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Functional neurologic disorder (FND) is characterized by a broad symptomatology, requiring a multidisciplinary approach to care. Rehabilitation professionals (eg, PT, OT, SLP) play a pivotal role in the management of FND following a positive rule-in diagnosis from a neurologist. Consensus guidelines have been published to guide rehabilitation of individuals with FND, however, there is a lack of evidence regarding specific components of supported interventions, which hinder their implementation. While some recent reviews have documented the multidisciplinary treatment interventions delivered by physical therapists (PT), few have documented specifics about the types of interventions delivered by occupational therapists (OT) and speech language pathologists (SLP). Thus, a scoping review characterizing the specifics of PT, OT, and SLP interventions for individuals with FND in relationship to the consensus guidelines is critical to inform clinical care.

Includes bibliographies

Includes bibliographies

This article is from BMC Neuroscience , volume 15 . Abstract Background: Angelman syndrome is a monogenic neurologic disorder that affects 1 in 15,000 children, and is characterized by ataxia, intellectual disability, speech impairment, sleep disorders, and seizures. The disorder is caused by loss of central nervous system expression of UBE3A, a gene encoding a ubiquitin ligase. Current treatments focus on the management of symptoms, as there have not been therapies to treat the underlying molecular cause of the disease. However, this outlook is evolving with advances in molecular therapies, including artificial transcription factors a class of engineered DNA-binding proteins that have the potential to target a specific site in the genome. Results: Here we review the recent progress and prospect of targeted gene expression therapies. Three main issues that must be addressed to advance toward human clinical trials are specificity, toxicity, and delivery. Conclusions: Artificial transcription factors have the potential to address these concerns on a level that meets and in some cases exceeds current small molecule therapies. We examine the possibilities of such approaches in the context of Angelman syndrome, as a template for other single-gene, neurologic disorders.

This article is from BMC Neuroscience , volume 15 . Abstract Background: Angelman syndrome is a monogenic neurologic disorder that affects 1 in 15,000 children, and is characterized by ataxia, intellectual disability, speech impairment, sleep disorders, and seizures. The disorder is caused by loss of central nervous system expression of UBE3A, a gene encoding a ubiquitin ligase. Current treatments focus on the management of symptoms, as there have not been therapies to treat the underlying molecular cause of the disease. However, this outlook is evolving with advances in molecular therapies, including artificial transcription factors a class of engineered DNA-binding proteins that have the potential to target a specific site in the genome. Results: Here we review the recent progress and prospect of targeted gene expression therapies. Three main issues that must be addressed to advance toward human clinical trials are specificity, toxicity, and delivery. Conclusions: Artificial transcription factors have the potential to address these concerns on a level that meets and in some cases exceeds current small molecule therapies. We examine the possibilities of such approaches in the context of Angelman syndrome, as a template for other single-gene, neurologic disorders.

This article is from BMC Neuroscience , volume 15 . Abstract Background: Angelman syndrome is a monogenic neurologic disorder that affects 1 in 15,000 children, and is characterized by ataxia, intellectual disability, speech impairment, sleep disorders, and seizures. The disorder is caused by loss of central nervous system expression of UBE3A, a gene encoding a ubiquitin ligase. Current treatments focus on the management of symptoms, as there have not been therapies to treat the underlying molecular cause of the disease. However, this outlook is evolving with advances in molecular therapies, including artificial transcription factors a class of engineered DNA-binding proteins that have the potential to target a specific site in the genome. Results: Here we review the recent progress and prospect of targeted gene expression therapies. Three main issues that must be addressed to advance toward human clinical trials are specificity, toxicity, and delivery. Conclusions: Artificial transcription factors have the potential to address these concerns on a level that meets and in some cases exceeds current small molecule therapies. We examine the possibilities of such approaches in the context of Angelman syndrome, as a template for other single-gene, neurologic disorders.

