Armstead, William
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1) The study investigated whether a catalytically inactive tPA variant (tPA-S481A) could prevent impairment of cerebral autoregulation and histopathology after traumatic brain injury (TBI) in piglets. 2) tPA-S481A prevented pial artery vasoconstriction and blunted dilation impairment during hypotension after TBI. 3) tPA-S481A also prevented neuronal cell loss in the hippocampus that normally occurs after TBI.
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The third poster examines the role of O-GlcNAc glycosylation in hippocampal synaptic
HB poster - AES2
This study investigated how immune signaling and cell stress gene expression changes in the hippocampus and cerebellum of a rat model for glutamate excitotoxicity neurodegeneration. RNA was extracted from these brain regions in mutant and normal rats at different ages. Gene expression analysis found that genes involved in cytokine signaling were downregulated while cell stress genes were upregulated in mutant rats, suggesting altered immune regulation contributes to neurodegeneration. Specifically, genes related to glutamate metabolism and clusterin expression changed over time and differed between brain regions in ways that could enhance excitotoxic cell damage and death. The results provide insight into how the immune system may initiate neurodegeneration during glutamate excitotoxicity.
Neurotossicità iperammoniemia martinelli
Disordini del ciclo dell'urea: la neurotossicità dell'iperammoniemia. Autore: Diego Martinelli, Unità Operativa Complessa Patologia Metabolica.
AN APPROACH TO NEUROLOGICAL EMERGENCIES IN DOGS
APPROACH TO A NEUROLOGICAL EMERGENCY CASE STARTS WITH THE BASIC TRIAGE APPROACH AS IN ANY OTHER EMERGENCY CASE. A NEUROLOGICAL ASSESSMENT IS ONLY DONE AFTER THE STABILIZATION OF THE PATIENT. THERE CAN BE MANY DIFFERENT APPROACHES BUT ALL BASICALLY AIM AT FIRST CONFIRMING IF AT ALL IT IS A NEURO CASE AND IF YES, WHERE IS THE LESION..IS IT IN THE CRANIUM OR BRAINSTEM OR THE SPINAL CORD? LESION LOCALISATION WILL NOT ONLY HELP TO UNDERSTAND BETTER THE TYPE OF THERAPY TO BE CHOSEN BUT WILL ALSO HELP TO TELL ABOUT THE PROGNOSIS OF THE CASE. MOST COMMONLY WE GET STATUS EPILEPTICUS, TRAUMATIC BRAIN INJURY, POISONING, SPINAL CORD INJURIES AND ACUTE VESTIBULAR DISEASES AS THOUGHT TO LINKED WITH NEUROLOGICAL EMERGENCY SITUATIONS. AN EMERGENCY MUST BE FAMILIAR WITH WITH THE RELEVANT HISTORY OF THE PATIENT. HE SHOULD ALSO BE KEEP A TEAM READY WHO CAN HELP HIM PUT THE IV ACCESS AND SEDATIONS WHILE HE CAN COLLECT THE BLOOD FOR BASIC ROUTINE BLOOD ANALYSIS. COUNTERING THE ONGOING STAGE OF SHOCK TO BRING IT TO NORMAL, CHECKING THE SYSTEMIC BLOOD PRESSURE, RECTAL TEMPERATURE AND OXYGEN CONCENTRATION ARE FEW OF THE MOST IMPORTANT FACTORS A CLINICIAN HAS TO DO WHILE ADMINISTERING THE MEDICS. SCORING SYSTEMS LIKE MODIFIED GLASSGOW COMA SCALE AS SUGGESTED BY DR PLATT ARE REALLY HELPFUL TO GIVE A PROGNOSTIC IDEA IN CASES LIKE CRANIO-CERBRAL INJURIES. RECENT TREATMENT UPDATES ARE REALLY HELPFUL TO KEEP HAVING BETTER OPTIONS IN CASE THE ROUTINE PROTOCOL FOR STABILIZING A SEIZURE PATIENT IS NOT WORKING.
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Investigations of TARP gamma-8 Null Mice
The document summarizes a study that characterized the behavioral and neurological effects of deleting the TARP γ-8 gene in mice. Key findings include:
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2) KO mice had enhanced stimulatory responses to d-amphetamine and phencyclidine.
3) KO mice engaged in less marble burying and digging behaviors.
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Yearly Clinical Review of a Patient’s WGS Results Leads to a New Gene Candida...
