The paper is to investigate eco-design flaws in equipments for medical simulation training and explore methods to improve. The eco-design flaws in equipments for medical simulation training were elaborated from the aspects of accessories, modules, model volumes, recycling of waste equipments, and production materials. The improved methods of the flaws were demonstrated. The designs of equipments for medical simulation training can be more environment friendly by means of getting rid of unnecessary accessories, developing replaceable modules for manikin models, curtailing volumes of equipments, recycling waste equipment and using degradable production materials. As the tendency of being environment friendly in medical equipments becomes increasingly obvious, the eco-friend merits must be considered by multi-objective optimizations in the processes of design, manufacture, and employment of equipments for medical simulation training.

Objective To evaluate the value of cranial MRI on diagnosing nonalcoholic Wernickes encephalopathy (WE). Methods The clinical characters, cranial MRI features, and outcomes materials in six cases of nonalcoholic Wernickes encephalopathy were analyzed.Results Cranial MR and Flair imaging of the patients exhibited areas of increased T 2W and flair signals symmetrically surrounding the aqueduct and third ventricle and within the medial thalamus. One patient who became persistent vegetative state coexistenced increased T 2W and flair signal of the cortex. According to the follow-up results, the alterations of four patients in T 2W and Flair signals showed to resolve being consistent with the clinical recovery. One patient with persistent vegetative state had no change within two years of the follow-up.Conclusions Cranial MRI is of great value in diagnosing nonalcoholic Wernickes encephalopathy and reflects appropriately the pathological evolution of this disease.

AIM: To study the protective effect of bone marrow stromal cells (MSCs) on ischemia /reperfusion hippocampal slices. METHODS: Ischemia/reperfusion models of hippocampal slices from newborn rats were established. MSCs obtained from adult bone marrow were cultured, isolated and purified. Cell death was assessed using propidium iodide fluorescence. And brain-derived neurotrophic factor (BDNF) expression in MSCs was determined by immunocytochemistry and Western blot. RESULTS: Maximal dead cells appeared in hippocampal slices 3 to 7 days after reperfusion. When the slices were co-cultured with MSCs, only a few cells were dead. The protective effect of MSCs on the slices was diminished significantly when anti-BDNF antibody was added to the medium. The protein of BDNF was faintly expressed in MSCs under normal conditions. When MSCs were co-cultured with ischemia /reperfusion hippocampal slices, the expression of BDNF in MSCs was increased gradually especially when co-cultured for 3 to 7 days. However, MSCs co-cultured with normal hippocampal slices expressed BDNF at a lower level at any times of co-culture. CONCLUSIONS: In an in vitro model of simulated ischemia, MSCs reduce cell death. Ischemia/reperfusion hippocampal slices co-cultured with MSCs promote the expression of BDNF in MSCs, which in turn protect the ischemic neurons.

A patient with multiple ischemic stroke due to spontaneous bilateral internal carotid artery dissection (ICAD) was reported and the epidemiology, neuroimaging, clinical characteristics and treatment of spontaneous bilateral ICAD were reviewed.Spontaneous bilateral ICAD mostly occurs in young and middle-aged individuals and the clinical manifestations are mainly stroke(71.1%), headache and neck pain(62.2%), Horner's syndrome(15.6%) and cranial nerve palsy(11.1%).Cervical axial T1-weighted fat-suppressed image is an alternative to DSA to make the definite diagnosis.Antithrombotic therapy is regularly used and the general clinical outcome is good.Cervical arterial dissection is one of the most common causes of stroke in young and middle-aged patients.Cervical MRI T1-weighted fat suppressed image is crucial for timely diagnosis and initiation of appropriate clinical intervention.

Our previous studies proposed that Alzheimer's disease (AD) is a metabolic disorder and hypothesized that abnormal brain glucose metabolism inducing multiple pathophysiological cascades contributes to AD pathogenesis. Aging is one of the great significant risk factors for AD. Membrane aging is first prone to affect the function and structure of the brain by impairing glucose metabolism. We presume that risk factors of AD, including genetic factors (e.g., the apolipoprotein E ε4 allele and genetic mutations) and non-genetic factors (such as fat, diabetes, and cardiac failure) accelerate biomembrane aging and lead to the onset and development of the disease. In this review, we further modify our previous hypothesis to demonstrate "membrane aging" as an initial pathogenic factor that results in functional and structural alterations of membranes and, consequently, glucose hypometabolism and multiple pathophysiological cascades.
Aging ; pathology ; Alzheimer Disease ; etiology ; pathology ; Animals ; Brain ; pathology ; Cell Membrane ; pathology ; Humans

The physiological functions of endogenous amyloid-β (Aβ), which plays important role in the pathology of Alzheimer's disease (AD), have not been paid enough attention. Here, we review the multiple physiological effects of Aβ, particularly in regulating synaptic transmission, and the possible mechanisms, in order to decipher the real characters of Aβ under both physiological and pathological conditions. Some worthy studies have shown that the deprivation of endogenous Aβ gives rise to synaptic dysfunction and cognitive deficiency, while the moderate elevation of this peptide enhances long term potentiation and leads to neuronal hyperexcitability. In this review, we provide a new view for understanding the role of Aβ in AD pathophysiology from the perspective of physiological meaning.
Humans ; Alzheimer Disease/pathology* ; Amyloid beta-Peptides/metabolism* ; Long-Term Potentiation ; Synaptic Transmission/physiology* ; Hippocampus

Brain ; pathology ; China ; Humans ; Organ Preservation ; standards ; Tissue Banks ; ethics ; standards