Zwitterionic Hydrogel Activates Autophagy to Promote Extracellular Matrix Remodeling for Improved Pressure Ulcer Healing

Pressure ulcer (PU) is a worldwide problem that is hard to heal because of its prolonged inflammatory response and impaired ECM deposition caused by local hypoxia and repeated ischemia/reperfusion. Our previous study discovered that the non-fouling zwitterionic sulfated poly (sulfobetaine methacrylate) (SBMA) hydrogel can improve PU healing with rapid ECM rebuilding. However, the mechanism of the SBMA hydrogel in promoting ECM rebuilding is unclear. Therefore, in this work, the impact of the SBMA hydrogel on ECM reconstruction is comprehensively studied, and the underlying mechanism is intensively investigated in a rat PU model. The in vivo data demonstrate that compared to the PEG hydrogel, the SBMA hydrogel enhances the ECM remolding by the upregulation of fibronectin and laminin expression as well as the inhibition of MMP-2. Further investigation reveals that the decreased MMP-2 expression of zwitterionic SBMA hydrogel treatment is due to the activation of autophagy through the inhibited PI3K/Akt/mTOR signaling pathway and reduced inflammation. The association of autophagy with ECM remodeling may provide a way in guiding the design of biomaterial-based wound dressing for chronic wound repair.

A Rare Complications of Sickle Cell Disease: Empyema and Chronic Subdural Hematoma

Sickle cell disease is a hemoglobinopathy responsible for many complications that are sometimes frightening. Brain damage is part of one of the complications that can affect the vital and/or functional prognosis of patients. We report two cases of neurological complications, patients with known homozygous sickle cell disease, admitted to the Resuscitation Service of the JRA University Hospital for neurological deficit of recent appearance. One presented a spontaneous bilateral chronic bilateral subdural hematoma, and the other an extradural empyema diagnosed on brain scan. The patients benefited from a neurosurgical intervention with favorable postoperative outcomes, marked by an improvement in neurological symptoms. This form of complication is relatively rare in patients with sickle cell disease. It is favoured by repeated vaso-occlusive crises responsible for vascular fragility following repeated ischemia and inflammatory phenomena. The surgical indication depends on the clinical condition and the radiological aspect

Motion Artefact in Voltage-Sensitive Fluorescent Dye Emission During Repeated Ischemia of Isolated Heart

Motion artefact (MA) in voltage-sensitive fluorescent signals causes significant debasement of action potential. During ischemia and reperfusion in isolated rabbit heart, this artefact develops in a manner which may be described by the time of its onset, level, and shape. The MA during ischemia: (a) may become substantial with approximately two minutes delay after establishing global ischemia; (b) may be almost twice as high as the physiological action potential and decreases both with time and repetition of ischemia; (c) the MA shape is unpredictable and depends on individual rabbit.

Repeated episodes of focal cerebral ischemia in a patient with mitral valve prolapse and migraine headache

Migraine is episodic, paroxysmal disorder where the headache represents the central symptom and is followed with different combinations of neurological gastrointestinal and vegetative changes. Not until the diagnostic procedures were developed, ischemic lesions were verified even in the patients with ordinary migraine. This is a report of a patient with migraine headache followed twice by verified episodes of temporary ischemic attacks and verified focal ischemic lesion of cerebral parenchyma. The mitral valve prolapse was also detected. This all imposed the administration of combined prophylactic antimigrainous and anticoagulant therapy as an imperative because of the risk of the development of repeated ischemia of cerebral tissue. This association also confirmed an opinion that migraine is a wider disorder with the dominant dysfunction of limbic system.