The rapid evolution of genetic disease understanding and expanding genetic databases behooves clinician specialists to regularly review the status of clinical genetic test panels, reevaluating the status of identified variants. With the increasing use of WES and WGS sequencing, these results likely also need regular review.
We present a four-generation family affected by sudden cardiac arrests, ventricular tachycardia and (within the last 2 generations) documented left ventricular non-compaction. An affected member underwent a 38-gene pan-cardiomyopathy clinical genetic panel with no identified pathogenic variants. Therefore, affected members from three surviving generations (*) agreed to undergo genetic testing by whole genome sequencing in 2016. Analysis with Golden Helix SVS identified 69 shared, rare (MAF≤0.00005) coding variants in 40 genes, but none were identified to be associated with cardiac phenotypes.
At clinical follow-up of the youngest family member in 2019, we elected to review our WGS results again. A recent review of the genetics and genomics of dilated cardiomyopathy now identifies the SRA1 gene as being potentially involved in this phenotype, although no human cases have yet been reported. Upon review of this families previous WGS sequencing using SVS, we identified a SRA1 c.328_329 ins GAC (p.Val110delinsGlyLeu) rare shared variant. This variant is only present in 2 of 142724 alleles in the gnomAD database and inserts an additional amino acid into a partially conserved two amino acid region within an otherwise highly conserved protein region.
Friedrichs and colleagues previously identified SRA1 as one of 3 genes within a 600kb haploblock associated with cardiomyopathy in three independent Caucasian populations. In zebrafish, sra1 morphants display severe pericardial edema. The human SRA1 region also encodes a long noncoding RNA, lnc-SRA1-2, that is modulated in heart failure, attenuates hypoxia-induced injury in experimental cardiomyocytes through PPARγ/NF-κB signalling, and promotes the activation of cardiac myofibroblasts. SRA1 knockdown in C2C12 mouse myoblast cells prevented proper muscle gene expression and cell differentiation.
Cardiac genetics assessments by whole genome or whole exome sequencing also need regular review, which can be easily performed by Golden Helix SVS software. Links to new and frequently updated gene tracks and other genetic databases facilitate these reviews.
JC paper-2009
The document examines the effects of the TACE inhibitor BMS-561392 on APP processing both in vitro and in vivo. In cell cultures expressing APP, BMS-561392 reduced secretion of sAPPα without increasing Aβ production. Conversely, a BACE inhibitor decreased sAPPβ and Aβ without affecting sAPPα. In vivo infusion of BMS-561392 into mouse brains decreased sAPPα levels but did not significantly change steady-state Aβ levels. The findings suggest that under normal conditions, BACE and TACE do not compete for APP as a substrate, though they share localization in the trans-Golgi network. Inhibition of TACE may therefore reduce TNFα levels in
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This document summarizes several research publications on neuroscience topics:
1. One study found that acetaminophen affects central monoaminergic neurotransmission in rats, increasing serotonin levels in various brain regions and decreasing dopamine metabolites, suggesting monoamines may be involved in its analgesic action.
2. Another study showed that the benzodiazepine triazolam suppresses the induction of long-term potentiation in hippocampal neurons, consistent with its positive modulation of GABA-A receptor function.
3. A third study found that chronic treatment with either a substance P receptor antagonist or conventional antidepressant increases burst firing of neurons in the locus coeruleus, similarly to how imipramine works.
epilepsy-recentadvancesandexistingpharmacotherapy-170112143509.pptx
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Sigma Xi Presentation
The document summarizes an experiment that investigated the effects of granulocyte colony stimulating factor (GCSF) on rats that experienced stroke. Rats were divided into groups that either received or did not receive GCSF treatment after experiencing induced stroke. Western blot analysis found that GCSF treatment decreased expression of caspase 12 and GRP78, markers of cell death, in the core region of the brain but increased expression of these markers in the penumbra region. However, the results lacked statistical significance likely due to small sample sizes and variation between groups. Future research with larger sample sizes is needed.
Sigma Xi Presentation
The document summarizes an experiment that investigated the effects of granulocyte colony stimulating factor (GCSF) on rats that experienced stroke. Rats were divided into groups that either received or did not receive GCSF treatment after experiencing induced stroke. Western blot assays were used to analyze and compare the molecular expression of caspase 12 and glucose regulated protein 78 (GRP78), which are indicators of cell death, between the treated and untreated groups in the core and penumbra regions of the brain. The results found decreased expression of both proteins in the core of treated rats but increased expression in the penumbra, though the results were not statistically significant. Future research with larger sample sizes is needed to better understand the effects.
