Various Types Of Brain Damage Research Articles

Brain Damage Detection Using Ensemble Classifier for Children Health Progress

Magnetic Resonance Imaging (MRI) is a medical imaging technique used to detect brain damage, particularly in children. Previous classification techniques for brain damage had low accuracy, complex edge detection, and high noise levels. In this proposed work, use an ensemble classification technique to analyze MRI brain images of 6-10 year old children. The input data is preprocessed using a Median filter to remove noise and improve image quality before being sent to a segmentation technique. Each part of the segmented image, such as tissue, inner layer, overall shape, and texture, is classified based on pixel size. The classification is done using an ensemble of Support Vector Machines (SVM) and K-Nearest Neighbors (KNN) techniques. The ensemble prediction is multiplied with several input values to classify the MRI image, aggregating different layer values. The output classified image is validated and developed using Mat Lab software simulation, with an accuracy of 97.86%. This method can accurately classify various types of brain damage and aid in early detection in children.

Role of c-Fos in DNA damage repair.

c-Fos, a member of the immediate early gene, serves as a widely used marker of neuronal activation induced by various types of brain damage. In addition, c-Fos is believed to play a regulatory role in DNA damage repair. This paper reviews the literature on c-Fos' involvement in the regulation of DNA damage repair and indicates that genes of the Fos family can be induced by various forms of DNA damage. In addition, cells lacking c-Fos have difficulties in DNA repair. c-Fos is involved in tumorigenesis and progression as a proto-oncogene that maintains cancer cell survival, which may also be related to DNA repair. c-Fos may impact the repair of DNA damage by regulating the expression of downstream proteins, including ATR, ERCC1, XPF, and others. Nonetheless, the underlying mechanisms necessitate further exploration.

Purpurin ameliorates D-galactose-induced aging phenotypes in mouse hippocampus by reducing inflammatory responses

Purpurin, an anthraquinone, has potent anti-oxidant and anti-inflammatory effects in various types of brain damage. In a previous study, we showed that purpurin exerts neuroprotective effects against oxidative and ischemic damage by reducing pro-inflammatory cytokines. In the present study, we investigated the effects of purpurin against D-galactose-induced aging phenotypes in mice. Exposure to 100 mM D-galactose significantly decreased cell viability in HT22 cells, and purpurin treatment significantly ameliorated the reduction of cell viability, formation of reactive oxygen species, and lipid peroxidation in a concentration-dependent manner. Treatment with 6 mg/kg purpurin significantly improved D-galactose-induced memory impairment in the Morris water maze test in C57BL/6 mice and alleviated the reduction of proliferating cells and neuroblasts in the subgranular zone of the dentate gyrus. In addition, purpurin treatment significantly mitigated D-galactose-induced changes of microglial morphology in the mouse hippocampus and the release of pro-inflammatory cytokines such as interleukin-1β, interleukin-6, and tumor necrosis factor-α. In addition, purpurin treatment significantly ameliorated D-galactose-induced phosphorylation of c-Jun N-terminal kinase and cleavage of caspase-3 in HT22 cells. These results suggest that purpurin can delay aging by reducing the inflammatory cascade and phosphorylation of the c-Jun N-terminal in the hippocampus.

Perioperative Changes in Serum Concentration of Glial Fibrillar Acid Protein and Delayed Cognitive Recovery: an Experimental Observational Study

