with the right drug”.