This article is from BMC Neuroscience , volume 15 . Abstract Background: Angelman syndrome is a monogenic neurologic disorder that affects 1 in 15,000 children, and is characterized by ataxia, intellectual disability, speech impairment, sleep disorders, and seizures. The disorder is caused by loss of central nervous system expression of UBE3A, a gene encoding a ubiquitin ligase. Current treatments focus on the management of symptoms, as there have not been therapies to treat the underlying molecular cause of the disease. However, this outlook is evolving with advances in molecular therapies, including artificial transcription factors a class of engineered DNA-binding proteins that have the potential to target a specific site in the genome. Results: Here we review the recent progress and prospect of targeted gene expression therapies. Three main issues that must be addressed to advance toward human clinical trials are specificity, toxicity, and delivery. Conclusions: Artificial transcription factors have the potential to address these concerns on a level that meets and in some cases exceeds current small molecule therapies. We examine the possibilities of such approaches in the context of Angelman syndrome, as a template for other single-gene, neurologic disorders.

Includes bibliographies and index

Includes bibliographies and index

Includes bibliographies and index

Neurologic Clinics 2025 Neurocritical Care

Neurologic Clinics 2025 Neurocritical Care

Includes bibliographical references (p. [312]-[315]) and index

Includes bibliographical references (p. [312]-[315]) and index

Includes bibliographical references (p. [312]-[315]) and index

Includes bibliographical references (p. [312]-[315]) and index

This article is from BMC Genetics , volume 13 . Abstract Because of dogs' unique population structure, human-like disease biology, and advantageous genomic features, the canine system has risen dramatically in popularity as a tool for discovering disease alleles that have been difficult to find by studying human families or populations. To date, disease studies in dogs have primarily employed either linkage analysis, leveraging the typically large family size, or genome-wide association, which requires only modest-sized case and control groups in dogs. Both have been successful but, like most techniques, each requires a specific combination of time and money, and there are inherent problems associated with each. Here we review the first report of mRNA-Seq in the dog, a study that provides insights into the potential value of applying high-throughput sequencing to the study of genetic diseases in dogs.Forman and colleagues apply high-throughput sequencing to a single case of canine neonatal cerebellar cortical degeneration. This implementation of whole genome mRNA sequencing, the first reported in dog, is additionally unusual due to the analysis: the data was used not to examine transcript levels or annotate genes, but as a form of target capture that revealed the sequence of transcripts of genes associated with ataxia in humans. This approach entails risks. It would fail if, for example, the relevant transcripts were not sufficiently expressed for genotyping or were not associated with ataxia in humans. But here it pays off handsomely, identifying a single frameshift mutation that segregates with the disease. This work sets the stage for similar studies that take advantage of recent advances in genomics while exploiting the historical background of dog breeds to identify disease-causing mutations.

This article is from BMC Genetics , volume 13 . Abstract Because of dogs' unique population structure, human-like disease biology, and advantageous genomic features, the canine system has risen dramatically in popularity as a tool for discovering disease alleles that have been difficult to find by studying human families or populations. To date, disease studies in dogs have primarily employed either linkage analysis, leveraging the typically large family size, or genome-wide association, which requires only modest-sized case and control groups in dogs. Both have been successful but, like most techniques, each requires a specific combination of time and money, and there are inherent problems associated with each. Here we review the first report of mRNA-Seq in the dog, a study that provides insights into the potential value of applying high-throughput sequencing to the study of genetic diseases in dogs.Forman and colleagues apply high-throughput sequencing to a single case of canine neonatal cerebellar cortical degeneration. This implementation of whole genome mRNA sequencing, the first reported in dog, is additionally unusual due to the analysis: the data was used not to examine transcript levels or annotate genes, but as a form of target capture that revealed the sequence of transcripts of genes associated with ataxia in humans. This approach entails risks. It would fail if, for example, the relevant transcripts were not sufficiently expressed for genotyping or were not associated with ataxia in humans. But here it pays off handsomely, identifying a single frameshift mutation that segregates with the disease. This work sets the stage for similar studies that take advantage of recent advances in genomics while exploiting the historical background of dog breeds to identify disease-causing mutations.

