Destruction Of Brain Tissue Research Articles

Клінічне спостереження тератоми головного мозку новонародженого

A congenital brain tumor is a tumor detected before birth or during the first two months of life. The frequency of congenital brain tumors is extremely low - 0.34 per 1 million newborns, and no more than 1.5% of all neoplasms of the central nervous system in children, but the rapid growth of the tumor and the destruction of normal brain tissue give them a fatal prognosis. Purpose - to expand knowledge on the possibilities of antenatal diagnosis and the features of the management of the early neonatal period of congenital mіalformations based on the clinical observation of fetal brain teratoma. An overview of literature sources is provided on the prevalence of pathology, histological structure (teratomas, neuroepithelial and mesenchymal tumors), features of the clinical course that distinguish them from childhood tumors - mainly supratentorial localization, lack of growth restriction due to the mobility of the bones of the skull, prognosis and tactics of pregnancy and childbirth . Ultrasound examination is the main method of diagnosis of brain tumors, which are visualized in the form of a solid or cystic calcified formation or not, and manifestations of hypervascularization can also be absent or present. The features of the structure and development of the teratoma, which contains cells of all 3 germ layers and has properties of rapid destructive growth, are also described. Hydrocephalus accompanying congenital brain tumors can be caused both by compression of the ventricular system and intracranial hemorrhages. Thanks to modern diagnostic capabilities, most cases are detected in terms of possible termination of pregnancy, in the case of childbirth with such a pathology, in 60% of cases, a cesarean section is used. The given clinical case shows the possibilities of antenatal diagnosis of a brain tumor and even clearly establishing the depth of the lesion, at the same time as the lack of treatment options. The research was carried out in accordance with the principles of the Helsinki Declaration. The informed consent of the patient was obtained for conducting the studies. No conflict of interests was declared by the authors.

Postnatal Effects of the Ethanol on the Encephalon Mass and Neocortex Architecture in Wistar Rat Offspring Submitted to Acute Prenatal Injection [E12] and in vitro Ethanol Effects on Wistar Rat and Human Erythrocytes

Aims: To verify the ethanol effects of the acute injections in pregnant Wistar rats (E12) on the offspring in P8. Additionally, measures of the brain and corporal masses and the stability of erythrocytes were performed in rats and humans.
 Study Design: Histological analysis and a spectrophotometer were used to count neural cells and osmotic fragility in erythrocytes.
 Place and Duration of Study: The immunohistochemistry study was partially performed at the Federal University of Uberlândia, and at the University of Toyama-Japan, the experiments on the brain, body masses, and stability of erythrocyte membranes in humans were performed from 2012 to 2014.
 Methodology: Eighteen pregnant female rats (180-230g) were housed in cages at 22 ± 0.4°C on a 12 h light/dark cycle with free access to food and water. On the 11th day of pregnancy (E12), 12 rats received three intraperitoneal (i.p.) injections of a 20% ethanol solution (3 g of ethanol/kg of body weight) at 8 hours intervals.
 Results: The number of neural cells was lower in rats treated with ethanol than to controls to each lobe and total count in all lobes (P = 0.001). Significant alterations of neocortical tissue in ethanol-treated were observed, as the decrease of brain mass (P = 0.05) in linear regression. The stability of erythrocyte membranes was verified with D50 equal to 0.46 g·dL-1 (± 0.05).
 Conclusion: According to this work, the ethanol injection in the rats showed marked brain tissue destruction relative to the control, and ethanol’s effects on erythrocytes indicated that membrane destruction could be one of the causes of brain cell disruption in neural migration.

Traumatic brain injury: Mechanisms, manifestations, and visual sequelae.

Traumatic brain injury (TBI) results when external physical forces impact the head with sufficient intensity to cause damage to the brain. TBI can be mild, moderate, or severe and may have long-term consequences including visual difficulties, cognitive deficits, headache, pain, sleep disturbances, and post-traumatic epilepsy. Disruption of the normal functioning of the brain leads to a cascade of effects with molecular and anatomical changes, persistent neuronal hyperexcitation, neuroinflammation, and neuronal loss. Destructive processes that occur at the cellular and molecular level lead to inflammation, oxidative stress, calcium dysregulation, and apoptosis. Vascular damage, ischemia and loss of blood brain barrier integrity contribute to destruction of brain tissue. This review focuses on the cellular damage incited during TBI and the frequently life-altering lasting effects of this destruction on vision, cognition, balance, and sleep. The wide range of visual complaints associated with TBI are addressed and repair processes where there is potential for intervention and neuronal preservation are highlighted.

