Is there a role for the pharmacist in screening for metabolic syndrome?

Evidence for a pharmacist role in the screening of MetS has been shown to be effective in at risk populations. Despite migrants being an at risk group for the development of MetS, no literature has described screening of migrants by pharmacists. The aim of this research was therefore to identify the impact of the pharmacist role in screening migrants on arrival in a Middle Eastern country and following 24 months of residency in the Middle East. This was a prospective longitudinal observational study. Migrants aged 18–65 years were informed about the research by pharmacists and consented to participate. Baseline screening for MetS risk factors was conducted. Parameters included glycated haemoglobin (HbA1c), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), blood pressure (BP) and waist circumference (WC). All migrants with identified metabolic abnormalities at this screening stage were referred to physicians by the pharmacist for further management. Migrants with normal metabolic parameters at baseline were invited to be re-screened by pharmacists. This will allow identification of an increase in any incidence of MetS, and will allow for earlier intervention and management. Of the 1379 identified migrants, 460 consented to participate; 70% were men and 82.2% (378) were Asians. Pharmacist-led screening revealed 13.9% (64) with abnormal BP, 6.7% (31) with pre-diabetes, 21.4% (91) with elevated TG, 25% (115) with low HDL–C and 47% (219) with high WC. 16% (75) were found to have MetS and were referred to the physician for follow-up. These participants were consequently identified as at risk for development of MetS at a much earlier stage. A total of 199 migrants with normal metabolic parameters will be followed-up following 24 months of residency in the Middle East. Throughout the study, migrants with metabolic abnormalities were referred by pharmacists to physicians for further management. The study indicates that pharmacist screening is effective for early identification and potential early management of MetS in this migrant population

Sanguinarine mediated apoptosis in Non-Small Cell Lung Cancer via generation of reactive oxygen species and suppression of JAK/STAT pathway

Effective treatment of lung cancer remains a significant clinical challenge due to its multidrug resistance and side effects of the current treatment options. The high mortality associated with this malignancy indicates the need for new therapeutic interventions with fewer side effects. Natural compounds offer various benefits such as easy access, minimal side effects, and multi-molecular targets and thus, can prove useful in treating lung cancer. Sanguinarine (SNG), a natural compound, possesses favorable therapeutic potential against a variety of cancers. Here, we examined the underlying molecular mechanisms of SNG in Non-Small Cell Lung Cancer (NSCLC) cells. SNG suppressed cell growth and induced apoptosis via downregulation of the constitutively active JAK/STAT pathway in all the NSCLC cell lines. siRNA silencing of STAT3 in NSCLC cells further confirmed the involvement of the JAK/STAT signaling cascade. SNG treatment increased Bax/Bcl-2 ratio, which contributed to a leaky mitochondrial membrane leading to cytochrome c release accompanied by caspase activation. In addition, we established the antitumor effects of SNG through reactive oxygen species (ROS) production, as inhibiting ROS production prevented the apoptosis-inducing potential of SNG. In vivo xenograft tumor model further validated our in vitro findings. Overall, our study investigated the molecular mechanisms by which SNG induces apoptosis in NSCLC, providing avenues for developing novel natural compound-based cancer therapies

The effect of migration on the incidence of new-onset metabolic syndrome in migrants to Qatar

Background: There is substantial evidence that migration to Western countries is associated with an increased risk of metabolic syndrome (MetS) 1 . However, there is a paucity of data on the incidence of MetS in migrants from different countries coming to Qatar. As a result, an important health problem is overlooked, and prevention measures are absent. This study aimed to investigate the effects of migration on the incidence of MetS following 24 months of residency in the Middle East (ME) among a group of migrants employed at Hamad Medical Corporation (HMC). Methods: This is a prospective longitudinal observational study. Migrants aged 18-65 years who joined HMC from June to December 2017 were invited to consent and participate. Baseline screening for MetS was conducted. Parameters included glycated hemoglobin (HbA1c), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), blood pressure (BP), and waist circumference (WC) measurement. Migrants with normal metabolic parameters at baseline were invited to be rescreened 24 months post-migration. The International Diabetes Federation (IDF) Consensus Worldwide Definition of MetS was employed to diagnose MetS 2 . Inferential statistics were applied to compare results before and after migration. Throughout the study, migrants with metabolic abnormalities were referred to physicians for further management. Results: Of the 1,379 screened migrants, 472 consented to participate. Of those, only 205 migrants had normal metabolic parameters. The incidence of MetS within the group with normal parameters rose to 17% (n = 27) after 24 months of residing in Qatar. Eighty-one percent (n = 129) developed at least one element of MetS. Migrants receiving medications that potentially induce MetS were more likely to develop MetS (odds ratio OR [(AOR 6.3, p < 0.001); 95% [CI], 0.07-0.59. p = 0.003). Conclusion: The incidence of MetS amongst migrants increases following residency in Qatar however, it is lower than that estimated in many developed countries (3, 4).qscienc

Greensporone A, a Fungal Secondary Metabolite Suppressed Constitutively Activated AKT via ROS Generation and Induced Apoptosis in Leukemic Cell Lines

Greensporone A is a fungal secondary metabolite that has exhibited potential in vitro for anti-proliferative activity in vitro. We studied the anticancer activity of greensporone A in a panel of leukemic cell lines. Greensporone A-mediated inhibition of proliferation is found to be associated with the induction of apoptotic cell death. Greensporone A treatment of leukemic cells causes inactivation of constitutively activated AKT and its downstream targets, including members GSK3 and FOXO1, and causes downregulation of antiapoptotic genes such as Inhibitor of Apoptosis (IAPs) and Bcl-2. Furthermore, Bax, a proapoptotic member of the Bcl-2 family, was found to be upregulated in leukemic cell lines treated with greensporone A. Interestingly, gene silencing of AKT using AKT specific siRNA suppressed the expression of Bcl-2 with enhanced expression of Bax. Greensporone A-mediated increase in Bax/Bcl-2 ratio causes permeabilization of the mitochondrial membrane leading to the accumulation of cytochrome c in the cytoplasm. Greensporone A-induced cytochrome c accumulation causes the activation of caspase cascade and cleavage of its effector, poly(ADP-ribose) polymerase (PARP), leading to apoptosis. Greensporone A-mediated apoptosis in leukemic cells occurs through the generation of reactive oxygen species (ROS) due to depletion of glutathione (GSH) levels. Finally, greensporone A potentiated the anticancer activity of imatinib in leukemic cells. In summary, our study showed that greensporone A suppressed the growth of leukemic cells via induction of apoptotic cell death. The apoptotic cell death occurs by inhibition of AKT signaling and activation of the intrinsic apoptotic/caspase pathways. These results raise the possibility that greensporone A could be developed as a therapeutic agent for the treatment of leukemia and other hematological malignancies