A number of studies have found an association between the increased concentration of glial fibrillar acid protein (GFAP) in blood serum in patients with various types of brain damage (ischemic stroke, traumatic brain injury, neurodegenerative and neuro-oncological diseases), as well as with a rapid decline in cognitive functions in elderly people with initially normal cognitive abilities.The objective: to identify the relationship between delayed cognitive recovery and changes in serum GFAP concentration in the perioperative period in patients operated for various oncological diseases.Subjects and Methods. The study included 30 patients who underwent surgical treatment for prostate cancer, colorectal cancer and pancreatic cancer under combined general anesthesia.The inclusion criteria were the expected duration of the operation over 300 minutes and the age over 60 years. GFAP was determined in plasma by enzyme immunoassay before anesthesia, the next day after surgery and on the 4th–5th day. Neuropsychological testing was performed before surgery and on the 4th–5th postoperative day. Delayed cognitive recovery was defined as a decrease in the composite z-score of more than one standard deviation (SD) compared to the preoperative assessment.Correlation analysis was performed between changes in the composite z-score (in absolute values) and the difference in GFAP concentration between the outcome and the first postoperative day, the outcome and the 4th–5th postoperative day and the first and 4th–5th postoperative days.Results. In five cases (16.6%), a decrease in the composite z-score > 1 SD was revealed indicating a delayed cognitive recovery. In the remaining 25 (83.4%) patients, changes in the composite z-score were less than one standard deviation. The median concentration of GFAP in patients with delayed cognitive recovery was 0.13 [0.1; 0.14] before surgery, 0.12 [0.09; 0.14] the day after surgery and 0.16 [0.05; 0.19] on the 4th–5th day after surgery. In patients without cognitive impairment, the concentration of GFAP was 0.15 [0.125; 0.184] before surgery, 0.15 [0.121; 0.163] 24 hours after surgery and 0.13 [0.079; 0.151] on the 4th–5th day after surgery. The correlation values between changes in the composite z-score and the difference in GFAP concentrations were: between the outcome and the first postoperative day – rs = 0.107, p = 0.37, outcome and the 4th–5th postoperative day – rs = 0.134, p = 0.37, the first and 4th‒5th postoperative days – rs = 0.21, p = 0.37.Discussion. There was no statistically significant difference in GFAP levels between patients with delayed cognitive recovery and patients without cognitive impairment. There was also no correlation between the difference in GFAP concentrations in plasma before surgery and 24 hours after, before surgery and on the 4th–5th day of the postoperative period and the composite z-score.Conclusions. The use of GFAP to predict cognitive decline associated with surgical treatment of colorectal cancer, prostate cancer and pancreatic cancer under general anesthesia is not yet possible.

Возможности исследования коннектома человека в связи с нарушением речевых функций

In this article we discuss the potential of human connectome research, particularly in connection with its applications in rehabilitation of speech disorders. The relevance of studying human connectome as a model reflecting all the connections in human brain stems from its potential for treating patients with various types of brain damage. The understanding of the hierarchical organization of human connectome can provide a new perspective on how various diseases affect brain topology and functioning. Social relevance of this study is defined by high demand for effective post-stroke rehabilitation techniques. Annually, there are 6 million stroke cases worldwide and 450,000 cases in Russia. Stroke is a major cause not only of deterioration of quality of life but also of partial or total loss of one’s ability to work. Thus, cognitive rehabilitation is the primary aim of psychological rehabilitation. Currently scientists employ a range of methods to investigate structural and functional organization of the brain on macro-, meso- and microlevels. It has been demonstrated that several areas with richer connections play the central role in network organization and participate in multiple communications, therefore being nodes of communication. Such multi-level connectome structure allows researchers to investigate how brain damage affects its morphology and functioning. Among the cognitive impairments prevalent in stroke survivors, aphasia is one of the gravest. Rehabilitation of speech is one of the main factors defining patients’ future quality of life. Research has shown that connectome analysis is effective in assessing auditory perception as well as its nominative function and repetition.

Clinical Features of Traumatic Brain Injury in Various Kinds of Brain Damage

Various circumstances of the injury lead to various types of brain damage. The main types of destructive effects are countracoup effect and acceleration/deceleration. The high intensity injuring force creates conditions for occurrence of combinations of different types of damage leading to aggravation of pathological processes caused by trauma, complication of clinical picture, difficulties of diagnosis and treatment, prolongation of hospital stay, and requires an additional methods of research and treating the injured. Finding the genesis of symptoms observed upon neurologic examination, and especially the differential diagnosis between primary and secondary lesions of the brain stem are nessesary to choose the emergency care for victims with severe traumatic brain injury, as well as to forecast the outcomes of treatment. The dynamics of neurological symptoms (level of wakefulness, pupil size, eyeball mobility, muscle tone and limb movement disorders, pathological plantar reflexes) have significant differences in patients with various types of brain damage, which makes a regular assessment of neurological status extremely important in these patients.