This article is from BMC Genetics , volume 13 . Abstract Because of dogs' unique population structure, human-like disease biology, and advantageous genomic features, the canine system has risen dramatically in popularity as a tool for discovering disease alleles that have been difficult to find by studying human families or populations. To date, disease studies in dogs have primarily employed either linkage analysis, leveraging the typically large family size, or genome-wide association, which requires only modest-sized case and control groups in dogs. Both have been successful but, like most techniques, each requires a specific combination of time and money, and there are inherent problems associated with each. Here we review the first report of mRNA-Seq in the dog, a study that provides insights into the potential value of applying high-throughput sequencing to the study of genetic diseases in dogs.Forman and colleagues apply high-throughput sequencing to a single case of canine neonatal cerebellar cortical degeneration. This implementation of whole genome mRNA sequencing, the first reported in dog, is additionally unusual due to the analysis: the data was used not to examine transcript levels or annotate genes, but as a form of target capture that revealed the sequence of transcripts of genes associated with ataxia in humans. This approach entails risks. It would fail if, for example, the relevant transcripts were not sufficiently expressed for genotyping or were not associated with ataxia in humans. But here it pays off handsomely, identifying a single frameshift mutation that segregates with the disease. This work sets the stage for similar studies that take advantage of recent advances in genomics while exploiting the historical background of dog breeds to identify disease-causing mutations.

This article is from BMC Genetics , volume 13 . Abstract Because of dogs' unique population structure, human-like disease biology, and advantageous genomic features, the canine system has risen dramatically in popularity as a tool for discovering disease alleles that have been difficult to find by studying human families or populations. To date, disease studies in dogs have primarily employed either linkage analysis, leveraging the typically large family size, or genome-wide association, which requires only modest-sized case and control groups in dogs. Both have been successful but, like most techniques, each requires a specific combination of time and money, and there are inherent problems associated with each. Here we review the first report of mRNA-Seq in the dog, a study that provides insights into the potential value of applying high-throughput sequencing to the study of genetic diseases in dogs.Forman and colleagues apply high-throughput sequencing to a single case of canine neonatal cerebellar cortical degeneration. This implementation of whole genome mRNA sequencing, the first reported in dog, is additionally unusual due to the analysis: the data was used not to examine transcript levels or annotate genes, but as a form of target capture that revealed the sequence of transcripts of genes associated with ataxia in humans. This approach entails risks. It would fail if, for example, the relevant transcripts were not sufficiently expressed for genotyping or were not associated with ataxia in humans. But here it pays off handsomely, identifying a single frameshift mutation that segregates with the disease. This work sets the stage for similar studies that take advantage of recent advances in genomics while exploiting the historical background of dog breeds to identify disease-causing mutations.

xiii, 1079 p

This article is from Asian Spine Journal , volume 6 . Abstract A 13-year-9-month-old female child presented with congenital kyphoscoliosis along with progressive paraparesis. Radiographs confirmed kyphoscoliosis and magnetic resonance imaging revealed a stretched and flattened spinal cord over the kyphotic deformity and a T7 hemivertebra. She underwent a posterior correction of the curve along with posterior decompression and a posterior to anterior excision of T7 hemivertebra to relieve her of the deteriorating neurology. While carrying out the excision of T7 hemivertebra, her trans cranial electrical motor evoke potential dropped. Consequently, she was administered a mega dose steroid therapy. After a positive wake-up test, the excision was discontinued and surgery was concluded by in situ fixation of the deformity with short rods. Thereafter, a gradual deterioration in the neurologic status was observed and patient became paraplegic on the fourth post operative day. In this case report, we try to analyze various causes for gradual deterioration in neurologic status.

