A novel ruthenium(III)–pyrimidine Schiff base was synthesized and characterized using different analytical and spectroscopic techniques. Molecular geometries of the ligand and ruthenium complex were investigated using the DFT-B3LYP level of theory. The quantum global reactivity descriptors were also calculated. Various biological and molecular docking studies of the complex are reported to explore its potential application as a therapeutic drug. Cytotoxicity of the complex was screened against cancer colorectal (HCT116), breast (MCF-7 and T47D), and hepatocellular (HepG2) cell lines as well as a human normal cell line (HSF). The complex effectively inhibited the tested cancer cells with variable degree with higher activity towards HepG2 (IC₅₀ values were 29 μM for HepG2, 38.5 μM for T47D, 39.7 μM for HCT, and 46.7 μM for MCF-7 cells). The complex induced apoptosis and cell cycle arrest in the S phase of HepG2 cells. The complex significantly induced the expression of H2AX and caspase 3 and caspase 7 gene and the protein level of caspase 3, as well as inhibited VEGF-A and mTOR/AKT, SND1, and NF-kB gene expression. The molecular docking studies supported the increased total apoptosis of treated HepG2 cells due to strong interaction of the complex with DNA. Additionally, the possible binding interaction of the complex with caspase 3 could be responsible for the elevated activity of caspase 3–treated cells. The score values for the two receptors were −3.25 and −3.91 kcal/mol.

Background: A variety of HIV-related endocrine dysfunctions including adrenal, gonadal and thyroid disorders have been reported. We aimed to compare between the markers of thyroid function in newly diagnosed HIV-infected patients and healthy volunteers as a control group. The prevalence of the thyroid abnormalities in HIV-infected patients was assessed and the levels of thyroid autoantibodies were also determined. Methods: A total of 100 newly diagnosed HIV-infected patients having a CD4 cell count of 180–350 cells/mm³ were enrolled in the study. Same number of healthy volunteers were also included for comparison. Measurements of thyroid function tests including thyroid-stimulating hormone (TSH), free thyroxin and free triiodothyronine levels beside thyroid autoantibodies, including antithyroglobulin (ATBG) and antithyroid peroxidase (ATPO), were carried out for all patients and volunteers. Results: In total, 70% of HIV-infected patients had normal thyroid function tests when compared with control individuals, while 30% of HIV-infected patients had abnormal thyroid function. Of the 30 cases, 11 cases had abnormal TSH values, with increased TSH predominant (7% of HIV cases) than decreased TSH (4% of patients) values. Incidence of thyroid abnormalities ranging from hypothyroidism (subclinical and overt: 6% and 1%, respectively) to hyperthyroidism (2%) and nonthyroidal illness (9%) were estimated in HIV-infected patients. The values of thyroid autoantibodies were almost normal in HIV-infected patients, except the three cases presented with elevated ATBG, indicating that thyroid abnormalities were not due to elevated ATBG and ATPO. Conclusions: Thyroid hormones are of great importance and due to high prevalence of thyroid function abnormality, it is recommended that thyroid function tests should be monitored in all HIV-infected patients before starting the treatment.

Vitamin D deficiency (VDD) and anemia are both public health nutrition concerns. An association between VDD and anemia has been suggested in various healthy and diseased populations. The current study aimed to elucidate the effect of VDD on iron status in children with type I diabetes mellitus (T1DM). The study recruited two groups of children with T1DM: control group comprised of 38 T1DM children with sufficient vitamin D (> 30 ng/ml) and a case group, consisted of 52 T1DM children with VDD (< 20 ng/ml). Both groups had comparable gender, age, BMI, and disease duration. The laboratory measurements included analysis of blood indices, markers of iron metabolism, hepcidin and inflammatory markers included interleukin 6 (IL-6) and C-reactive protein (CRP). Compared to control group, T1DM children with VDD differs specifically in terms of some markers of blood indices, such as decreased hemoglobin and increased red blood cell distribution width. Moreover, decreased serum iron, ferritin, total iron-binding capacity and transferrin along with elevated inflammatory markers were observed in case group. Results of the study indicated that VDD had increased the risk of iron deficiency anemia in children with T1DM as well as inflammatory related anemia. Furthermore, in T1DM children, VDD had raised the incidence of both absolute and functional iron deficiency, with greater incidence of the former. This study may indicate that VDD may be a risk factor that may worsen iron deficiency anemia in T1DM.