Sigma xi presentation
This document summarizes an experiment that investigated the effects of granulocyte colony stimulating factor (GCSF) on rats that experienced stroke induced by focal cerebral ischemia. Western blot assays were used to analyze the molecular expression of caspase 12 and glucose regulated protein 78 (GRP78) in GCSF treated and untreated rats, as indicators of cell death. The results found decreased expression of these markers in the core region of treated rats' brains but increased expression in the penumbra region, though the results were not statistically significant. Future research with larger sample sizes is needed to better understand the effects of GCSF on apoptotic pathways following stroke.
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Studies during the last 10 years have revealed a new category of brain diseases in which crucial neuronal receptors are attacked by autoantibodies. As a result of this attack there is a reduction of the target synaptic proteins leading to alterations in synaptic transmission. The clinical manifestations vary according to the receptor involved, and may resemble many of the symptoms caused by neurodegenerative diseases in which specific receptors are involved, including among others Parkinson, epilepsy, chronically progressive sleep disease, or schizophrenia.
Nature of psychosis and schizophrenia
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1) Assessment of effort is important in TBI clinical practice and research to generate valid data on patients' true cognitive capacities, as poor effort is common and can invalidate test results.
2) Formal effort tests should be integrated into evaluations to detect exaggeration and rule out other factors, given the effects of poor effort can dwarf those of mild TBI.
3) Various external incentives like compensation can adversely impact effort, so it is important to consider effort and response bias in clinical and research work involving people with TBI.
Zafonte, Ross
Ross Zafonte is a professor and chairman at Harvard Medical School. He holds the position of chairman, which is a leadership role within an academic department. As chairman, he oversees the department and provides guidance to faculty and students.
Youcha, Vicki
The document discusses strategies for translating scientific research on traumatic brain injury (TBI) and clinical practices to end users through social media. It outlines results from surveys of people with TBI or caring for someone with TBI that found they are interested in topics like memory, depression, and relationships and prefer video and text formats. The document recommends partnering with popular websites and social media to distribute information on TBI to a wider audience in multiple formats and lay language.
Ungerstedt, Urban
The document discusses using microdialysis catheters to monitor brain chemistry in patients with brain injuries. Monitoring markers like glucose, lactate, pyruvate, and glycerol levels can provide information about brain energy metabolism and cell damage. Optimizing factors like blood flow, oxygen and glucose delivery through drugs or surgery may improve tissue repair and survival. Different brain regions may require different intensive care treatments based on their chemistry profiles to reverse pathology and improve outcomes. Case studies are presented showing how monitoring chemistry over time can demonstrate the effects of interventions.
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The document discusses brain tissue oxygenation (PbtO2) monitoring in neurointensive care units. PbtO2 directly measures oxygen levels in brain tissue and is used to detect cerebral ischemia. Low PbtO2 values are associated with increased mortality risk and various treatments can be used to improve PbtO2 levels and outcomes for patients with severe traumatic brain injury. The document reviews guidelines, indications, techniques, and complications of PbtO2 monitoring.
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This document summarizes research on diverse mechanisms of blast-induced neurotrauma in rat models. It finds that exposure to a single "composite" blast, which includes head acceleration, results in cerebrovascular damage, astrocyte activation (glyosis), and neuronal injury. A single "primary" blast exposure instigated predominantly systemic/vascular changes and glyosis. The positional orientation of the animal relative to the shock wave influences whether a composite or primary blast is experienced. Responses depend on the type and magnitude of blast exposure.
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This document summarizes a presentation on mitochondrial dysfunction following traumatic brain injury (TBI) and spinal cord injury (SCI). It discusses how mitochondrial dysfunction manifests over time after injury and contributes to cell death through calcium overload and oxidative damage. The presentation shows that mitochondrial function is acutely lost after injury in a severity-dependent manner. Mitochondrial calcium buffering capacity, bioenergetics, and markers of oxidative damage are disrupted for up to 24 hours following injury. Early treatment with antioxidants may help preserve mitochondrial integrity and reduce oxidative damage in the first hours after injury.