This article is from Journal of Injury and Violence Research , volume 4 . Abstract Background:: To examine whether spinal cord decompression improves functional recovery and decreases lesion volumes in paraplegic rats two studies were conducted. At the first study, a comparative study was conducted to evaluate decompression timing of 3-seconds, 1 hour, 6 hours, 3 weeks and 10 weeks in 63 rats. The second study was performed to compare the electro-microscopic findings and motor function recovery in a group of 10 rats receiving compression for 3 seconds and 10 minutes. Methods:: Compressive injury was produced using an aneurysmal clip method. Behavioral assessment was performed through inclined plane test, tail-flick reflex and Basso, Beattie and Bresnahan (BBB) rating scales. At the end of the study, the rats were sacrificed and spinal cord specimens were studied under light and electron microscopic techniques. Results:: The first experiment showed that rats sustaining 3-second immediate spinal cord compression showed significant improved functional recovery (P less than 0.05) and smaller lesion volumes (P = 0.039) than rats subjected to compression times of 1 hour, 6 hours, 3 weeks, and 10 weeks after spinal cord injury. BBB rating scales were significantly better in the early compression group after the 4th week of evaluation (P less than 0.05) and persisted throughout the rest of the study. Histopathology demonstrated decreased normal tissue, more severe gliosis and cystic formation in the late group, compared to the early group (P less than 0.05). In EM study, injuries in the late group including injury to the myelin and axon were more severe than the early compression group and there was more cytoplasmic edema in the late compression group. Conclusions:: Our findings show that the early 3-second decompression after spinal cord injury improves functional motor recovery, spares more functional tissue, which is accompanied by lower intracellular edema and myelin and axon damage, whereas higher myelin regeneration in rats compared to those with 10 minutes of compression. Inclined plane and tail-flick reflex assessments showed no significant difference. Keywords:: Decompression, BBB rating scal , Histopathology, Electron microscopy, Spinal cord injury

xii, 499 pages ; 22 cm

Neurologic Clinics 2002: Volume 20 , Issue Index. Digitized from IA1631613-04 . Previous issue: sim_neurologic-clinics_2001-11_19_4 . Next issue: sim_neurologic-clinics_2002-02_20_1 .

Neurologic Clinics 2002: Volume 20 , Issue Index. Digitized from IA1631613-04 . Previous issue: sim_neurologic-clinics_2001-11_19_4 . Next issue: sim_neurologic-clinics_2002-02_20_1 .

Neurologic Clinics 2002: Volume 20 , Issue Index. Digitized from IA1631613-04 . Previous issue: sim_neurologic-clinics_2001-11_19_4 . Next issue: sim_neurologic-clinics_2002-02_20_1 .

Despite a well established connection between maternal metabolism and nutrition and subsequent child neurodevelopment, this topic has rarely been studied outside of the United States and Europe. As such, the primary objective of this study is to synthesize and examine the ways in which a mother’s metabolic profile will affect her child’s neurodevelopment in mothers and children from the Caribbean region. This study examines a wide range of maternal metabolic conditions to determine if there is any link to subsequent non-genetic neurodevelopmental delays in their children. Following the Arksey and O’Malley methodology for scoping reviews and JBI guidelines for protocol development, articles from MEDLINE (PubMed), CINAHL (EBSCO), SCOPUS, and grey literature related to the topic will be collected. Articles of all designs as well as those printed in either English or Spanish will be included for analysis. Data will be analyzed from all included articles to determine whether or not there is an identifiable link between maternal metabolism and nutrition and child neurodevelopment in the Caribbean region.

Despite a well established connection between maternal metabolism and nutrition and subsequent child neurodevelopment, this topic has rarely been studied outside of the United States and Europe. As such, the primary objective of this study is to synthesize and examine the ways in which a mother’s metabolic profile will affect her child’s neurodevelopment in mothers and children from the Caribbean region. This study examines a wide range of maternal metabolic conditions to determine if there is any link to subsequent non-genetic neurodevelopmental delays in their children. Following the Arksey and O’Malley methodology for scoping reviews and JBI guidelines for protocol development, articles from MEDLINE (PubMed), CINAHL (EBSCO), SCOPUS, and grey literature related to the topic will be collected. Articles of all designs as well as those printed in either English or Spanish will be included for analysis. Data will be analyzed from all included articles to determine whether or not there is an identifiable link between maternal metabolism and nutrition and child neurodevelopment in the Caribbean region.