Prevalence of death due to Firearm (Gunshot) injuries in Forensic Cases, in Kabul city, Afghanistan

Introduction: firearms (rifles, pistols, grenades, mines, and suicide bombers) cause gunshot injuries. In addition to destructive damage, the use of these weapons causes severe health damage, including bed sentences, disability, and death, which impose a heavy burden on the health sector and society with many adverse consequences for the social system. Objective: to assess the prevalence of deaths due to firearm injuries in the cases brought to the Kabul Forensic Medicine Center. Methods and Materials: This is a descriptive cross-sectional study. We have collected the data in a census manner from March 21, 2019, to March 19, 2020. We have retrieved the demographic information from the database of Kabul Forensic Medicine Center and analyzed it using SPSS version 26. Results: we went through the files and reviewed the demographic information of 1538 dead bodies which were brought to the Kabul Forensic Medicine Center, from March 21, 2019, to March 19, 2020, of which 466 (30.29%) were due to firearm injuries. Among those victims, 428 cases (91, 84%), were men, and 28 cases (8.16%) were female. The youngest age of the victims was 18 years and the oldest age of the victims was 40 years. The most common site of injury was the head (34.97%), and the most common cause of death was the destruction of brain tissue and severe internal and external bleeding (34.97%). The distance of gunshot was distant in most of the cases (52.78%). In most of the cases (69.74%), the type of wound canal originated with the exit wound. Conclusion: the death prevalence due to firearm injuries was 30.29%. Male, in the second, third, and fourth decades of life were victims in the majority of cases. In terms of anatomical location, the causes of death in most cases were firearm injuries to the head, destruction of brain tissues, and severe internal and external bleeding.

Pro-inflammatory cytokines in cystic glioblastoma: A quantitative study with a comparison with bacterial brain abscesses. With an MRI investigation of displacement and destruction of the brain tissue surrounding a glioblastoma.

Cystic glioblastomas are aggressive primary brain tumors that may both destroy and displace the surrounding brain tissue as they grow. The mechanisms underlying these tumors’ destructive effect could include exposure of brain tissue to tumor-derived cytokines, but quantitative cytokine data are lacking. Here, we provide quantitative data on leukocyte markers and cytokines in the cyst fluid from 21 cystic glioblastomas, which we compare to values in 13 brain abscess pus samples. The concentration of macrophage/microglia markers sCD163 and MCP-1 was higher in glioblastoma cyst fluid than in brain abscess pus; lymphocyte marker sCD25 was similar in cyst fluid and pus, whereas neutrophil marker myeloperoxidase was higher in pus. Median cytokine levels in glioblastoma cyst fluid were high (pg/mL): TNF-α: 32, IL-6: 1064, IL-8: 23585, tissue factor: 28, the chemokine CXCL1: 639. These values were not significantly different from values in pus, pointing to a highly pro-inflammatory glioblastoma environment. In contrast, levels of IFN-γ, IL-1β, IL-2, IL-4, IL-10, IL-12, and IL-13 were higher in pus than in glioblastoma cyst fluid. Based on the quantitative data, we show for the first time that the concentrations of cytokines in glioblastoma cyst fluid correlate with blood leukocyte levels, suggesting an important interaction between glioblastomas and the circulation. Preoperative MRI of the cystic glioblastomas confirmed both destruction and displacement of brain tissue, but none of the cytokine levels correlated with degree of brain tissue displacement or peri-tumoral edema, as could be assessed by MRI. We conclude that cystic glioblastomas are highly pro-inflammatory environments that interact with the circulation and that they both displace and destroy brain tissue. These observations point to the need for neuroprotective strategies in glioblastoma therapy, which could include an anti-inflammatory approach.

