Neonatal Cerebral Hypoxia Ischemia ( Hi ) Remains A Major Cause Of Death And Neurological Disability

According to the article, “A Squirt of Stem Cell Gel Heals Brain Injuries,” was written by Sandeep Ravindran discussed about a scientist name, Dr. Ning Zhang who works at Clemson University in South Carolina, developed a gel that injected into the injured brain that helps recover from any traumatic injuries including people who suffered from fall, car accidents, gunshot wounds, and combat. This procedure is to insert the gel into the injured brain and stimulates the growth of stem cells. Even though, it’s hard to fix an injured brain because of swollen tissues and can cause more damage to the cells. They already did the experiment, the gel injection is to change the temperature or release the pressure of the injured brain, but it’s often not

of anesthetics by 50%, provides neuroprotection against focal cerebral ischemia. Perinatal asphyxia can lead to death and severe disability. Brain hypoxia-ischemia (HI) injury is the major pathophysiology contributing to death and severe disability after perinatal asphyxia. Ren et al. studied the effects of dexmedetomidine on seven-day old Sprague Dawley rats with

As a Neonatal Nurse Practitioner, Hypoxic ischemic encephalopathy (HIE) is one of the most serious birth complications affecting full term infants that are seen in the NICU. Perinatal asphyxia, more appropriately known as hypoxic-ischemic encephalopathy, is clinical and laboratory evidence of a brain injury due to asphyxia. The primary causes of this condition are low cerebral blood flow. Birth asphyxia causes 840,000 or 23% of all neonatal deaths worldwide (Zanelli.) By the age of two, up to 60% of infants with HIE will die or have severe disabilities including mental retardation, epilepsy, and cerebral palsy (Allen).

Stroke is considered as second leading reason of death in the world with over zillions of individuals suffering from this. With the increasing hazard of developing this feared disease, particularly in developed nations, scientists and medical investigators are rushing to find a cure for stroke. One of the newest breakthroughs is an investigation being conducted that deals with the use of stem cells.

The sub-acute phase continues from the acute phase and characterized by new events such as formation of free radicals, delayed calcium influx, apoptotic cell death, inflammatory response, central cavitation initiation, and astroglial scar initiation (28). Neutrophils are the first immune cells to respond/arrive at injury, removing microbial intruders and tissue debris. Neutrophils release protease metalloproteinase, ROS, TNF-α, IFN-γ, IL-1, 8, 12 and other pro-inflammatory factors to activate other inflammatory and glial cells (29, 30). While initially beneficial, neutrophil persistence significantly increases damage through continuous production of pro-inflammatory cytokines and proteolytic enzymes (31). Therefore, neutrophil activation is limited to a couple days, and is contained to the sub-acute phase. Microglia and macrophages become active in response to neutrophils and the injury, also releasing numerous

In an in vitro model of cerebral ischemia, increase of miR-497 expression following oxygen-glucose deprivation, correlated with increased cell death and down regulation of its anti-apoptotic proteins, Bcl2 and Bclw [17]. Temporal regulation of miRNA expression has been shown in the brain of rat models subjected to middle cerebral artery occlusion (MCAo) [20]. An up regulation of the anti-apoptotic miR-21 has been shown to protect neurons from death in cerebral ischemic model. The temporal and biphasic regulation of these miRNAs have been proposed to play a crucial role either in the acute injury phase or the late recovery phase [16]. In addition, biphasic expression of miRNAs has also been demonstrated in the same animal models. Cerebral ischemia

The results presented here are logical extension of previous studies focusing on Nrf2 as a control point for the maintenance of GSH homeostasis in response to E-induced redox shifts in cultured neurons and in the developing brain. The Nrf2-related studies illustrated that the transcription factor does play a vital role in neuroprotection against E damage [7]. Yet, the neuroprotective setting remained incomplete in that GSH homeostasis was not preserved in a subpopulation of neurons in the E-exposed fetal brain [7], even in the presence of E-dependent up-regulation of Nrf2 expression. To mitigate this gap in our understanding, these new studies address a role of Cys homeostasis and their control points which could be

The population of world is growing each and every year. With more people the more food needs to be made and the greater the strain on healthcare and many other things. However, there is still much room to grow throughout the world. China is an nation with a very large population and has an extremely high birth rate, in fact it is over 17 million live births a year. However, with such a large number of births there is also the problem of of the infant death rate (Matandrea, 2009). The death rate is 29.2 per 1000 births (Matandrea, 2009). That is very high. Over twenty percent of deaths are caused by asphyxia, or lack of oxygen to the body. Through recent efforts, a company called the Freedom of Breath helped

ML had neurological involvement before admission. This included a history of stroke which contributed to the anoxic encephalopathy. This loss of oxygen and blood flow to areas of the brain was evident on his results from a CT of the head. The CT showed that patient ML had mild to moderate ischemia and low attenuation in multiple parts of the brain. The CT scan also made evident that this patient had suffered from cerebral volume loss. These results were not surprising considering the patient was unresponsive except for pain stimuli and was also nonverbal due to having a trach and being on mechanical ventilation. Due to him being unresponsive it was difficult to assess if his current infection had any effect on his neurological state.