This article is from PLoS ONE , volume 9 . Abstract Backgrounds: Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). Neuronal apoptosis is involved in the pathological process of EBI. Hydrogen can inhibit neuronal apoptosis and attenuate EBI following SAH. However, the molecular mechanism underlying hydrogen-mediated anti-apoptotic effects in SAH has not been elucidated. In the present study, we aimed to evaluate whether hydrogen alleviates EBI after SAH, specifically neuronal apoptosis, partially via the Akt/GSK3β signaling pathway. Methods: Sprague-Dawley rats (n = 85) were randomly divided into the following groups: sham group (n = 17), SAH group (n = 17), SAH + saline group (n = 17), SAH + hydrogen-rich saline (HS) group (n = 17) and SAH + HS + Ly294002 (n = 17) group. HS or an equal volume of physiological saline was administered immediately after surgery and repeated 8 hours later. The PI3K inhibitor, Ly294002, was applied to manipulate the proposed pathway. Neurological score and SAH grade were assessed at 24 hours after SAH. Western blot was used for the quantification of Akt, pAkt, GSK3β, pGSK3β, Bcl-2, Bax and cleaved caspase-3 proteins. Neuronal apoptosis was identified by double staining of terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining and NeuN, and quantified by apoptosis index. Immunohistochemistry and immunofluorescent double-labeling staining was performed to clarify the relationships between neuronal apoptosis and pAkt or pGSK3β. Results: HS significantly reduced neuronal apoptosis and improved neurological function at 24 hours after SAH. The levels of pAkt and pGSK3β, mainly expressed in neurons, were markedly up-regulated. Additionally, Bcl-2 was significantly increased while Bax and cleaved caspase-3 was decreased by HS treatment. Double staining of pAkt and TUNEL showed few colocalization of pAkt-positive cells and TUNEL-positive cells. The inhibitor of PI3K, Ly294002, suppressed the beneficial effects of HS. Conclusions: HS could attenuate neuronal apoptosis in EBI and improve the neurofunctional outcome after SAH, partially via the Akt/GSK3β pathway.

This article is from PLoS ONE , volume 9 . Abstract Backgrounds: Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). Neuronal apoptosis is involved in the pathological process of EBI. Hydrogen can inhibit neuronal apoptosis and attenuate EBI following SAH. However, the molecular mechanism underlying hydrogen-mediated anti-apoptotic effects in SAH has not been elucidated. In the present study, we aimed to evaluate whether hydrogen alleviates EBI after SAH, specifically neuronal apoptosis, partially via the Akt/GSK3β signaling pathway. Methods: Sprague-Dawley rats (n = 85) were randomly divided into the following groups: sham group (n = 17), SAH group (n = 17), SAH + saline group (n = 17), SAH + hydrogen-rich saline (HS) group (n = 17) and SAH + HS + Ly294002 (n = 17) group. HS or an equal volume of physiological saline was administered immediately after surgery and repeated 8 hours later. The PI3K inhibitor, Ly294002, was applied to manipulate the proposed pathway. Neurological score and SAH grade were assessed at 24 hours after SAH. Western blot was used for the quantification of Akt, pAkt, GSK3β, pGSK3β, Bcl-2, Bax and cleaved caspase-3 proteins. Neuronal apoptosis was identified by double staining of terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining and NeuN, and quantified by apoptosis index. Immunohistochemistry and immunofluorescent double-labeling staining was performed to clarify the relationships between neuronal apoptosis and pAkt or pGSK3β. Results: HS significantly reduced neuronal apoptosis and improved neurological function at 24 hours after SAH. The levels of pAkt and pGSK3β, mainly expressed in neurons, were markedly up-regulated. Additionally, Bcl-2 was significantly increased while Bax and cleaved caspase-3 was decreased by HS treatment. Double staining of pAkt and TUNEL showed few colocalization of pAkt-positive cells and TUNEL-positive cells. The inhibitor of PI3K, Ly294002, suppressed the beneficial effects of HS. Conclusions: HS could attenuate neuronal apoptosis in EBI and improve the neurofunctional outcome after SAH, partially via the Akt/GSK3β pathway.

