Detection of some virulence factors genes in Staphylococcus aureus isolated from different clinical cases

Staphylococcus aureus is one of the most important pathogenic type to humans, and the most common species responsible for a wide range of diseases such as furuncles, various abscesses, wounds abscesses resulting from surgical operations, dermatitis, soft tissue inflammation, arthritis, bones inflammation, bronchial pneumonia, inflammation of internal parts of the heart and injuries caused by toxins such as toxic shock syndorome and staphylococcus aureus syndrome and food poisoning. The current study aimed by finding the genes responsible for the virulence factors in S. aureus isolates by using the Single and Multiplex PCR mechanism (technology). A total of 60 specimens (urine, burn swabs, wound swaabs) from different clinical cases were collected from patients (in different age groups) who admitted to several health centers in Al-Diwaniyah Teaching Hospital, Iraq, during a period extending from October 2016 to January 2017. Some virulence factors were investigated for 30 isolate only of MRSA using Single and Multiplex PCR for detection virulence factor genes which both coa gene encoding production of coagulase, clfA gene encoding for clumpting factor, spa gene encoding for protein A, fnbA gene encoding for fibronectin binding proteins, luks gene encoding prouction of Panton Valentine Leukocidin (PVL). Results 30 (100%) were possess coa, clfA, spa and fnbA genes, 13 (43.3%) were possess luks gene

Effects of a brief high-fat diet and acute exercise on the mTORC1 and IKK/NF-κB pathways in rat skeletal muscle.

One exercise session can improve subsequent insulin-stimulated glucose uptake by skeletal muscle in healthy and insulin-resistant individuals. Our first aim was to determine whether a brief (2 weeks) high-fat diet (HFD) that caused muscle insulin resistance would activate the mammalian target of rapamycin complex 1 (mTORC1) and/or inhibitor of κB kinase/nuclear factor κB (IKK/NF-κB) pathways, which are potentially linked to induction of insulin resistance. Our second aim was to determine whether acute exercise that improved insulin-stimulated glucose uptake by muscles would attenuate activation of these pathways. We compared HFD-fed rats with rats fed a low-fat diet (LFD). Some animals from each diet group were sedentary and others were studied 3 h postexercise, when insulin-stimulated glucose uptake was increased. The results did not provide evidence that brief HFD activated either the mTORC1 (including phosphorylation of mTOR(Ser2448), TSC2(Ser939), p70S6K(Thr412), and RPS6(Ser235/236)) or the IKK/NF-κB (including abundance of IκBα or phosphorylation of NF-κB(Ser536), IKKα/ß(Ser177/181), and IκB(Ser32)) pathway in insulin-resistant muscles. Exercise did not oppose the activation of either pathway, as evidenced by no attenuation of phosphorylation of key proteins in the IKK/NF-κB pathway (NF-κB(Ser536), IKKα/ß(Ser177/181), and IκB(Ser32)), unaltered IκBα abundance, and no attenuation of phosphorylation of key proteins in the mTORC1 pathway (mTOR(Ser2448), TSC2(Ser939), and RPS6(Ser235/236)). Instead, exercise induced greater phosphorylation of 2 proteins of the mTORC1 pathway (PRAS40(Thr246) and p70S6K(Thr412)) in insulin-stimulated muscles, regardless of diet. Insulin resistance induced by a brief HFD was not attributable to greater activation of the mTORC1 or the IKK/NF-κB pathway in muscle, and exercise-induced improvement in insulin sensitivity was not attributable to attenuated activation of these pathways in muscle.