Regulating eEF2 and eEF2K in skeletal muscle by exercise.

Skeletal muscle is a flexible and adaptable tissue that strongly responds to exercise training. The skeletal muscle responds to exercise by increasing muscle protein synthesis (MPS) when energy is available. One of protein synthesis's major rate-limiting and critical regulatory steps is the translation elongation pathway. The process of translation elongation in skeletal muscle is highly regulated. It requires elongation factors that are intensely affected by various physiological stimuli such as exercise and the total available energy of cells. Studies have shown that exercise involves the elongation pathway by numerous signalling pathways. Since the elongation pathway, has been far less studied than the other translation steps, its comprehensive prospect and quantitative understanding remain in the dark. This study highlights the current understanding of the effect of exercise training on the translation elongation pathway focussing on the molecular factors affecting the pathway, including Ca2+, AMPK, PKA, mTORC1/P70S6K, MAPKs, and myostatin. We further discussed the mode and volume of exercise training intervention on the translation elongation pathway.What is the topic of this review? This review summarises the impacts of exercise training on the translation elongation pathway in skeletal muscle focussing on eEF2 and eEF2K.What advances does it highlight? This review highlights mechanisms and factors that profoundly influence the translation elongation pathway and argues that exercise might modulate the response. This review also combines the experimental observations focussing on the regulation of translation elongation during and after exercise. The findings widen our horizon to the notion of mechanisms involved in muscle protein synthesis (MPS) through translation elongation response to exercise training.

Amyand's hernia: non incarcerated, inflamed appendix in inguinal sac case report.

Inguinal hernia is described as protrusion of abdominal structures into inguinal canal, such as intestinal loop and abdominal fascia. Appendix rarely bulges into inguinal canal which is called Amyand's hernia. A 55-year-old diabetic male presented to an outpatient clinic with right inguinal bulging since 2 years ago which was non-tender, without erythema and became non reducible since 2 days ago. Also bulging worsened by physical activity. The patient went through operation and an inflamed appendix was found stuck in hernia sac. Non incarcerated inguinal hernia can be diagnosed with physical examination and there is no need of further imaging which makes it hard to diagnose the nature of protrusion. Amyand's hernia usually presents with pain due to appendicitis which mimics incarcerated hernia and makes it easier to suspect the etiology and request for further investigation. However in this case, pain was suppressed and this patient was candidate for elective inguinal herniotomy.

Donepezil attenuates injury following ischaemic stroke by stimulation of neurogenesis, angiogenesis, and inhibition of inflammation and apoptosis.

Donepezil has proven to be an effective drug to reduce neuronal death and subsequently injury in neurodegenerative diseases. The current study evaluated the neuroprotective effects of donepezil in a rat model of ischaemic stroke and explored possible mechanisms which by this drug may reduce cell death. Temporary middle cerebral artery occlusion (tMCAO) was exerted for 45 min to induce ischaemic stroke. The animals were assigned into five groups: sham, control, and three groups treated with different doses of donepezil. Donepezil was intraperitoneally (IP) injected 4 h after reperfusion for 10 consecutive days. Infarct size was determined using TTC staining. The expression of proteins was evaluated using immunohistochemistry assays. Compared with the control group, infarct size was significantly reduced in tMCAO rats treated with different doses of donepezil. Moreover, our results showed significant decreased expression levels of apoptotic markers and pro-inflammatory mediators after treatment with different doses of donepezil for 10 days (P < 0.05). Likewise, significant increase of brain-derived neurotrophic factor (BDNF) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) proteins were found in tMCAO rats treated with donepezil compared with the control group (P < 0.05). Collectively, our findings show the validity of donepezil as a new therapeutic agent for attenuation of injury following ischaemic stroke through attenuation of inflammation and improvement of mitochondrial function, neurogenesis, and angiogenesis.