This article is from PLoS ONE , volume 9 . Abstract Backgrounds: Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). Neuronal apoptosis is involved in the pathological process of EBI. Hydrogen can inhibit neuronal apoptosis and attenuate EBI following SAH. However, the molecular mechanism underlying hydrogen-mediated anti-apoptotic effects in SAH has not been elucidated. In the present study, we aimed to evaluate whether hydrogen alleviates EBI after SAH, specifically neuronal apoptosis, partially via the Akt/GSK3β signaling pathway. Methods: Sprague-Dawley rats (n = 85) were randomly divided into the following groups: sham group (n = 17), SAH group (n = 17), SAH + saline group (n = 17), SAH + hydrogen-rich saline (HS) group (n = 17) and SAH + HS + Ly294002 (n = 17) group. HS or an equal volume of physiological saline was administered immediately after surgery and repeated 8 hours later. The PI3K inhibitor, Ly294002, was applied to manipulate the proposed pathway. Neurological score and SAH grade were assessed at 24 hours after SAH. Western blot was used for the quantification of Akt, pAkt, GSK3β, pGSK3β, Bcl-2, Bax and cleaved caspase-3 proteins. Neuronal apoptosis was identified by double staining of terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining and NeuN, and quantified by apoptosis index. Immunohistochemistry and immunofluorescent double-labeling staining was performed to clarify the relationships between neuronal apoptosis and pAkt or pGSK3β. Results: HS significantly reduced neuronal apoptosis and improved neurological function at 24 hours after SAH. The levels of pAkt and pGSK3β, mainly expressed in neurons, were markedly up-regulated. Additionally, Bcl-2 was significantly increased while Bax and cleaved caspase-3 was decreased by HS treatment. Double staining of pAkt and TUNEL showed few colocalization of pAkt-positive cells and TUNEL-positive cells. The inhibitor of PI3K, Ly294002, suppressed the beneficial effects of HS. Conclusions: HS could attenuate neuronal apoptosis in EBI and improve the neurofunctional outcome after SAH, partially via the Akt/GSK3β pathway.

This article is from PLoS ONE , volume 9 . Abstract Backgrounds: Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). Neuronal apoptosis is involved in the pathological process of EBI. Hydrogen can inhibit neuronal apoptosis and attenuate EBI following SAH. However, the molecular mechanism underlying hydrogen-mediated anti-apoptotic effects in SAH has not been elucidated. In the present study, we aimed to evaluate whether hydrogen alleviates EBI after SAH, specifically neuronal apoptosis, partially via the Akt/GSK3β signaling pathway. Methods: Sprague-Dawley rats (n = 85) were randomly divided into the following groups: sham group (n = 17), SAH group (n = 17), SAH + saline group (n = 17), SAH + hydrogen-rich saline (HS) group (n = 17) and SAH + HS + Ly294002 (n = 17) group. HS or an equal volume of physiological saline was administered immediately after surgery and repeated 8 hours later. The PI3K inhibitor, Ly294002, was applied to manipulate the proposed pathway. Neurological score and SAH grade were assessed at 24 hours after SAH. Western blot was used for the quantification of Akt, pAkt, GSK3β, pGSK3β, Bcl-2, Bax and cleaved caspase-3 proteins. Neuronal apoptosis was identified by double staining of terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining and NeuN, and quantified by apoptosis index. Immunohistochemistry and immunofluorescent double-labeling staining was performed to clarify the relationships between neuronal apoptosis and pAkt or pGSK3β. Results: HS significantly reduced neuronal apoptosis and improved neurological function at 24 hours after SAH. The levels of pAkt and pGSK3β, mainly expressed in neurons, were markedly up-regulated. Additionally, Bcl-2 was significantly increased while Bax and cleaved caspase-3 was decreased by HS treatment. Double staining of pAkt and TUNEL showed few colocalization of pAkt-positive cells and TUNEL-positive cells. The inhibitor of PI3K, Ly294002, suppressed the beneficial effects of HS. Conclusions: HS could attenuate neuronal apoptosis in EBI and improve the neurofunctional outcome after SAH, partially via the Akt/GSK3β pathway.