Preeclampsia (PE) is characterized by new onset hypertension and proteinuria. Undoubtedly, some individuals do not fit precisely into this description, and it could be challenging to spot newly developed PE in females who already have hypertension or renal illness. Monitoring the disease's progression enables the optimization of delivery time while minimizing premature births. The current study explores the diagnostic benefits of serum endostatin and cystatin C in addition to serum and urinary magnesium (Mg) and fractional excretion magnesium (FEMg) for early prediction of PE. The population sample included 82 pregnant women divided into 3 groups: normal pregnancy group served as a control (n = 26), nonpreeclampsia (NPE, n = 34) group included pregnant women with one or more risk factors but did not progress to PE, and pregnant women who developed preeclampsia (PE, n = 22) group. Blood samples were withdrawn at two sampling times: at 12th to 16th and 24th to 26th weeks of gestation. Compared to normal pregnancy, results (X̅ ± SD) indicated a significant increase in serum endostatin in NPE at the first sample (10.78 ± 3.63 ng/mL) and the second sample (28.03 ± 3.79 ng/mL), while cystatin C was at the first sample (0.68 ± 0.06 mg/dL) and the second sample (0.71 ± 0.07 mg/dL). In the PE group, the serum endostatin was 18.86 ± 4.37 ng/mL at the first sampling time and 53.56 ± 9.76 ng/mL for the second sample. Serum cystatin C was also elevated in PE with X̅ ± SD equivalent to 0.73 ± 0.08 and 0.89 ± 0.08 mg/dL at the first and second samples, respectively. On the other hand, serum and urinary Mg in addition to FEMg levels did not significantly differ across the groups under study. Receiver operating characteristic (ROC) curve analysis proved that both endostatin and cystatin C could be good indicators for PE. The findings imply that measuring endostatin and cystatin C at early pregnancy and before progression to PE may be effective in detecting the likelihood of PE. Endostatin could be more precise and sensitive in assessing the probability of PE than cystatin C; however, coupling of the two parameters may be promising.

Gestational diabetes mellitus (GDM) is among the most common complications during pregnancy. It is characterized by hyperglycemia that is first identified during pregnancy, typically in the second or third trimesters. However, the relatively late diagnosis limits timely glycemic control and preventive interventions. The present study aimed to evaluate the diagnostic potential of serum afamin and fibroblast growth factor 21 (FGF21) as early predictive biomarkers for GDM. The study involved 17 healthy pregnant women and 26 pregnant women with one or more risk factors for developing GDM. Fasting blood samples were collected in the 1st (8–12 weeks) and 2nd (22–28 weeks) trimesters of pregnancy. Higher serum afamin level was observed in GDM group at 1st trimester (92.9 ± 34.51 ng/ml) compared to normal pregnancy (57.1 ± 25.15 ng/ml). At 2nd trimester, no significant difference in circulated serum afamin was noted between the two groups (73.2 ± 20.30 ng/ml and 68.3 ± 18.74 ng/ml, for GDM and normal pregnancy, respectively). The study also indicated higher serum FGF21 in pregnancy complicated with GDM compared to normal pregnancy at both sampling times (1st trimester: 140.8 ± 32.83 and 97.1 ± 21.43 Pg/ml for GDM and normal; 2nd trimester: 123.8 ± 41.85 and 89.4 ± 32.53 Pg/ml for GDM and normal). At 1st trimester no significant correlations were noted between afamin and all parameters in normal pregnancy, however, in pregnancy complicated with GDM, positive correlations were noted between the hormone and the diabetic profile parameters and baby birth weight. At both 1st and 2nd trimesters, no correlation between FGF21 with all tested parameters, either in normal or complicated pregnancies. ROC curve analysis demonstrated that afamin (AUC = 0.826, P < 0.001), FGF21 (AUC = 0.877, P < 0.001), and their combined assessment (AUC = 0.9, P < 0.001) were strong predictors of GDM development at 1st trimester before the development of the disease than expectant mothers with normal pregnancy.