Constructing Domain Ontology for Alzheimer Disease Using Deep Learning Based Approach

Facts can be exchanged in multiple fields with the help of disease-specific ontologies. A range of diverse values can be produced by mining ontological approaches for demonstrating disease mechanisms. Alzheimer’s disease (AD) is an incurable neurological brain illness. An early diagnosis of AD can be helpful for better treatment and the prevention of brain tissue destruction. Researchers have used machine learning techniques to predict the early detection of AD. However, Alzheimer’s disorders are still underexplored in the knowledge domain. In the biomedical field, the illustration of terminologies and notions is essential. Multiple methods are adopted to represent these notions, but ontologies are the most frequent and accurate. Ontology construction is a complex and time-consuming process. The designed ontology relies on Disease Ontology (DO), which is considered the benchmark in medical practice. Ontology reasoning mechanisms can be adopted for AD identification. In this paper, a deep convolutional neural network-based approach is proposed to diagnose Alzheimer’s disease, using an AD dataset acquired from Kaggle. Machine learning-based approaches (logistic regression, gradient boosting, XGB, SGD, MLP, SVM, KNN, random forest) are also used for a fair comparison. The simulation results are generated using three strategies (default parameters, 10-cross validation, and grid search), and MLP provides superior results on a default parameter strategy with an accuracy of 92.12%. Furthermore, the deep learning-based approach convolutional neural network (CNN) achieved an accuracy of 94.61%. The experimental results indicate that the construction of ontology, with the help of deep learning knowledge, can produce better results where the robustness and scalability can be enhanced. In comparisons to other methods, the CNN results are excellent and encouraging.

Development of a Novel Biomarker for an early detection of Alzheimer disease

BackgroundAlzheimer’s disease (AD), a neurodegenerative disease, is the most common form of dementia among older patients and is the 6th leading cause of death in the US. Almost 1 in 10 people over the age of 65 have AD and every 65 second someone in the US develop AD. Worldwide 30 million people have AD, and 5.8 million American are living with this disease where by 2050, it is projected to be 14 million. Problems in AD and other forms of dementia involve an irreversible brain tissue damage and destruction, leading to progressive cognitive impairment led difficulty of performing simple tasks. In 2019, AD and other dementia in US costed $290 billion. By 2050, these costs could rise as high as 1.1 trillion. Due to technological advancements in artificial intelligence, the computer can not only plan & predict the path or course for a robot, but for multiple proteins and their metabolites. Several digital models and simulations can determine the interactions and commonality between proteins of all sorts. The goal of this project is to identify biological markers by metabolomic meta‐analysis that correlate with the progression of AD and be integrated to a prototype biosensor capable of detecting the stable biomarker for an early detection of dementia. This project analyzes the commonalties in dementia related proteins through data mining and analysis of the cerebrospinal fluid and blood metabolome to see (when altered in Alzheimer disease) the metabolic reactions that could potentially relate to phenotypes detectable for an early onset Alzheimer's. Along with that, the project utilizes the novel findings to assemble a detection system via electrochemical analysis by observing the difference in the relative resistance between varying solution of key analyte changed in Alzheimer’s patient.Material and MethodsPlastic straw, Hydrogel, Electrical resistant measuring machine and specialized Electrode. Protein sequences analysis: Information on the proteins that are associated with the Alzheimer diseases were obtained from PubMed; Amino acid sequences of these proteins (in FASTA format) were obtained through ExPASy. The amino acid sequences of proteins in FASTA format were obtained from the UniProt database in Expasy. Clastalw‐Multiple Alignment: The commonality in the protein sequences was deduced obtained by aligning multiple protein sequences through the Clustal‐W.Results and ConclusionBioinformatics tools and computer algorithms shows three dimensional structures of Alzheimer’s disease associated proteins where majority of them were associated with the membrane. Mutational analysis indicated that most of them in AD fall into transmembrane regions of the protein which may be due to change in lipid composition of the cells. Metabolomics studies indicated that the relative abundance of lipid metabolites was relatively low in the blood of AD compared to healthy or MCI. In contrast, the cerebrospinal fluid levels of lipid metabolites were higher in AD/dementia patients compared to their healthy counterparts. Increased lipid metabolomic disturbances in CSF also correlated with enlarged ventricle filled with CSF in AD patients. Digital models and simulations studies of this project demonstrated the interactions and commonality between proteins of AD and demonstrated their folding. Analysis of the CSF and blood metabolome provided a strong AD phenotypes detectability for early onset Alzheimer and may be useful as detectable marker for the cognitive impairment.

