Obesity is a risk factor for several comorbidities and complications, including iron deficiency anemia. Iron deficiency anemia is a serious global public health problem, with a worldwide prevalence. The high prevalence of obesity in combination with iron deficiency incidence observed in different age and sex categories suggests an association between obesity and iron status. Obesity may disrupt iron homeostasis, resulting in iron deficiency anemia. The association between obesity and iron deficiency may be due to increased hepcidin levels mediated by chronic inflammation. Hepcidin is a small peptide hormone that functions as a negative regulator of intestinal iron absorption. Significant body weight loss in overweight and obese individuals decreases chronic inflammation and serum hepcidin levels, resulting in improved iron status due to increased iron absorption. However, further randomized controlled trials are required to confirm this effect. Contents 1. Introduction 2. Iron metabolism 3. Hepcidin and iron homeostasis 4. Obesity and low-grade chronic inflammation 5. Association between overweight and obesity, and iron status 6. Effect of weight loss on iron status 7. Future research and clinical implications 8. Conclusions

To date, natural products are widely used as pharmaceutical agents for many human diseases and cancers. One of the most popular natural products that have been studied for anticancer properties is thymoquinone (TQ). As a bioactive compound of Nigella sativa, TQ has shown anticancer activities through the inhibition of cell proliferation, migration, and invasion. The anticancer efficacy of TQ is being investigated in several human cancers such as pancreatic cancer, breast cancer, colon cancer, hepatic cancer, cervical cancer, and leukemia. Even though TQ induces apoptosis by regulating the expression of pro- apoptotic and anti-apoptotic genes in many cancers, the TQ effect mechanism on such cancers is not yet fully understood. Therefore, the present review has highlighted the TQ effect mechanisms on several signaling pathways and expression of tumor suppressor genes (TSG). Data from relevant published experimental articles on TQ from 2015 to June 2020 were selected by using Google Scholar and PubMed search engines. The present study investigated the effectiveness of TQ alone or in combination with other anticancer therapeutic agents, such as tyrosine kinase inhibitors on cancers, as a future anticancer therapy nominee by using nanotechnology.

ObjectiveSo far no studies have been performed in Malaysia to look at association of diabetes mellitus (DM) with blood groups. We studied the association of ABO blood groups with DM type 2.Patients and methodologyIt was a case control study conducted at Kepala Batas Hospital Batas, Penang, Malaysia in the year 2009, involving 70 patients with DM type 2 and 140 healthy controls. Ethical approval was obtained from Universiti Sains Malaysia. Blood samples were collected from the patients after consent. Samples were tested for ABO blood groups using ID-Card gel method.ResultsChi-square test results showed that there was an association between the ABO blood groups and DM type 2. It was found that A and O blood groups were negatively associated with DM type 2 (P<0.05) with higher percentage of A and O groups individuals were non-diabetic. No significant association was noted between DM type 2 and blood groups B (P=0.423) and AB (P=0.095). It was also noted that B blood group was distributed with highest percentage among patients with DM type 2 (53.71%) compared to controls (22.52%), but no statistical significance achieved.ConclusionThe results obtained suggest that there was a negative association between ABO blood groups A and O with DM type 2, with A and O group having less chances of diabetes. Large studies in other ethnic groups are needed to confirm these results.

BackgroundTumor-suppressor genes are inactivated by methylation in several cancers including acute myeloid leukemia (AML). Src homology-2 (SH2)-containing protein-tyrosine phosphatase 1 (SHP-1) is a negative regulator of the JAK/STAT pathway. Transcriptional silencing of SHP-1 plays a critical role in the development and progression of cancers through STAT3 activation. 5-Azacytidine (5-Aza) is a DNA methyltransferase inhibitor that causes DNA demethylation resulting in re-expression of silenced SHP-1. Lestaurtinib (CEP-701) is a multi-targeted tyrosine kinase inhibitor that potently inhibits FLT3 tyrosine kinase and induces hematological remission in AML patients harboring the internal tandem duplication of the FLT3 gene (FLT3-ITD). However, the majority of patients in clinical trials developed resistance to CEP-701. Therefore, the aim of this study, was to assess the effect of re-expression of SHP-1 on sensitivity to CEP-701 in resistant AML cells.MethodsResistant cells harboring the FLT3-ITD were developed by overexposure of MV4-11 to CEP-701, and the effects of 5-Aza treatment were investigated. Apoptosis and cytotoxicity of CEP-701 were determined using Annexin V and MTS assays, respectively. Gene expression was performed by quantitative real-time PCR. STATs activity was examined by western blotting and the methylation profile of SHP-1 was studied using MS-PCR and pyrosequencing analysis. Repeated-measures ANOVA and Kruskal–Wallis tests were used for statistical analysis.ResultsThe cytotoxic dose of CEP-701 on resistant cells was significantly higher in comparison with parental and MV4-11R-cep + 5-Aza cells (p = 0.004). The resistant cells showed a significant higher viability and lower apoptosis compared with other cells (p < 0.001). Expression of SHP-1 was 7-fold higher in MV4-11R-cep + 5-Aza cells compared to parental and resistant cells (p = 0.011). STAT3 was activated in resistant cells. Methylation of SHP-1 was significantly decreased in MV4-11R-cep + 5-Aza cells (p = 0.002).ConclusionsThe restoration of SHP-1 expression induces sensitivity towards CEP-701 and could serve as a target in the treatment of AML. Our findings support the hypothesis that, the tumor-suppressor effect of SHP-1 is lost due to epigenetic silencing and its re-expression might play an important role in re-inducing sensitivity to TKIs. Thus, SHP-1 is a plausible candidate for a role in the development of CEP-701 resistance in FLT3-ITD+ AML patients.

ObjectiveRegular physical activity is essential for lifelong optimal health. Contrarily, physical inactivity is linked with risk for many chronic diseases. This study was conducted to evaluate the physical activity levels and factors associated with physical inactivity among a multi-ethnic population of young men living in Saudi Arabia.MethodsThis is a cross-sectional study involving 3,600 young men (20–35 years) living in Riyadh, Saudi Arabia. Sociodemographic and physical activity data were collected from subjects by face-to-face interviews. Physical activity characteristics were evaluated by using the Global Physical Activity Questionnaire. Weight and height were measured following standardized methods, then body mass index was calculated.ResultsPhysical inactivity was reported among 24.9% of study subjects. The lowest and highest rates of physical inactivity were reported among subjects from the Philippines (14.0%) and Saudi Arabia (41.5%), respectively. There is a high variation in daily minutes spent on physical activities related to work, transport, recreation, vigorous and moderate-intensity physical activities and sedentary behaviors among study participants based on their nationalities. Nationality, increasing age, longer residency period in Saudi Arabia, living within a family household, having a high education level, earning a high monthly income, and increasing body mass index were significantly associated with a higher risk of physical inactivity among the study participants.ConclusionPhysical inactivity prevalence is relatively high among a multi-ethnic population of young men living in Saudi Arabia. The findings confirmed notable disparities in the physical activity characteristics among participants from different countries living in Saudi Arabia.