Response accuracy of ChatGPT 3.5 Copilot and Gemini in interpreting biochemical laboratory data a pilot study.

With the release of ChatGPT at the end of 2022, a new era of thinking and technology use has begun. Artificial intelligence models (AIs) like Gemini (Bard), Copilot (Bing), and ChatGPT-3.5 have the potential to impact every aspect of our lives, including laboratory data interpretation. To assess the accuracy of ChatGPT-3.5, Copilot, and Gemini responses in evaluating biochemical data. Ten simulated patients' biochemical laboratory data, including serum urea, creatinine, glucose, cholesterol, triglycerides, low-density lipoprotein (LDL-c), and high-density lipoprotein (HDL-c), in addition to HbA1c, were interpreted by three AIs: Copilot, Gemini, and ChatGPT-3.5, followed by evaluation with three raters. The study was carried out using two approaches. The first encompassed all biochemical data. The second contained only kidney function data. The first approach indicated Copilot to have the highest level of accuracy, followed by Gemini and ChatGPT-3.5. Friedman and Dunn's post-hoc test revealed that Copilot had the highest mean rank; the pairwise comparisons revealed significant differences for Copilot vs. ChatGPT-3.5 (P = 0.002) and Gemini (P = 0.008). The second approach exhibited Copilot to have the highest accuracy of performance. The Friedman test with Dunn's post-hoc analysis showed Copilot to have the highest mean rank. The Wilcoxon Signed-Rank Test demonstrated an indistinguishable response (P = 0.5) of Copilot when all laboratory data were applied vs. the application of only kidney function data. Copilot is more accurate in interpreting biochemical data than Gemini and ChatGPT-3.5. Its consistent responses across different data subsets highlight its reliability in this context.

The impact of omentin-1 gene polymorphisms (rs2274907 and rs2274908) on serum lipid concentrations and coronary artery disease in a sample of Iraqi individuals (A pilot study).

BACKGROUND: Coronary artery disease (CAD) is the primary cause of death worldwide. It is mainly caused by atherosclerosis that initiates from a genetic-environmental interaction. Studies highlighted the association of numerous gene polymorphisms with CAD. Omentin-1 is secreted from visceral adipose tissues, intestine, and others; it has anti-inflammatory and insulin sensitivity improving roles. AIM: To explore the association of the omentin-1 gene polymorphisms (rs2274907 and rs2274908) with serum lipid concentrations and CAD in a sample of the Iraqi population. METHODS: A case-control study was followed, in which CAD patients were analyzed versus a group of healthy persons. Serum lipid concentrations were measured by enzymatic methods. Genotyping of the omentin-1 gene for rs2274907 SNP was achieved by ARMS-PCR, while for rs2274908 SNP by allele-specific PCR (AS-PCR) techniques. RESULTS: Atherogenic serum lipid concentrations increased significantly in CAD patients relative to the control group. Genotyping of the omentin-1 gene for rs2274907 SNP revealed a significant (OR = 4.11, P = 0.035) elevation of the AT genotype carriers in CAD versus the control groups. The genotype analysis of the rs2274908 SNP failed to exhibit a significant variation. The two analyzed SNPs were indicated to be in linkage disequilibrium (r = 0.772, P < 0.0001). The global haplotype association of the 2 SNPs was demonstrated to be significant (P = 0.006). Serum lipid concentrations were found to be independent of the genotype distribution of the rs2274907 SNP. CONCLUSION: Carriers of the AT genotype of rs2274907 SNP in the omentin-1gene may have a four-fold risk of developing CAD compared to those of the wild genotype. Alterations of serum lipid concentrations may do not depend on the genotypes of this SNP.

Adiponectin gene polymorphisms as a predictor for development of type 2 diabetes mellitus in Iraqi population.

BACKGROUND: Type 2 diabetes mellitus (T2DM) incidence is increasing globally and nationally. The etiology of the disease includes environmental and genetic factors. Polymorphism of adiponectin gene was found to be implicated in the pathogenesis of T2DM in numerous populations. METHODS: A case-control study was conducted to assess the association of rs2241766 and rs822395 SNPs of adiponectin gene (ADIPOQ) with T2DM in Iraqi population. The study included 400 patients with T2DM and 400 healthy individuals served as a control group. Serum lipid concentrations, insulin level and the index of insulin resistance (HOMA) were measured. The genotyping of ADIPOQ for rs2241766 and rs822395 SNPs was performed by PCR-RFLP. RESULTS: The genotype distribution of rs2241766 SNP indicated a significant increase of carriers of the homozygous GG (OR: 5.04, CI95%: 2.27-11.19, P: 0.0001) and heterozygous TG (OR: 1.7, CI95%: 1.22-2.39, P: 0.002) variants when compared with those of the wild type, suggesting a risk factor of 2 and 5 to develop the disease. The minor allele frequency (MAF) G was observed to be significantly (P: 0.0001) higher in patients (22%) when compared with the control group (11.74%). Results of rs822395 SNP failed to exhibit a significant difference. Changes of BMI, cholesterol, triglycerides, insulin and insulin resistance index values in the diabetic patients seemed to be parallel with the presence of MAF of rs2241766 SNP. CONCLUSION: The rs2241766T>G SNP of adiponectin gene is a risk factor for the development of T2DM in Iraqi population and directs the changes of serum lipid concentrations as well as insulin resistance.

Association of adiponectin gene polymorphism rs266729 with type two diabetes mellitus in Iraqi population. A pilot study.

BACKGROUND: Diabetes incidence is increasing worldwide. Many studies demonstrated that polymorphisms within the adiponectin gene could be associated with type 2 diabetes mellitus (T2DM). METHODS: A case-control study was conducted to find the association between SNP rs266729 and T2DM in Iraqi population. The study included 135 patients referring to diabetic clinic in Najaf city randomly selected based on World Health Organization (WHO) guidelines and 135 healthy controls. DNA was extracted from blood and genotyped by PCR-RFLP by using (HhaI) enzyme. Multinomial logistic regression was applied to compare the proportions of genotypes and alleles. The odds ratio for risk of developing T2DM was calculated with and without adjustment for age, sex, and BMI. RESULTS: The frequency of the G allele of rs266729 (C/G) polymorphism was significantly higher (p=0.00) in diabetic subjects (28%) compared to that in normal subjects (14%). The homozygous genotype (GG) significantly (OR=3.67, CI 95%(1.25-10.76), P=0.01) increased the risk of T2DM by three folds with respect to those of the wild type (CC) after adjustment for age, sex and BMI, furthermore the heterozygous CG genotype significantly (OR=2.45, CI 95%(1.41-4.26), P=0.001) raised the risk of T2DM by two folds. Homozygous and heterozygous genotypes of rs266729 polymorphism exhibited significant association with raised fasting insulin values (p=0.01), and decreased HDL levels (p=0.00). CONCLUSION: Adiponectin gene polymorphism rs266729 is involved in the pathogenesis of T2DM. In addition this SNP may play a role in the development of cardiovascular diseases and metabolic syndrome by affecting HDL and insulin levels.