The role of adipokines and ghrelin in interactions and clinical implications in childhood obesity.

BACKGROUND: Childhood obesity is a growing global health concern, especially prevalent in the Arabian Peninsula, and is known to contribute to metabolic syndrome and insulin resistance. This study aimed to investigate the interplay between adipokines (leptin and adiponectin), ghrelin, and insulin homeostasis in childhood obesity. MATERIAL AND METHODS: A case-control study was conducted in Babylon involving 120 children/adolescents (7-17 years). The participants were divided into two groups: 60 obese and 60 healthy controls. Anthropometric and biochemical measures were examined, applying World Health Organization (WHO) growth standards to categorize weight status. Data on blood lipids, glucose, adipokines, and ghrelin were collected in Babylon (Merjan Medical City), ensuring accuracy and providing insights into pediatric obesity's metabolic and hormonal status. RESULT: Clinical, anthropometric, and laboratory attributes of children were evaluated, with classification as normal-weight or obese based on BMI/Z-score and Waist Circumference. The obese group exhibited elevated triglycerides and insulin levels, as well as reduced adiponectin levels (P ≤ 0.001). Leptin levels showed a positive correlation with BMI/Z-score (r = 0.352, P = 0.006). A diagnostic model demonstrated the significant diagnostic capacity of leptin (AUC > 99%) and its importance in predicting childhood obesity. Each unit increase in leptin elevated the probability of obesity by a factor of 1.197 (95% CI: 1.0507-1.3632, P = 0.0068). CONCLUSION: The study revealed significant differences in clinical, biochemical, and biological markers of obesity between the research groups and the control group. Leptin emerged as a significant predictor of obesity, demonstrating high diagnostic accuracy. The complex interactions among these adipokines underscore the necessity for comprehensive obesity management strategies.

Comparison of some hematological parameters between male and female patients infected with COVID-19.

BACKGROUND: COVID-19 is a highly contagious virus that is rapidly spreading across the world. As the number of COVID-19 patients is quickly rising, and certain nations and areas, such as the third world countries, lack the medical resources, it is critical to track and monitor a patient's status using blood parameters on regular testing. The aim of this study is to compare the serum D-dimer levels, Ferritin, CRP, WBCs, Lymphocytes, and Neutrophils in male and female patients infected with COVID-19. OBJECTIVE AND METHODS: The study procedure includes evaluating the D-dimer level, Ferritin, CRP, WBCs, lymphocytes, and neutrophils in 116 patients infected with COVID-19 (48 Females and 68 Males). RESULT: The result of this study shows a significant increase in the D-dimer level in males 1618 ± 247.7 ng/ml compared to females 684.5 ± 53.69 ng/ml and a significant increase in Ferritin level in males 525.6 ± 69.55 µg/L compared to females 254.1 ± 33.73 µg/L. However, no other significant change is seen in the other parameters (CRP, LDH, and WBCs, L, and N) although all of these parameters are abnormal, compared to the normal reference values. CONCLUSION: This study concludes that there is a significant increase in the D-dimer and Ferritin concentrations in male patients compared to female patients, who were infected with COVID-19. Also there are no significant differences in other parameters (CRP, LDH, WBCs, L, and N) between male and female patients.

Newcastle disease virus suppress glycolysis pathway and induce breast cancer cells death.

Newcastle disease virus (NDV) can modulate cancer cell signaling pathway and induce apoptosis in cancer cells. Cancer cells increase their glycolysis rates to meet the energy demands for their survival and generate ATP as the primary energy source for cell growth and proliferation. Interfering the glycolysis pathway may be a valuable antitumor strategy. This study aimed to assess the effect of NDV on the glycolysis pathway in infected breast cancer cells. Oncolytic NDV attenuated AMHA1 strain was used in this study. AMJ13 and MCF7 breast cancer cell lines and a normal embryonic REF cell line were infected with NDV with different multiplicity of infections (moi) to determine the IC50 of NDV through MTT assay. Crystal violet staining was done to study the morphological changes. NDV apoptosis induction was assessed using AO/PI assay. NDV interference with the glycolysis pathway was examined through measuring hexokinase (HK) activity, pyruvate, and ATP concentrations, and pH levels in NDV infected and non-infected breast cancer cells and in normal embryonic cells. The results showed that NDV replicates efficiently in cancer cells and spare normal cells and induce morphological changes and apoptosis in breast cancer cells but not in normal cells. NDV infected cancer cells showed decreased in the HK activity, pyruvate and ATP concentrations, and acidity, which reflect a significant decrease in the glycolysis activity of the NDV infected tumor cells. No effects on the normal cells were observed. In conclusion, oncolytic NDV ability to reduce glycolysis pathway activity in cancer cells can be an exciting module to improve antitumor therapeutics.

Hexokinase inhibition using D-Mannoheptulose enhances oncolytic newcastle disease virus-mediated killing of breast cancer cells.

BACKGROUND: Most cancer cells exhibit increased glycolysis and use this metabolic pathway cell growth and proliferation. Targeting cancer cells' metabolism is a promising strategy in inhibiting cancer cell progression. We used D-Mannoheptulose, a specific hexokinase inhibitor, to inhibit glycolysis to enhance the Newcastle disease virus anti-tumor effect. METHODS: Human breast cancer cells were treated by NDV and/or hexokinase inhibitor. The study included cell viability, apoptosis, and study levels of hexokinase enzyme, pyruvate, ATP, and acidity. The combination index was measured to determine the synergism of NDV and hexokinase inhibitor. RESULTS: The results showed synergistic cytotoxicity against breast cancer cells by combination therapy but no cytotoxic effect against normal cells. The effect was accompanied by apoptotic cell death and hexokinase downregulation and inhibition to glycolysis products, pyruvate, ATP, and acidity. CONCLUSIONS: The combination treatment showed safe significant tumor cell proliferation inhibition compared to monotherapies suggesting a novel strategy for anti-breast cancer therapy through glycolysis inhibition by hexokinase downregulation.