This article is from PLoS ONE , volume 9 . Abstract Backgrounds: Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). Neuronal apoptosis is involved in the pathological process of EBI. Hydrogen can inhibit neuronal apoptosis and attenuate EBI following SAH. However, the molecular mechanism underlying hydrogen-mediated anti-apoptotic effects in SAH has not been elucidated. In the present study, we aimed to evaluate whether hydrogen alleviates EBI after SAH, specifically neuronal apoptosis, partially via the Akt/GSK3β signaling pathway. Methods: Sprague-Dawley rats (n = 85) were randomly divided into the following groups: sham group (n = 17), SAH group (n = 17), SAH + saline group (n = 17), SAH + hydrogen-rich saline (HS) group (n = 17) and SAH + HS + Ly294002 (n = 17) group. HS or an equal volume of physiological saline was administered immediately after surgery and repeated 8 hours later. The PI3K inhibitor, Ly294002, was applied to manipulate the proposed pathway. Neurological score and SAH grade were assessed at 24 hours after SAH. Western blot was used for the quantification of Akt, pAkt, GSK3β, pGSK3β, Bcl-2, Bax and cleaved caspase-3 proteins. Neuronal apoptosis was identified by double staining of terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining and NeuN, and quantified by apoptosis index. Immunohistochemistry and immunofluorescent double-labeling staining was performed to clarify the relationships between neuronal apoptosis and pAkt or pGSK3β. Results: HS significantly reduced neuronal apoptosis and improved neurological function at 24 hours after SAH. The levels of pAkt and pGSK3β, mainly expressed in neurons, were markedly up-regulated. Additionally, Bcl-2 was significantly increased while Bax and cleaved caspase-3 was decreased by HS treatment. Double staining of pAkt and TUNEL showed few colocalization of pAkt-positive cells and TUNEL-positive cells. The inhibitor of PI3K, Ly294002, suppressed the beneficial effects of HS. Conclusions: HS could attenuate neuronal apoptosis in EBI and improve the neurofunctional outcome after SAH, partially via the Akt/GSK3β pathway.

This article is from Critical Care , volume 17 . Abstract Introduction: Several methods have been proposed to evaluate neurological outcome in out-of-hospital cardiac arrest (OHCA) patients. Blood lactate has been recognized as a reliable prognostic marker for trauma, sepsis, or cardiac arrest. The objective of this study was to examine the association between initial lactate level or lactate clearance and neurologic outcome in OHCA survivors who were treated with therapeutic hypothermia. Methods: This retrospective cohort study included patients who underwent protocol-based 24-hour therapeutic hypothermia after OHCA between January 2010 and March 2012. Serum lactate levels were measured at the start of therapy (0 hours), and after 6 hours, 12 hours, 24 hours, 48 hours and 72 hours. The 6 hour and 12 hour lactate clearance were calculated afterwards. Patients’ neurologic outcome was assessed at one month after cardiac arrest; good neurological outcome was defined as Cerebral Performance Category one or two. The primary outcome was an association between initial lactate level and good neurologic outcome. The secondary outcome was an association between lactate clearance and good neurologic outcome in patients with initial lactate level >2.5 mmol/l. Results: Out of the 76 patients enrolled, 34 (44.7%) had a good neurologic outcome. The initial lactate level showed no significant difference between good and poor neurologic outcome groups (6.07 ±4 .09 mmol/L vs 7.13 ± 3.99 mmol/L, P = 0.42), However, lactate levels at 6 hours, 12 hours, 24 hours, and 48 hours in the good neurologic outcome group were lower than in the poor neurologic outcome group (3.81 ± 2.81 vs 6.00 ± 3.22 P