Targeting C-C Chemokine Receptor 5: Key to Opening the Neurorehabilitation Window After Ischemic Stroke.

Stroke is the world’s second major cause of adult death and disability, resulting in the destruction of brain tissue and long-term neurological impairment; induction of neuronal plasticity can promote recovery after stroke. C–C chemokine receptor 5 (CCR5) can direct leukocyte migration and localization and is a co-receptor that can mediate human immunodeficiency virus (HIV) entry into cells. Its role in HIV infection and immune response has been extensively studied. Furthermore, CCR5 is widely expressed in the central nervous system (CNS), is engaged in various physiological activities such as brain development, neuronal differentiation, communication, survival, and learning and memory capabilities, and is also involved in the development of numerous neurological diseases. CCR5 is differentially upregulated in neurons after stroke, and the inhibition of CCR5 in specific regions of the brain promotes motor and cognitive recovery. The mechanism by which CCR5 acts as a therapeutic target to promote neurorehabilitation after stroke has rarely been systematically reported yet. Thus, this review aims to discuss the function of CCR5 in the CNS and the mechanism of its effect on post-stroke recovery by regulating neuroplasticity and the inflammatory response to provide an effective basis for clinical rehabilitation after stroke.

Protective Effects of Cannabinoid Type 2 Receptor Activation Against Microglia Overactivation and Neuronal Pyroptosis in Sepsis-Associated Encephalopathy

Sepsis-associated encephalopathy (SAE) has close association with long-term cognitive deficits, resulting in increased mortality. The mechanism of SAE is complicated, including excessive microglial activation and neuroinflammation. Cannabinoid type 2 receptor (CB2R) has been proved to be effective in neuronal protection and survival promotion. Microglia play a role in CB2R mediated neuronal protection when neurons are exposed to noxious stimuli. Pyroptosis is a type of programmed proinflammatory cell death. However, the underlying mechanisms involved in this process still remain to be explored. Here, the SAE model was derived from cecal ligation and puncture (CLP). Tests used to evaluate behavior phenotypes included the open-field test (OFT), novel object recognition test (NORT), and Morris water maze (MWM). Hematoxylin and eosin (H&E) staining, enzyme-linked immunosorbent assays (ELISA), Western blotting, and immunofluorescence staining were performed to detect cell injury, cytokine, CB2R and pyroptosis-associated protein expression. Conclusion from these results, we conclude that CLP could induce microglia hyperactivation and neuronal pyroptosis, aggravating brain tissue destruction and cognitive dysfunction. The CB2R-specific agonist HU308 could have protective effects against SAE by inhibiting microglia activity and neuronal pyroptosis. This study provides a new therapeutic option for the treatment of SAE.

Overexpressed ski efficiently promotes neurorestoration, increases neuronal regeneration, and reduces astrogliosis after traumatic brain injury.

Traumatic brain injury (TBI) survivors suffer from long-term disability and neuropsychiatric sequelae due to irreparable brain tissue destruction. However, there are still few efficient therapies to promote neurorestoration in damaged brain tissue. This study aimed to investigate whether the pro-oncogenic gene ski can promote neurorestoration after TBI. We established a ski-overexpressing experimental TBI mouse model using adenovirus-mediated overexpression through immediate injection after injury. Hematoxylin-eosin staining, MRI-based 3D lesion volume reconstruction, neurobehavioral tests, and analyses of neuronal regeneration and astrogliosis were used to assess neurorestorative efficiency. The effects of ski overexpression on the proliferation of cultured immature neurons and astrocytes were evaluated using imaging flow cytometry. The Ski protein level increased in the perilesional region at 3 days post injury. ski overexpression further elevated Ski protein levels up to 14 days post injury. Lesion volume was attenuated by approximately 36-55% after ski overexpression, with better neurobehavioral recovery, more newborn immature and mature neurons, and less astrogliosis in the perilesional region. Imaging flow cytometry results showed that ski overexpression elevated the proliferation rate of immature neurons and reduced the proliferation rate of astrocytes. These results show that ski can be considered a novel neurorestoration-related gene that effectively promotes neurorestoration, facilitates neuronal regeneration, and reduces astrogliosis after TBI.

