Allogeneic human umbilical cord blood for acute ischemic stroke: Phase I clinical trial.

Objectives: Transplantation of human umbilical cord blood cells (hUCB) may enhance neuroprotection, and thus, the intravenous (IV) infusion of hUCB in patients with acute ischemic stroke (AIS) is being tested for its safety and efficacy.

Materials And Methods: We conducted a 12-month, open-label, and single-center, phase I trial of hUCB treatment in AIS patients at the age of 45-80 years, with magnetic resonance imaging evidence of acute infarction in the internal carotid artery supplied territory and the National Institute of Health Stroke Scale (NIHSS) score between 6 and 18. Eligible participants received a single-dose IV infusion of hUCB followed by the two doses of mannitol infusion within 9 days after the onset of stroke symptoms.

Modulation of parietal cytokine and chemokine gene profiles by mesenchymal stem cell as a basis for neurotrauma recovery.

Background & Purpose: Following traumatic brain injury (TBI), primary mechanical injury to the brain may cause blood-brain-barrier damage followed by secondary injury, ultimately culminating in cell death. We aimed to test whether one injection of mesenchymal stem cells (MSC) derived from the human umbilical cord can modulate brain cytokine and chemokine gene profiles and attenuate neurological injury in rats with TBI.

Methods: One-day post-TBI, the injured rats were treated with one injection of MSC (4 × 10/rat, i.

Vascular, Cognitive, and Psychomental Survey on Elderly Recycling Volunteers in Northern Taiwan.

Stroke and dementia represent frequent causes of psychophysical and socioeconomic burdens. We conducted a vascular, cognitive, and psychomental survey involving elderly volunteers at community-based recycling stations in Northern Taiwan. Recycling volunteers aged ≥60 years were surveyed.

EphA2-positive human umbilical cord-derived mesenchymal stem cells exert anti-fibrosis and immunomodulatory activities via secretion of prostaglandin E2.

Objective: Previous study has demonstrated that EphA2 is a biomarker of mesenchymal stem cells (MSCs) from human placenta or umbilical cord and is able to distinguish MSCs from fibroblasts. In this study, we further examine the potential efficacy of EphA2 human umbilical cord-derived MSCs (hUC-MSCs).

Materials And Methods: MSCs specific markers, EphA2 and CD146 expression on the surface of hUC-MSCs were determined by flow cytometry analysis.

MRI tracking of polyethylene glycol-coated superparamagnetic iron oxide-labelled placenta-derived mesenchymal stem cells toward glioblastoma stem-like cells in a mouse model.

Mesenchymal stem cells (MSCs) that display homing and infiltration properties towards tumor cells are a promising cellular targeting vector for brain tumor therapy but are limited to local-regional delivery in current preclinical models. Here, we investigated whether placenta-derived MSCs (P-MSCs) are a superior cellular vector for systemic targeting of glioblastoma stem-like cells (GSCs), with an imaging modality to real-time monitor the trafficking P-MSCs to glioblastoma sites. Results demonstrated that P-MSCs had greater migratory activity towards GSCs and across blood-brain barrier compared with bone marrow-derived MSCs, and this activity was enhanced by hypoxia precondition.

Impact of code stroke on thrombolytic therapy in patients with acute ischemic stroke at a secondary referral hospital in Taiwan.

Background: Efficacy of thrombolytic therapy decreases with time elapsed from symptom onset. We sought to identify the impact of code stroke on the thrombolytic therapy.

Methods: Code stroke is activated by the emergency physician when a patient is eligible for thrombolytic therapy.

Nuclear targeting of the betanodavirus B1 protein via two arginine-rich domains induces G1/S cell cycle arrest mediated by upregulation of p53/p21.

The molecular functions of betanodavirus non-structural protein B and its role in host cell survival remain unclear. In the present study, we examined the roles of specific nuclear targeting domains in B1 localization as well as the effect of B1 nuclear localization on the cell cycle and host cell survival. The B1 protein of the Red spotted grouper nervous necrosis virus (RGNNV) was detected in GF-1 grouper cells as early as 24 hours post-infection (hpi).

CD34 human placenta-derived mesenchymal stem cells protect against heat stroke mortality in rats.

CD34 is a transmembrane phosphoglycoprotein used to selectively enrich bone marrow in hematopoietic stem cells for transplantation. Treating rats with CD34 cells derived from human umbilical cord blood before or after heat stroke has been shown to promote survival. We investigated whether CD34 human placenta-derived stem cells (PDMSCs) could improve survival following heat stroke in rats.