Effects of FABP7 on functional recovery after spinal cord injury in adult mice.

Elucidating the mechanisms of neuronal injury is crucial for the development of spinal cord injury (SCI) treatments. Brain-type fatty acid-binding protein 7 (FABP7) is expressed in the adult rodent brain, especially in astrocytes, and has been reported to play a role in astrocyte function in various types of brain damage; however, its role after SCI has not been well studied. In this study, the authors evaluated the expression change of FABP7 after SCI using a mouse spinal cord compression model and observed the effect of FABP7 gene knockout on neuronal damage and functional recovery after SCI. Female FABP7 knockout (KO) mice with a C57BL/6 background and their respective wild-type littermates were subjected to SCI with a vascular clip. The expression of FABP7, neuronal injury, and functional recovery after SCI were analyzed in both groups of mice. Western blot analysis revealed upregulation of FABP7 in the wild-type mice, which reached its peak 14 days after SCI, with a significant difference in comparison to the control mice. Immunohistochemistry also showed upregulation of FABP7 at the same time points, mainly in proliferative astrocytes. The number of surviving ventral neurons in the FABP7-KO mice at 28 days after SCI was significantly lower than that observed in the wild-type mice. In addition, motor functional recovery in the FABP7-KO mice was significantly worse than that of the wild-type mice. The findings of this study indicate that FABP7 could have a neuroprotective role that might be associated with modulation of astrocytes after SCI. FABP7 could potentially be a therapeutic target in the treatment of SCI.

Carbon dots based immunosorbent assay for the determination of GFAP in human serum

Glial fibrillary acidic protein (GFAP) is expressed in the central nervous system and the level of GFAP normally rises with brain injury and astroglial tumors. So, serum GFAP is used as a marker for diagnosing various types of brain damage and astroglial tumors. In this study, a new sensor based on carbon dots (CDs) linked with antibodies to specifically detect GFAP in human serum was developed. Anti-GFAP (Ab1) linked with protein A/G agarose resin (PA/G) as a capture antibody (PA/G-Ab1) and anti-GFAP (Ab2) labeled with CDs as a detection antibody (CDs-Ab2) were prepared firstly. Then the CD-linked antibody immunosorbent assay (CLAISA) method was constructed based on the sandwich conjunction reaction among PA/G-Ab1, GFAP, and CDs-Ab2. CLAISA, using the fluorescence of PA/G-Ab1-GFAP-Ab2-CDs as the direct signal, enabled the proposed immunosensor to detect GFAP sensitively with a linear range of 0.10–8.00 ng ml−1 and a detection limit of 25 pg ml−1. This method was applied to the determination of GFAP in human serum by the standard addition method, and the results showed high accuracy and precision. Considering the easy synthetic process and excellent performance of CLAISA, this method has great potential to be used to monitor GFAP in the clinic.

Chapter 23 - Thermoregulation and age

The thermoregulatory functions may vary with age. Thermosensitivity is active in neonates and children; both heat production and heat loss effector mechanisms are functional but easily exhaustable. Proportional and lasting defense against thermal challenges is difficult, and both hypothermia and hyperthermia may easily develop. Febrile or hypothermic responses to infections or endotoxin can also develop, together with confusion. In small children febrile convulsions may be dangerous. In old age the resting body temperature may be lower than in young adults. Further, thermosensitivity decreases, the thresholds for activating skin vasomotor and evaporative responses or metabolism are shifted, and responses to thermal challenges are delayed or insufficient: both hypothermia and hyperthermia may develop easily. Infection-induced fevers are often limited or absent, or replaced by hypothermia. Various types of brain damage may induce special forms of hypothermia, hyperthermia, or severe fever. Impaired mental state often accompanies hypothermia and hyperthermia, and may occasionally be a dominant feature of infection (instead of the most commonly observed fever). Aging brings about a turning point in women's life: the menopause. The well-known influence of regular hormonal cycles on the thermoregulation of a woman of fertile age gives way to menopausal hot flushes caused by estrogen withdrawal. Not all details of this thermoregulatory anomaly are fully understood yet.