The effect of (Mg, Co) bis (citrate) germanates on morphological changes in brain tissue

Introduction. The problem of safety of pharmacotherapy is becoming more and more urgent all over the world. This is primarily due to the increase in the number of medicines and their widespread use. The use of pharmacotherapeutic agents is usually accompanied by the occurrence of adverse reactions, which differ in their manifestations and degree of severity. Safe use of medicines is one of the priority tasks of modern health care. Therefore, when studying new biologically active substances – future medicines, special attention is paid to information about their toxicity. The search for new effective and safe medicines is a rather complex and long process. One of the well-known ways of searching is based on the detection of biologically active substances (BAS) involved in life processes, pathophysiological and pathochemical processes that underlie the pathogenesis of various diseases. Guided by these principles under the leadership of Professor Seyfullina I.Y. at the Department of Inorganic Chemistry and Chemical Education of Odesa National University named after I.I. Mechnikov, a number of biologically active substances were synthesized – coordination compounds based on germanium, vitamins, microelements, and organic acids acted as bioligands. Purposefully synthesized: magnesium bis(citrato)germanate – hermacite, cobalt bis(citrato)germanate – hercocite. The acute toxicity of BAR was studied: magnesium bis (citrato) germanate LD50= (3049.55±42.54) mg/kg of rat weight, cobalt bis (citrato) germanate LD50= (185.00±4.23) mg/kg. The aim of the work was to study the morphological changes in the brain tissue of rats after administration of (Mg, Co) bis (citrate) germanates in subacute and subchronic experiments. Research methodology and methods. An experimental study was conducted on sexually mature male Wistar rats weighing 180-250 g, which were injected intraperitoneally with (Mg, Co) bis (citrate) germanates in doses of 1/40, 1/110 and 1 /135 LD50. At the same time, it was previously proven that the main pharmacological properties of the compound were manifested by doses of 1/110 and 1/135 LD50. After decapitation, macro- and microscopic examination of the brain tissue was carried out. When conducting the experiment, the general principles of the European Convention for the Protection of Vertebrate Animals, Directive 2010/63/EU of the European Parliament and the Council of the European Union dated September 21, 2010 on the protection of animals used for scientific purposes were observed. Research results and their discussion. The introduction of coordination compounds of metals for 28 days at a dose of 1/40 LD50 caused the appearance of perivascular and pericellular edema in the tissue of the brain, which was more pronounced for the cobalt-containing compound. Administration of hermacyt in doses of 1/40 LD50 for 3 months led to the appearance of areas of necrotized brain tissue, and administration of hercocyte led to the appearance of areas of destruction of brain tissue with the formation of small cavities. Administration of BAR in doses of 1/110 LD50 for 28 days and 3 months was accompanied by minor morphological changes (moderately expressed perivascular and pericellular edema). When BAR was used in doses of 1/135 LD50, the tissue of the brain of rats had minor changes (fullness of individual vessels of the microcirculatory channel, around which there is moderate edema). Conclusions. Thus, new multimetallic coordination compounds (Mg, Co) bis(citrate) germanate in effective doses in subacute and subchronic experiments did not show toxic effects on brain tissues and are promising for further study and establishment of pharmacological properties.

Memory Modulation Factors in Hippocampus Exposed to Radiation.