Human Umbilical Cord Mesenchymal Stem Cells Preserve Adult Newborn Neurons and Reduce Neurological Injury after Cerebral Ischemia by Reducing the Number of Hypertrophic Microglia/Macrophages.

Microglia are the first source of a neuroinflammatory cascade, which seems to be involved in every phase of stroke-related neuronal damage. Two weeks after transient middle cerebral artery occlusion (MCAO), vehicle-treated rats displayed higher numbers of total ionized calcium-binding adaptor molecule 1 (Iba-1)-positive cells, greater cell body areas of Iba-1-positive cells, and higher numbers of hypertrophic Iba-1-positive cells (with a cell body area over 80 μm) in the ipsilateral ischemic brain regions including the frontal cortex, striatum, and parietal cortex. In addition, MCAO decreased the number of migrating neuroblasts (or DCX- and 5-ethynyl-2'-deoxyuridine-positive cells) in the cortex, subventricular zone, and hippocampus of the ischemic brain, followed by neurological injury (including brain infarct and neurological deficits).

Betanodavirus B2 protein triggers apoptosis and necroptosis in lung cancer cells that suppresses autophagy.

The betanodavirus B2 protein targets the mitochondria and acts as a "death factor", but its effect on lung cancer cells is unknown. We examined the effect of the B2 protein on triggering apoptosis or necroptosis P53-dependent and P53-independent pathways and increased in suppression of autophagy. The B2 protein targets the mitochondria of A549 (P53) and H1299 (P53) lung cancer cells due to a specific signal sequence (RTFVISAHAA).

Anti-apoptotic genes Bcl-2 and Bcl-xL overexpression can block iridovirus serine/threonine kinase-induced Bax/mitochondria-mediated cell death in GF-1 cells.

Although serine/threonine (ST) kinase is known to induce host cell death in GF-1 cells, it remains unclear how ST kinase induces mitochondrial function loss. In the present study, we addressed the issue of mitochondrial function loss by determining whether the Bcl-2 family members Bcl-2 and Bcl-xL can prevent ST kinase-induced cell death activity via interacting with the pro-apoptotic gene Bax. Grouper fin cells (GF-1) carrying EGFP-Bal-xL and EGFP-Bcl-2 fused genes were selected, established in cell culture, and used to examine the involvement of Bcl-2 and Bcl-xL overexpression in protection of GF-1 cells from the effects of the giant sea perch iridovirus (GSIV) ST kinase gene.

Evaluation of cerebral blood flow in acute ischemic stroke patients with atrial fibrillation: A sonographic study.

Background/purpose: Although cerebral emboli are a frequent cause of cardiogenic stroke, the possibility of a reduction in cerebral perfusion consequent to arrhythmia or impaired cardiac function should be considered in patients with atrial fibrillation (AF).

Methods: We reviewed sonographic studies and clinical features of patients with acute ischemic stroke. A total of 144 patients with AF and 144 age- and sex-matched patients with small vessel occlusion but without AF were included.

MOAP-1 Mediates Fas-Induced Apoptosis in Liver by Facilitating tBid Recruitment to Mitochondria.

Fas apoptotic signaling regulates diverse physiological processes. Acute activation of Fas signaling triggers massive apoptosis in liver. Upon Fas receptor stimulation, the BH3-only protein Bid is cleaved into the active form, tBid.

A New Visual Stimulation Program for Improving Visual Acuity in Children with Visual Impairment: A Pilot Study.

The purpose of this study was to investigate the effectiveness of visual rehabilitation of a computer-based visual stimulation (VS) program combining checkerboard pattern reversal (passive stimulation) with oddball stimuli (attentional modulation) for improving the visual acuity (VA) of visually impaired (VI) children and children with amblyopia and additional developmental problems. Six children (three females, three males; mean age = 3.9 ± 2.

Elevation of troponin I in acute ischemic stroke.

Background. Cardiac morbidities account for 20% of deaths after ischemic stroke and is the second commonest cause of death in acute stroke population. Elevation of cardiac troponin has been regarded as a prognostic biomarker of poor outcome in patients with acute stroke.

Common Neurological Disorders Involving Inpatient Liaisons at a Secondary Referral Hospital in Taiwan: A Retrospective Cross-Sectional Study.

