Articles: function.
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The aim of this registry study was to evaluate the efficacy of Pycnogenol® in controlling signs/symptoms and temporary impairment of cognitive function (COFU) associated with jet lag. Previous flight studies have shown a decrease in the level of jet lag symptoms with Pycnogenol®. The control of jet lag signs/symptoms appeared to be correlated with flight-related microangiopathy and peripheral edema. Pycnogenol® - a standardized extract from the bark of French maritime pine - has significant antiedema, anti-inflammatory and antioxidant properties. ⋯ In conclusion, in this registry study Pycnogenol® was effective in preventing jet lag-related symptoms and preserving cognitive functions without tolerability problems. These observations should be tested in a larger group of subjects including complex individuals prone to edema (i.e. diabetics, hypertensive or older patients).
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The voltage-gated sodium channel Na V 1.7 is an essential component of human pain signaling. Changes in Na V 1.7 trafficking are considered critical in the development of neuropathic pain. SUMOylation of collapsin response mediator protein 2 (CRMP2) regulates the membrane trafficking and function of Na V 1.7. ⋯ Moreover, enhancing SENP1 expression did not affect the activity of TRPV1 channels or voltage-gated calcium and potassium channels. Intrathecal injection of CRISPRa SENP1 lentivirus reversed mechanical allodynia in male and female rats with spinal nerve injury. These results provide evidence that the pain-regulating effects of SENP1 overexpression involve, in part, the modulation of Na V 1.7 channels through the indirect mechanism of CRMP2 deSUMOylation.
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Volatile anesthetics induce hyperpolarizing potassium currents in spinal cord neurons that may contribute to their mechanism of action. They are induced at lower concentrations of isoflurane in noncholinergic neurons from mice carrying a loss-of-function mutation of the Ndufs4 gene, required for mitochondrial complex I function. The yeast NADH dehydrogenase enzyme, NDi1, can restore mitochondrial function in the absence of normal complex I activity, and gain-of-function Ndi1 transgenic mice are resistant to volatile anesthetics. The authors tested whether NDi1 would reduce the hyperpolarization caused by isoflurane in neurons from Ndufs4 and wild-type mice. Since volatile anesthetic behavioral hypersensitivity in Ndufs4 is transduced uniquely by glutamatergic neurons, it was also tested whether these currents were also unique to glutamatergic neurons in the Ndufs4 spinal cord. ⋯ Bypassing complex I by overexpression of NDi1 eliminates increases in potassium currents induced by isoflurane in the spinal cord. The isoflurane-induced potassium currents in glutamatergic neurons represent a potential downstream mechanism of complex I inhibition in determining minimum alveolar concentration.
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Curr Opin Anaesthesiol · Apr 2024
ReviewGuidelines in trauma-related bleeding and coagulopathy: an update.
The diagnosis and treatment of patients with severe traumatic bleeding and subsequent trauma-induced coagulopathy (TIC) is still inconsistent, although the implementation of standardized algorithms/treatment pathways was repeatedly linked to improved outcome. Various evidence-based guidelines for these patients now exist, three of which have recently been updated. ⋯ Treatment of trauma-related bleeding begins at the scene with local compression, use of tourniquets and pelvic binders and rapid transport to a certified trauma centre. After arrival at the hospital, measures to record, monitor and support coagulation function should be initiated immediately. Surgical bleeding control is carried out according to 'damage control' principles. Modern coagulation management includes individualized treatment based on target values derived from point-of-care viscoelastic test procedures.