Background and Aim: Type 2 diabetes mellitus is a metabolic disease characterized by insulin resistance which gives it the place of chronic inflammatory disease. The aim of this study was to show the value of assaying us CRP in Type 2 Diabetics (T2DM) in the prediction of proathherogenic inflammation. Methods: This is a case-control study carried out in 33 T2DM followed in the metabolic diseases service of the University Hospital of Brazzaville (CHUB) between October and December 2020 and 30 controls separated into two subgroups, 15 subjects at risk intermediates and 15 professional athletes. Results: The comparison of the means of the concentrations of the biological parameters between the controls and the diabetic subjects of group I and group II showed a significant difference for CRP-us (p = 0.002), fasting blood glucose (p <0.0001) , the level of HBA1c (p <0.0001). A significant difference for creatinine was observed only for group II and controls. Conclusion: A correlation was obtained between CRP-us and fasting blood sugar, HBA1c, LDL-C and BMI. CRP-us is an excellent marker to predict the onset of vascular disease.

Background and Objective: Cardiovascular disease is the leading cause of morbidity and mortality in diabetic patients. The objective of this study was to determine the frequency of diabetic patients with a serum BNP level greater than 100 pg / ml and to establish the relationship between BNP and other variables. Methods: This is a cross-sectional study carried out in 50 diabetic patients admitted to the metabolic diseases department of the University Hospital of Brazzaville between May and October 2018. Results: A single type 2 diabetic patient presented a BNP = 187.4 pg / ml, a frequency of 2%. BNP level was associated with age (p = 0.005) and creatinine (p = 0.003). The small number of samples and an untargeted population did not allow us to profile BNP in diabetic patients. Conclusion: the mean BNP is high in diabetics in Congo Brazzaville despite a small sample size which does not allow the results to be generalized.

Background?Pulmonary arterial hypertension (PAH), a life-limiting condition characterized by dysfunction of pulmonary microvascular endothelium, is predisposed by mutations in several genes that are critical for the proper activation of specific bone morphogenetic protein (BMP) receptor complexes that phosphorylate intracellular Smad1/5/8 in endothelial cells. However, the functional importance of BMP-9 (GDF2), one of the high affinity ligands for ALK1 (ACVRL1) and BMPR-II (BMPR2), for the pulmonary microvasculature remains imperfectly understood. Objective—The aim of this study was first to determine the in vivo impact of BMP-9 deficiency on pulmonary vascular growth and remodeling, then to assess whether ALK1 expression can alter BMP-9 transcriptional signatures in human pulmonary microvascular endothelial cells (PMECs). Methods—CRISPR-Cas9 gene editing was used to create Gdf2 knockout rats in Sprague Dawley background. Computed micro-tomography (Micro-Ct) scan after Microfil perfusion was performed to generate high-resolution 3D-images of the pulmonary arterial tree. The influence of ALK1 abundance on the transcriptional signatures of BMP-9 responses in human PMECs was assessed by single cell (sc)-RNAseq. Functional studies were performed using human PMECs exposed to BMP-9, the ALK1/2 inhibitor ML347, and ALK1-Fc fusion protein that neutralizes BMP9/10 and two animal models of severe pulmonary hypertension (PH). Results—Micro-Ct angiography revealed structural and functional remodeling along the pulmonary vascular tree in BMP-9 deficient rats, resulting in vasodilation and increase in vascular density. scRNA-seq experiments identified distinct transcriptional signatures in human PMECs in response to BMP-9 responses. ALK1 expression had a direct impact on both proangiogenic capacities and transcriptional responses of PMECs to BMP-9. Functional studies performed in human PMECs confirmed that abundance of BMP-9 and ALK1 acted as modulators of PMEC tube formation, migration and proliferation, and also of vascular endothelial growth factor (VEGF)/VEGFR activities. The structural and functional remodeling observed in Gdf2 knockout rats coincided with a lower susceptibility to develop severe PH induced by monocrotaline (MCT) and SU5416+hypoxia (SuHx). Conclusion—BMP-9 and ALK1 are critical modulators of pulmonary vascular growth and remodeling. Our results provide potential mechanisms explaining why BMP-9 deficient animals are less susceptible to the rise in pulmonary vascular resistance in experimental models of PH.