Although the key scene of the hippocampus in memory processes is obvious, the specificity of its participation in information processing is far from being established. Current advanced neuroimaging enables to operate with precise morphometric parameters.The aim of the study was to reveal fine memory rearrangements under mechanical impact on the hippocampus by a neoplasm and radiation exposure in the course of therapy.Materials and MethodsWe used a homogeneous sample of 28 patients with parasellar meningiomas adjacent to hippocampus. In 10 patients (5 with left-sided and 5 with right-sided meningiomas), the tumor was located near the hippocampus but exhibited no mechanical effect on it. In 18 patients (10 with left-sided and 8 with right-sided tumors), the neoplasm compressed the adjacent hippocampus. The control group consisted of 39 healthy subjects. All three groups were comparable in age, education, and gender characteristics. In order to control tumor growth, the patients underwent radiotherapy when the hippocampus involuntary was exposed to a dose comparable to that in the tumor (30 sessions with a single focal dose of 1.8 Gy, total dose — 54.0 Gy).Based on the literature data on hippocampus involved in mnestic processes, a special methodology to investigate memory was developed. Incorrect responses the subjects made when identifying previously memorized images were classified as neutralizing the novelty factor of an identified stimulus or as wrongly emphasizing its novelty.ResultsAt the first observation point (before radiation therapy) all groups underwent a complete standardized neuropsychological examination and performed a battery of cognitive tests. The overall results of the tests assessing attention, memory, thinking processes, and neurodynamic indicators corresponded to standard values. A mild brain compression by the tumor without brain tissue destruction was not accompanied by focal neuropsychological symptoms and deficit manifestations in the cognitive sphere. However, as early as in the first observation point, the number of “pattern separation” errors in the clinical group was significantly higher than that in healthy subjects.The second observation point (immediately after radiotherapy) and the third observation point — 6 months after the treatment — showed that, in general, the patients’ cognitive sphere condition was not deteriorating, and in a number of parameters was characterized by positive dynamics, apparently associated with some tumor reduction due to the therapy provided. However, the distribution of errors in the original method significantly changed. When previously memorized stimuli were recognized, the errors neutralizing the novelty factor of the evaluated stimulus increased, while the number of errors with overestimating the stimuli novelty decreased.All tendencies hypothetically (according to the published data) associated with the changes in functional activity of the hippocampus were more pronounced in the subgroup of patients with mechanical impact of the tumor on hippocampus.ConclusionThe continuous flow of impressions any person has at any moment of his activity is most likely marked by the hippocampus in a continuum “old–similar–new”. The present study has shown that mechanical impact on the hippocampus combined with radiation exposure changes the range of assessments towards the prevailing labeling “old, previously seen, already known”.

Antiatherogenic Effects of Quercetin in the THP-1 Macrophage Model In Vitro, With Insights Into Its Signaling Mechanisms Using In Silico Analysis

Background: Atherosclerosis (AS), a major risk factor for stroke and brain tissue destruction, is an inflammatory disease of the blood vessels, and the underlying pathology is inflammation mediated by various chemokines and cytokines. Quercetin, a natural flavonol, is reported to have both anti-inflammatory and antioxidant properties. As such, in the present study, we evaluated the antiatherogenic effects of quercetin in a human THP-1 cell line in vitro and also the signaling mechanisms using in silico analysis.Materials and Methods: THP-1 macrophages exposed to different concentrations of quercetin (5–100 μM for 24 h) were tested for cytotoxicity. Real-time gene expression assay for intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) was carried out following treatment with quercetin at 15 and 30 μM for 24 h either in the absence or presence of interferon (IFN-γ) for 3 h to induce inflammation. Monocyte migration and cholesterol efflux were also assessed.Results: Quercetin did not exert any cytotoxic effects on THP-1 cells at the various concentrations tested. The gene expression assay showed a significant decrease in ICAM-1 (by 3.05 and 2.70) and MCP-1 (by 22.71 and 27.03), respectively. Quercetin at 15 µM decreased THP-1 monocyte migration by 33% compared to the MCP-1-treated cells. It also increased cholesterol efflux significantly by1.64-fold and 1.60-fold either alone or in combination with IFN-γ, respectively. Ingenuity Pathway Analysis of the molecular interactions of quercetin identified canonical pathways directly related to lipid uptake and cholesterol efflux. Furthermore, CD36, SR-A, and LXR-α also demonstrated significant increases by 72.16-, 149.10-, and 29.68-fold, respectively.Conclusion: Our results from both in vitro and in silico studies identified that quercetin inhibited the THP-1 monocyte migration, MCP-1, and ICAM-1 and increased cholesterol efflux probably mediated via the LXR/RXR signaling pathway. Therefore, quercetin will help prevent cell infiltration in atherosclerotic plaques and reduce the risk of stroke or brain destruction.