Stewart, William
This document discusses diffuse axonal injury (DAI), a type of traumatic brain injury seen in fatal TBI cases. It provides a historical perspective on DAI and reviews the pathology, including microscopic findings. DAI involves damage to axons throughout the brain and is graded based on its severity and location. While commonly seen in fatal TBI, the pathology of mild DAI requires further study. The document also describes a unique brain tissue archive containing over 2,000 traumatic brain injury cases accrued over decades that has been used in over 150 publications to better understand DAI and its association with neurodegenerative conditions.
Snyder, Evan
The document summarizes a presentation given by Evan Y. Snyder on strategies for enhancing neural stem cell efficacy in the central nervous system. Some key points:
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1) Demyelination is a major feature of many central nervous system disorders and injuries like traumatic brain injury, but it has not been extensively examined in TBI.
2) Studies show oligodendrocyte death and loss of myelin occurring acutely and for weeks/months after TBI in humans and animal models.
3) It is unknown whether demyelination and dysfunctional myelin play a role in long-term axonal degeneration observed after TBI, or if myelin and oligodendrocyte damage are merely epiphenomena with no causal link to neurodegeneration. More research is needed to investigate these questions.
Smith, Doug H.
1) The document discusses whether diffuse axonal injury (DAI), the primary pathology seen in non-blast traumatic brain injury, is also present following mild blast brain injury.
2) Animal studies using shock tubes have found only limited axonal swelling and darker staining of brain regions following blast, without extensive DAI.
3) The pathologies observed do not fully match current hypotheses about mild blast brain injury in humans, which have not found hemorrhage or extensive DAI seen in non-blast injury.
4) It remains unclear whether swollen axons are the predominant pathology in DAI or if blast causes an as yet undetected type of subcellular damage.
Sanchez, Justin
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Rowitch, David
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Noble, Marc
1. The document discusses how small changes in redox state, or oxidative status, can have big effects on precursor cell function, survival, death, and differentiation.
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This document discusses diffusion tensor imaging (DTI) and its ability to detect microstructural changes in white matter following mild traumatic brain injury (mTBI). It summarizes several studies conducted by the author and colleagues using 3T MRI-DTI showing that DTI measures of white matter anisotropy correlate with cognitive processing speed and are sensitive to damage in specific tracts related to attention and memory. The document also discusses newer analytical techniques for DTI, such as independent component analysis and connectomics, and their potential for gaining insights into global brain connectivity changes and importance maps for network disruption caused by mTBI.
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Armstead, William
- 1. tPA Variant tPA-S481A prevents impairment of cerebral autoregulation during hypotension and histopathology after TBI William M. Armstead, John Riley, Serge Yarovoi, Douglas B. Cines, Douglas H. Smith, and Abd Al-Roof Higazi Departments of Anesthesiology and Critical Care, Pharmacology, Pathology, and Neurosurgery University of Pennsylvania
- 2. Freeman, Udomphorn, Armstead, Fisk, Vavilala Anesthesiology 108: 588-595, 2008. Impairment of autoregulation correlates with GCS Impaired Cerebral Autoregulation MAP or CPP CBF (ml/100g/min) Intact Cerebral Autoregulation MAP or CPP CBF (ml/100g/min)
- 3. Cerebral autoregulation (ARI) is more impaired after moderate-severe TBI in children < 4 years. Glasgow outcome score (6 month GOS) is worse after moderate-severe TBI in children < 4 yrs. Freeman, Udomphorn, Armstead, Fisk, Vavilala Anesthesiology 108: 588-595, 20008 0.001 23 3 ARI > 0 (intact autoregulation) 5 8 ARI = 0 (absent autoregulation) 0.65 ± 0.31 0.33 ± 0.32 Mean ARI p Age ≥ 4 ( 12 ± 3) years (n=27) Age < 4 (2 ± 1) years (n=11) Table 2: 0.005 17 3 Age > 4 years 6 7 Age < 4 years p 6 month GOS > 4 (n=23) 6 month GOS < 4 (n=10) Table 4:
- 5. tPA contributes to impaired NMDA cerebrovasodilation through activation of JNK and ERK MAPK. Neurologic Res, in press. Impaired NMDA receptor mediated cerebrovasodilation contributes to disturbed autoregulation during hypotension after TBI. Develop Brain Res 139: 19-28, 2002.
- 8. FPI produces pial artery vasoconstriction, which was Blocked by tPA-S481A (1 mg/kg iv) 30 min post injury Pial artery dilation during hypotension blunted after FPI, but tPA-S481A prevented such impairment.
- 9. FPI was associated with marked neuronal cell loss in CA1 and CA3 hippocampus, which was prevented by tPA-S481A