Extracellular poly(ADP-ribose) is a neurotrophic signal that upregulates glial cell line-derived neurotrophic factor (GDNF) levels in vitro and in vivo

Synthesis of poly(ADP-ribose) (PAR) is catalyzed by PAR polymerase-1 (PARP-1) in neurons. PARP1 plays a role in various types of brain damage in neurodegenerative disorders. In neurons, overactivation of PARP-1 during oxidative stress induces robust PAR formation, which depletes nicotinamide adenine dinucleotide levels and leads to cell death. However, the role of the newly-formed PAR in neurodegenerative disorders remains elusive. We hypothesized that the effects of PAR could occur in the extracellular space after it is leaked from damaged neurons. Here we report that extracellular PAR (EC-PAR) functions as a neuroprotective molecule by inducing the synthesis of glial cell line-derived neurotrophic factor (GDNF) in astrocytes during neuronal cell death, both in vitro and in vivo. In primary rat astrocytes, exogenous treatment with EC-PAR produced GDNF but not other neurotrophic factors. The effect was concentration-dependent and did not affect cell viability in rat C6 astrocytoma cells. Topical injection of EC-PAR into rat striatum upregulated GDNF levels in activated astrocytes and improved pathogenic rotation behavior in a unilateral 6-hydroxydopamine model of Parkinson disease in rats. These findings indicate that EC-PAR acts as a neurotrophic enhancer by upregulating GDNF levels. This effect protects the remaining neurons following oxidative stress-induced brain damage, such as that seen with Parkinson disease.

Differences in Cognitive Function of Rats with Traumatic Brain Injuries Following Hyperbaric Oxygen Therapy.

BackgroundHyperbaric oxygen (HBO) is a historical therapeutic option in the treatment of various types of brain damage. At present, clinical treatment of hypoxic-ischemic injury is giving priority to cognitive training. The effects of HBO on cognitive dysfunction were observed in a controlled cortical impact (CCI) rat model.Material/MethodsSeventy male SD rats were randomly divided into control (n=10) and intervention (n=60) groups. All rats underwent baseline water maze testing 1 day before modeling, and were retested 8 weeks after modeling. The percentage of residence time during escape latency in the target quadrant and the total time were recorded. Data were analyzed by SPSS 16.0 software. P<0.05 was considered statistically significant.ResultsAfter 8 weeks, no statistical difference (P>0.05) existed in spatial learning ability in the 3-day and 5-day groups when compared with baseline. The other groups were statistically different by auto-comparison (P<0.05). No statistical difference (P>0.05) in spatial memory existed in the 5-day and 1-week groups when compared with baseline, while a significant difference was noted in the other groups by self-comparison (P<0.05). No statistical difference (P>0.05) was noted in the level of expression of growth-associated protein-43 (GAP-43) and synaptophysin (Syn) in the 1-day group compared with the control group. The remaining groups and the control group were statistically different (P<0.05), while the level of expression of GAP-43 and Syn in the 5-day, 1-week, and 2-week groups was significantly different compared with that in the control group (P<0.01).ConclusionsIf HBO therapy was provided 5–7 days after craniocerebral trauma, there was apparent improvement in cognitive function and neuroplasticity.

Cortical regulation of striatal projection neurons and interneurons in a Parkinson's disease rat model.

Striatal neurons can be either projection neurons or interneurons, with each type exhibiting distinct susceptibility to various types of brain damage. In this study, 6-hydroxydopamine was injected into the right medial forebrain bundle to induce dopamine depletion, and/or ibotenic acid was injected into the M1 cortex to induce motor cortex lesions. Immunohistochemistry and western blot assay showed that dopaminergic depletion results in significant loss of striatal projection neurons marked by dopamine- and cyclic adenosine monophosphate-regulated phosphoprotein, molecular weight 32 kDa, calbindin, and μ-opioid receptor, while cortical lesions reversed these pathological changes. After dopaminergic deletion, the number of neuropeptide Y-positive striatal interneurons markedly increased, which was also inhibited by cortical lesioning. No noticeable change in the number of parvalbumin-positive interneurons was found in 6-hydroxydopamine-treated rats. Striatal projection neurons and interneurons show different susceptibility to dopaminergic depletion. Further, cortical lesions inhibit striatal dysfunction and damage induced by 6-hydroxydopamine, which provides a new possibility for clinical treatment of Parkinson's disease.