This article is from AIDS Research and Therapy , volume 9 . Abstract Background: Even though the prevalence of HIV infection among the adult population in Ethiopia was estimated to be 2.2% in 2008, the studies on the pattern of neurological manifestations are rare. The aim of this retrospective study was to assess the pattern and predictors of mortality of HIV/AIDS patients with neurologic manifestations. Methods: Medical records of 347 patients (age ≥13 years) admitted to Tikur Anbesa Hospital from September 2002 to August 2009 were reviewed and demographic and clinical data were collected. Results: Data from 347 patients were analysed. The mean age was 34.6 years. The diagnosis of HIV was made before current admission in 33.7% and 15.6% were on antiretroviral therapy (ART). Causes of neurological manifestation were: cerebral toxoplasmosis (36.6%), tuberculous meningitis (22.5%), cryptococcal meningitis (22.2%) and bacterial meningitis (6.9%). HIV-encephalopathy, primary central nervous system (CNS) lymphoma and progressive multifocal leukoencephalopathy were rare in our patients. CD4 count was done in 64.6% and 89.7% had count below 200/mm3[mean = 95.8, median = 57] and 95.7% were stage IV. Neuroimaging was done in 38% and 56.8% had mass lesion. The overall mortality was 45% and the case-fatality rates were: tuberculous meningitis (53.8%), cryptococcal meningitis (48.1%), cerebral toxoplasmosiss (44.1%) and bacterial meningitis (33.3%). Change in sensorium and seizure were predictors of mortality. Conclusions: CNS opportunistic infections were the major causes of neurological manifestations of HIV/AIDS and were associated with high mortality and morbidity. Almost all patients had advanced HIV disease at presentation. Early diagnosis of HIV, prophylaxis and treatment of opportunistic infections, timely ART, and improving laboratory services are recommended. Mortality was related to change in sensorium and seizure.

This article is from Iranian Journal of Child Neurology , volume 6 . Abstract Children with rheumatic disorders may have a wide variety of clinical features ranging from fever or a simple arthritis to complex multisystem autoimmune diseases. Information about the prevalence of neurological manifestations in children with rheumatologic disorders is limited. This review describes the neurologic complications of childhood Rheumatic disease either solely or combined with symptoms of other organs involvement, as a primary manifestation or as a part of other symptoms, additionally.

This article is from Iranian Journal of Child Neurology , volume 6 . Abstract Children with rheumatic disorders may have a wide variety of clinical features ranging from fever or a simple arthritis to complex multisystem autoimmune diseases. Information about the prevalence of neurological manifestations in children with rheumatologic disorders is limited. This review describes the neurologic complications of childhood Rheumatic disease either solely or combined with symptoms of other organs involvement, as a primary manifestation or as a part of other symptoms, additionally.

This article is from Retrovirology , volume 11 . Abstract None

This article is from Retrovirology , volume 11 . Abstract None

The promise of recent success demonstrating the immunologic recognition of tumor cells has been limited by the paucity of native human tumor specific antigens that might serve as targets for attack. This work focused on a human disorders, paraneoplastic neurologic degeneration (PND), in which breast tumors express tumor specific antigens--proteins normally made only in the nervous system--and come under immunologic attack. In the first Aim we characterized the expression of PND genes in normal tissue and tumor. We found that cdr2, Nova-1 and Nova-2 are all highly restricted in normal tissues, but are expressed in breast and other tumors. This specificity underlies the antigenicity of these proteins in tumor cells, and provides a potential focus for tumor therapy. In Aims II-III we set out to generate animal models of breast tumor immunity against the cdr2 antigen. In parallel, we recently examined tumor immunity in human PND patients, based on our identification of cdr2 as the tumor antigen in these tumors (Aim 1). These studies allowed us to identify cdr2-specific killer T cells in breast cancer patients, and helped guide our approach to animal models. We have now generated cdr2-specific CTLs in mice inoculated with genetically defined transfected tumor cell lines. These studies allow us to overcome unanticipated difficulties originally encountered in these experiments.

This report documents the fifth reported occurrance of cerebral phaeophyphomycosis in cats. Because mycotic encephalitis was not considered in the differential diagnosis, fungal cultures were not performed. The most likely etiologic agent, based on site specificity and morphology, is Xylohypha (Cladosporium) bantiana. The most common route of transmission is by aerosol. Although rare, it should be considered in the differential diagnosis of slowly progressive neurologic disease, especially in immunosuppressed individuals. (sdw)

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