Background And Purpose: The requirement for neurology liaison is increasing in accordance with the growing health care demands associated with aging populations. The aim of this study was to characterize the nature of neurological inpatient liaisons (NILs) to help plan for the appropriate use of neurology resources.

Methods: This was a retrospective cross-sectional study of NILs in a secondary referral hospital over a 12-month period.

Giant seaperch iridovirus (GSIV) induces mitochondria-mediated cell death that is suppressed by bongkrekic acid and cycloheximide in a fish cell line.

Giant seaperch iridovirus (GSIV) induces cell death by an unknown mechanism. We postulated that this mechanism involves mitochondria-mediated cell death. Cell viability assays revealed a steady increase in dead grouper fin cells (GF-1) after GSIV infection, from 11% at 2 days post-infection (dpi) to 67% at 5 dpi.

Modulator of apoptosis 1 (MOAP-1) is a tumor suppressor protein linked to the RASSF1A protein.

Modulator of apoptosis 1 (MOAP-1) is a BH3-like protein that plays key roles in cell death or apoptosis. It is an integral partner to the tumor suppressor protein, Ras association domain family 1A (RASSF1A), and functions to activate the Bcl-2 family pro-apoptotic protein Bax. Although RASSF1A is now considered a bona fide tumor suppressor protein, the role of MOAP-1 as a tumor suppressor protein has yet to be determined.

Threonine 56 phosphorylation of Bcl-2 is required for LRRK2 G2019S-induced mitochondrial depolarization and autophagy.

The G2019S leucine-rich repeat kinase 2 (LRRK2) mutation is the most common cause of genetic Parkinson's disease (PD). However, the molecular mechanism underlying LRRK2 G2019S-induced cellular pathology is poorly understood. Here, we demonstrated that LRRK2 G2019S bound to and phosphorylated Bcl-2, a mitochondrial anti-apoptotic protein, at Threonine 56.

Inhibition of excessive mitochondrial fission reduced aberrant autophagy and neuronal damage caused by LRRK2 G2019S mutation.

LRRK2 G2019S mutation is the most common genetic cause of Parkinson's disease (PD). Cellular pathology caused by this mutant is associated with mitochondrial dysfunction and augmented autophagy. However, the underlying mechanism is not known.

Effects of visual rehabilitation on a child with severe visual impairment.

We examined the effects of visual rehabilitation, including a chromatic luminance discrimination program and a fixation training program, on a 6-yr-old boy with severe visual impairment. Single-subject ABA and AB designs were used. The programs were conducted 2×/wk and included 6 to 7 sessions for the baseline phase and 10 to 11 sessions for the intervention phase.

A novel Drp1 inhibitor diminishes aberrant mitochondrial fission and neurotoxicity.

Excessive mitochondrial fission is associated with the pathology of a number of neurodegenerative diseases. Therefore, inhibitors of aberrant mitochondrial fission could provide important research tools in addition to potential leads for drug development. Using a rational approach, we designed a novel and selective peptide inhibitor, P110, of excessive mitochondrial fission.

Betanodavirus induces oxidative stress-mediated cell death that prevented by anti-oxidants and zfcatalase in fish cells.

The role of oxidative stress in the pathogenesis of RNA nervous necrosis virus infection is still unknown. Red-spotted grouper nervous necrosis virus (RGNNV) induced free radical species (ROS) production at 12-24 h post-infection (pi; early replication stage) in fish GF-1 cells, and then at middle replication stage (24-48 h pi), this ROS signal may upregulate some expressions of the anti-oxidant enzymes Cu/Zn SOD and catalase, and eventually expression of the transcription factor Nrf2. Furthermore, both antioxidants diphenyliodonium and N-acetylcysteine or overexpression of zebrafish catalase in GF-1 cells also reduced ROS production and protected cells for enhancing host survival rate due to RGNNV infection.

Betanodavirus up-regulates chaperone GRP78 via ER stress: roles of GRP78 in viral replication and host mitochondria-mediated cell death.

Whether viral pathogens that induce ER stress responses benefit the host or the virus remains controversial. In this study we show that betanodavirus induced ER stress responses up-regulate GRP78, which regulates the viral replication and host cellular mitochondrial-mediated cell death. Betanodavirus (redspotted grouper nervous necrosis virus, RGNNV) infection resulted in the following increased ER stress responses in fish GF-1 grouper fin cells: (1) IRE-1 and ATF-6 sensors at 48 h post-infection (p.