A retrospective case-study to determine the efficacy of Zolpidem in neurologically impaired patients to improve brain functioning and mental cognition

A retrospective case-study to determine the efficacy of Zolpidem in neurologically impaired patients to improve brain functioning and mental cognition The prescription drug Zolpidem, originally used for treating insomnia, has recently been found to have significant beneficial effects on patients with various types of brain damage. This retrospective study will investigated the nature and extent of improvements observed in patients with brain damage due to hypoxic injury, stroke, birth defects, and trauma.

A retrospective case-study to determine the efficacy of Zolpidem in neurologically impaired patients to improve brain perfusion and function.

A retrospective case-study to determine the efficacy of Zolpidem in neurologically impaired patients to improve brain perfusion and function The prescription drug Zolpidem, generally used as a sleep induction agent, has been found to have significant beneficial effects on patients with various types of brain damage. The initial findings of this study support the paradoxical conclusion that Zolpidem is able to restore varying degrees of brain perfusion within subpopulations of brain damaged patients.

APOE genotype alters glial activation and loss of synaptic markers in mice

The ε4 allele of the Apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), and affects clinical outcomes of chronic and acute brain damages. The mechanisms by which apoE affect diverse diseases and disorders may involve modulation of the glial response to various types of brain damage. We examined glial activation in a mouse model where each of the human APOE alleles are expressed under the endogenous mouse APOE promoter, as well as in APOE knock-out mice. APOE4 mice displayed increased glial activation in response to intracerebroventricular lipopolysaccharide (LPS) compared to APOE2 and APOE3 mice by several measures. There were higher levels of microglia/macrophage, astrocytes, and invading T-cells after LPS injection in APOE4 mice. APOE4 mice also displayed greater and more prolonged increases of cytokines (IL-1β, IL-6, TNF-α) than APOE2 and APOE3 mice. We found that APOE4 mice had greater synaptic protein loss after LPS injection, as measured by three markers: PSD-95, drebin, and synaptophysin. In all assays, APOE knock-out mice responded similar to APOE4 mice, suggesting that the apoE4 protein may lack anti-inflammatory characteristics of apoE2 and apoE3. Together, these findings demonstrate that APOE4 predisposes to inflammation, which could contribute to its association with Alzheimer's disease and other disorders.

Abnormal Cortical Network Activation in Human Amnesia: A High-resolution Evoked Potential Study

Little is known about how human amnesia affects the activation of cortical networks during memory processing. In this study, we recorded high-density evoked potentials in 12 healthy control subjects and 11 amnesic patients with various types of brain damage affecting the medial temporal lobes, diencephalic structures, or both. Subjects performed a continuous recognition task composed of meaningful designs. Using whole-scalp spatiotemporal mapping techniques, we found that, during the first 200 ms following picture presentation, map configuration of amnesics and controls were indistinguishable. Beyond this period, processing significantly differed. Between 200 and 350 ms, amnesic patients expressed different topographical maps than controls in response to new and repeated pictures. From 350 to 550 ms, healthy subjects showed modulation of the same maps in response to new and repeated items. In amnesics, by contrast, presentation of repeated items induced different maps, indicating distinct cortical processing of new and old information. The study indicates that cortical mechanisms underlying memory formation and re-activation in amnesia fundamentally differ from normal memory processing.