Suicide with Very Close Shot Wounds, A Case Report

Background: Currently victims of gunshot wound violence are very often found because more and more members of civil society have firearms, both for self-defense and for other purposes. In principle, examination of gunshot wound victims is the same as examination of wounds in other traumas, but there is one specific thing, namely, doctors must know and understand about firearms, ammunition and bullets. Without understanding this, it will be difficult to provide adequate assistance, because injury to the body is ultimately based on these three elements. In gunshot wounds, there are two types of wounds, including incoming gunshot wounds and exit gunshot wounds. incoming gunshot wounds consist of: contact wound, close gunshot wound (near wound), and distant gunshot wound (distant wound). This case report aims to determine the cause of death of the victim, which was found through forensic and histopathological examination, whether the victim died due to suicide, murder or accident. The case that occurred in Serdang Bedagai on October 6, 2019 at 07:30 WIB, the victim was a 44 years old male, the victim was found dead in his house. On external examination, he found one incoming gunshot wound to the right side of the head and one exit gunshot wound to the left head. On internal examination, there was blood absorption in the brain and its layers. There was a penetrating wound that entered the right scalp and a penetrating wound on the left side of the scalp. From the results of forensic and histopathological examinations on a male victim aged 44 years, especially the internal examination of the corpse, it can be concluded that the cause of death of the victim is the destruction of brain tissue which causes loss of function of body organs due to very close gunshot wounds. And the victim allegedly committed suicide.

Repetitive Transcranial Magnetic Stimulation Improves Mild Cognitive Impairment Associated with Alzheimer's Disease in Mice by Modulating the miR-567/NEUROD2/PSD95 Axis.

BackgroundMild cognitive impairment (MCI) is a typical symptom of early Alzheimer’s disease (AD) and is driven by the dysfunction of microRNAs (miRs). Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive technique for handling neuropsychiatric disorders and has universally effects on the functions of miRs. In the current study, the improvement effects of rTMS on MCI associated with AD were explored by focusing on miR-567/NEUROD2/PSD95 axis.MethodsMCI was induced in mice using scopolamine and was treated with rTMS of two frequencies (1 Hz and 10 Hz). The changes in cognitive function, brain structure, neurotrophic factor levels, and activity of miR-567/NEUROD2/PSD95 axis were assessed. The interaction between rTMS and miR-567 was further verified by inducing the level of miR-567 in AD mice.ResultsThe administrations of rTMS improved the cognitive function of AD mice and attenuated brain tissue destruction, which were associated with the restored production of BDNF and NGF. Additionally, rTMS administrations suppressed the expression of miR-567 and up-regulated the expressions of NEUROD2 and PSD95, which contributed to the improved condition in central nerve system. With the induced level of miR-567, the effects of rTMS were counteracted: the learning and memorizing abilities of mice were impaired, the brain neuron viability was suppressed, and the production of neurotrophic factors was suppressed even under the administration of rTMS. The changes in brain function and tissues were associated with the inhibited expressions of NEUROD2 and PSD95.ConclusionThe findings outlined in the current study demonstrated that rTMS treatment could protect brain against AD-induced MCI without significant side effects, and the function depended on the inhibition of miR-567.

An alleged murder due to blunt head injury from a viewpoint of forensic investigation: a case report

Background: Blunt violence on the head often occurs in the community, which often causes fatal conditions and even death. Death due to blunt force on the head can be caused by intracranial bleeding or destruction of brain tissue. Case description: A case of suspected murder was reported due to blunt violence on the victim's head with the initials RA, 16 years old, a student at an official school. On forensic medical examination found signs of blunt violence in the form of bruises on the forehead and face, and the results of an autopsy found the destruction of the bones forming the face, fracture of the skull with the release of brain tissue. In the police investigation, the suspect admitted to committing violence with a kick on the head of the victim using shoes without other tools. There was a mismatch between the strength of the violence recognized by the suspect and the autopsy findings so that the forensic examination focused on seeing whether blunt violence that occurred on the victim could result in death or not. Conclusion: It is necessary to deepen police checks on suspects about how violence was carried out, how the power of violence was carried out, and what were the motives for violence. During the trial, the panel of judges stated that there was a possibility that the perpetrators would use hard objects to attack the victim.