Murine chronic cerebral hypoperfusion (CCH) results in white matter (WM) injury and behavioral deficits. Pericytes influence blood-brain barrier (BBB) integrity and cerebral blood flow. Under hypoxic conditions, perictyes detach from perivascular locations, increasing vessel permeability and neuronal injury. This study characterizes the time course of BBB dysfunction and pericyte coverage following murine experimental CCH secondary to bilateral carotid artery stenosis (BCAS). Mice underwent BCAS or sham operation. On post-procedure days 1, 3, 7 and 30, corpus callosum BBB permeability was characterized using Evans blue (EB) extravasation and IgG staining and pericyte coverage was calculated. The BCAS cohort demonstrated increased EB extravasation on postoperative days 1 (p=.03) and 3 (p=.01) when compared to sham mice. Further, EB extravasation was significantly greater (p=.03) at day 3 than at day 30 in BCAS mice. Positive IgG staining was seen at post-procedure day 3 in the BCAS group. BCAS mice demonstrated a nadir in pericyte coverage on post-operative day 3 (p50%) was reported to be 7% in women and 9% in men3. Clinical carotid endarterectomy studies of cerebral hypoperfusion, demonstrate a nearly 25% incidence of subtle cognitive decline in the absence of overt neurologic change or radiographic evidence of stroke4. Neurodegenerative diseases such as Alzheimer’s disease and vascular dementia have become increasingly more common as the population ages5-8.

Ischemia produces necrosis by starving neurons of oxygen and glucose, which results in failure of mitochondria to produce ATP. In absence of ATP , membrane ion pumps stop functioning and neurons depolarize,allowing intracellular calcium to rise. Cellular depolarization causes glutamate release from synaptic terminals,excess extracellular glutamate produces neurotoxicity by activating the postsynaptic glutamate receptors that increase neuronal calcium influx. Free radicals cause catalytic destruction of membranes.

. Overview of processes involved ischemic stroke and high potential therapeutic microRNAs. Cerebral ischemia includes several injurious mechanisms (excitotoxicity, oxidative stress, inflammation and apoptosis) to confer neuronal injury. Potential therapeutic areas to compensate these pathogenic process include promoting angiogenesis, neurogenesis and neuroprotection which they are as recovery and repair

Currently, 285,000 US citizens suffer from spinal cord injury (SCI), and 99.6% of these individuals are paralyzed to some extent.1 SCI is the result of a mechanical insult to the spine that damages the spinal cord. This is followed by secondary SCI, which involves a series of biochemical events resulting in further neuronal and glial cell death.2 Astrocytes, the most abundant glial cell of the central nervous system (CNS), provide neurons with structural and neurotrophic support as well as protection from toxins. Following primary injury, damaged glia are unable to provide damaged neurons with the support necessary for axonal regeneration. Individuals that suffer from SCI are limited to two forms of treatment: 1) administration

The hypoxia-inducible factor prolyl hydroxylase domain enzymes (HIF-PHDs) are a family of oxygen sensors that has been implicated in neuronal survival. Catalysis by the HIF-PHDs destabilizes the transcriptional activator HIF-1a under normoxia. HIF-PHDs are promising target candidates for mitochondrial protection in paradigms of oxidative stress. The inhibition of HIF-PHDs prevented neuronal cell death induced by mitochondrial toxins [1][2].

Fetal tissues are advantageous in medical therapy for a myriad of ways. Most commonly, the fetal tissue cells would be used to treat neurodegenerative diseases such as Parkinson’s, Huntington’s disease, and Alzheimer’s disease. More recent breakthroughs show possibilities of the use of fetal tissues for diabetes and an assortment of blood and immune disorders. (Bachoud, 2000) Fetal tissues divide more rapidly than matured tissues, making them better candidates for the experimental medical therapy. (Fackleman,1995) In addition, by using fetal tissues in the transplant, the possibility of the host rejecting the transplant is significantly lower than that of the use of matured tissues. (McCloskey) The objective behind the transplant is to restore the lost functions in a person ridden with a neurodegenerative and otherwise incurable disease. (Bensoussan, 2002)