Prostaglandins and Cyclooxygenases in Glial Cells During Brain Inflammation

Many brain disorders such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Huntington, stroke, head trauma, and infection, are associated with inflammation that is involved in neuropathologenesis and hyperalgesis. Microglia and astrocytes act as immune cells in the inflamed brain. Both cell types, but especially microglia, are thought to contribute to the onset of inflammation in many brain diseases by producing deleterious proinflammatory mediators. Prostaglandins (PGs), which are critical mediators of physiologic processes and inflammation, are largely produced by activated microglia and reactive astrocytes during brain inflammation. These compounds are converted from arachnoidic acid (AA) by two isoforms of the cyclooxygenase (COX) enzyme, namely COX-1 and COX-2. In particular, the action of COX-2 and PGs in CNS inflammation has gained much attention recently. PGs have been found to act neuroprotectively by elevating intracellular cAMP levels in neurons. These molecules also function as anti-inflammatory molecules to reduce the production of nitric oxide and proinflammatory cytokines, and to increase the expression of anti-inflammatory cytokines. However, accumulating evidence also shows that COX inhibitors alleviate various types of brain damage via suppressing inflammatory reactions. Accordingly, the roles of two COX enzymes in mediating inflammation and anti-inflammation have recently been debated. We provide here a review of recent findings indicating that the reciprocal interaction of glial cell activation, COX enzymes and PGs mediates neurodegeneration and neuroprotection during brain inflammation. In addition, the mechanism by which PGs mediate signaling is discussed.

Assessing nonverbal memory with the Biber Figure Learning Test—Extended in temporal lobe epilepsy patients

Material-specific memory dysfunction was assessed using a nonverbal, visuospatial, supraspan learning test, the Biber Figure Learning Test-Extended (BFLT-E), in 71 left-hemisphere language-dominant epilepsy patients prior to anterior temporal lobectomy (ATL) and in 48 age-matched healthy subjects. Two matched forms of the BFLT-E yielded comparable scores, indicating that this task may be used to track memory performance over time in individual patients. Right temporal lobe epilepsy (RTLE) and left temporal lobe epilepsy (LTLE) patients performed below healthy subjects on all free-recall measures. RTLE, but not LTLE, patients also differed from healthy subjects in recognition memory discrimination. Furthermore, the RTLE patients performed below LTLE patients on measures specific to long-term memory abilities. The BFLT-E appears to be a useful clinical tool for assessing different components of visuospatial memory in patients with lateralized mesial temporal lobe (MTL) dysfunction. The test is sensitive to visuoconstructional problems associated with various types of brain damage, but it also distinguishes material-specific, nonverbal, visuospatial memory impairments in patients with neurological dysfunction in the non language-dominant right temporal lobe.

Assessing nonverbal memory with the Biber Figure Learning Test--Extended in temporal lobe epilepsy patients

Material-specific memory dysfunction was assessed using a nonverbal, visuospatial, supraspan learning test, the Biber Figure Learning Test-Extended (BFLT-E), in 71 left-hemisphere language-dominant epilepsy patients prior to anterior temporal lobectomy (ATL) and in 48 age-matched healthy subjects. Two matched forms of the BFLT-E yielded comparable scores, indicating that this task may be used to track memory performance over time in individual patients. Right temporal lobe epilepsy (RTLE) and left temporal lobe epilepsy (LTLE) patients performed below healthy subjects on all free-recall measures. RTLE, but not LTLE, patients also differed from healthy subjects in recognition memory discrimination. Furthermore, the RTLE patients performed below LTLE patients on measures specific to long-term memory abilities. The BFLT-E appears to be a useful clinical tool for assessing different components of visuospatial memory in patients with lateralized mesial temporal lobe (MTL) dysfunction. The test is sensitive to visuoconstructional problems associated with various types of brain damage, but it also distinguishes material-specific, nonverbal, visuospatial memory impairments in patients with neurological dysfunction in the non language-dominant right temporal lobe.

What Neuropsychology Tells us About Consciousness

I argue that, contrary to some critics, the notion of conscious experience is a good candidate for denoting a distinct and scientifically interesting phenomenon in the brain. I base this claim mainly on an analysis of neuropsychological data concerning deficits resulting from various types of brain damage as well as some additional supporting empirical evidence. These data strongly point to the hypothesis that conscious experience expresses information that is available for global, integrated, and flexible behavior.