Neuroinflammation evoked by brain injury in a rat model of lacunar infarct

Stroke is the leading cause of long-term, severe disability worldwide. Immediately after the stroke, endogenous inflammatory processes are upregulated, leading to the local neuroinflammation and the potentiation of brain tissue destruction. The innate immune response is triggered as early as 24 h post-brain ischemia, followed by adaptive immunity activation. Together these immune cells produce many inflammatory mediators, i.e., cytokines, growth factors, and chemokines. Our study examines the immune response components in the early stage of deep brain lacunar infarct in the rat brain, highly relevant to the clinical scenario. The lesion was induced by stereotactic injection of ouabain into the adult rat striatum. Ouabain is a Na/K ATPase pump inhibitor that causes excitotoxicity and brings metabolic and structural changes in the cells leading to focal brain injury. We have shown a surge of neurodegenerative changes in the peri-infarct area in the first days after brain injury. Immunohistochemical analysis revealed early microglial activation and the gradual infiltration of immune cells with a significant increase of CD4+ and CD8+ T lymphocytes in the ipsilateral hemisphere. In our studies, we identified the higher level of pro-inflammatory cytokines, i.e., interleukin-1α, interleukin-1β, tumor necrosis factor-α, and interferon-γ, but a lower level of anti-inflammatory cytokines, i.e., interleukin-10 and transforming growth factor-β2 in the injured brain than in normal rats. Concomitantly focal brain injury showed a significant increase in the level of chemokines, i.e., monocyte chemoattractant protein-1 and CC motif chemokine ligand 5 compared to control. Our findings provide new insights into an early inflammatory reaction in our model of the deep-brain lacunar infarct. The results of this study may highlight future stroke immunotherapies for targeting the acute immune response accompanied by the insult.

Stroke and the immune system: A review of the new strategies

The immunology of stroke can be approached in several ways. By viewing stroke from an immunological standpoint, we are trying to achieve new insights in its pathogenesis and reach new therapeutic options. To review and summarize the findings from publications on immunology of stroke. Infections are a well-known risk factor for stroke. This is due to activated immune cells interacting with throm-bocytes and releasing coagulation factors, which affect the formation of the thrombus. Aseptic inflammation in the ischemic lesion leads to cellular invasion of the area and triggers a pro-inflammatory response, which has an impact on further destruction of ischemic brain tissue. Another aspect of stroke is systemic immune suppression, which is a predisposing factor towards a systemic bacterial infection. Infection itself is also an independent risk factor for negative clinical outcomes and increased mortality. The immunological approach to the topic of ischemic stroke holds significant value for future research.

NR2 antibodies as diagnostic and prognostic stroke biomarker

Given the high percentage of disability and mortality resulting from a stroke, search of new ways to improve early diagnosis and optimize therapeutic approaches is highly relevant. The article reviews the studies of NR2 antibodies to glutamate N-methyl-D-aspartate (NMDA) receptors as a biomarker in acute stroke. The review shows that this biomarker is suitable for determining the presence of ischemic process in the brain and the degree of destruction of brain tissue, both in the first hours of stroke and at follow-up. In addition, the analysis of NR2 antibodies can be informative to predict the worsening, the increase in the locus size, which can contribute to the timely correction of treatment and will improve the effectiveness of the therapy. The prognostic potential of NR2 antibodies can be used for personalized therapeutic approach. However, currently the lack of studies of NR2 antibodies in acute stroke requires further study of this biomarker.

THE POSSIBILITY OF USING GLIAL FIBRILLARY ACIDIC PROTEIN AS A BIOMARKER IN THE ACUTE PERIOD OF STROKE

High mortality and disability resulting from a stroke throughout the world is the cause of fi nding new opportunities to improve early diagnosis and optimize therapeutic approaches. The article presents a review of the literature devoted to the study of glial fi brillary acidic protein (GFAP) as a biomarker in the acute period of stroke, which showed that its use is possible not only to diff erentiate the ischemic and hemorrhagic process, but also to determine the degree of destruction of brain tissue, as in the fi rst hours of a stroke, and in the dynamics. In addition, the GFAP analysis can be useful for monitoring the course of the disease, control the eff ectiveness of therapy, as well as to predict outcomes.