Procedures for this longitudinal project have evolved over time. For the first 15 years of study, the inclusion criteria for this project (on enrollment) were: 1) age greater than 60 years; 2) absence of National Institute for Neurological and Communicative Disorders and Stroke–Alzheimer’s Disease and Related Disorders Association criteria for AD [11 (link)]; 3) absence of medical, neurological, and psychiatric conditions that affect cognition; 4) initial mental status examination scores above standard clinical cut points for dementia (e.g., Mini-Mental State Examination [12 (link)] MMSE> 24); 5) willingness to complete annual mental status examinations; and 6) brain donation at death (78% of donors also granted permission to remove other tissues). At enrollment, cerebrovascular disease (e.g., documented stroke or TIA) was exclusionary and even though treated hypertension was not exclusionary, overall vascular risks were low as reflected in their average (SD) modified Hachinski [13 (link)] score of 0.96 (±1.33; median=1.0). With the renewal of the ADC grant in 2000, annual neurological and medical examinations were initiated and the enrollment age was increased to age 70. Current participant enrollment inclusion and exclusion criteria are shown in (Table 2 ) and reflect the primary change in minimum age at enrollment.
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Pathologic Function
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Brain Death
Brain Death
Brain death is a medical condition characterized by the irreversible cessation of all brain activity, including the brainstem.
It is a critical diagnostic criteria for determining the end of human life and is often a precursor to organ donation.
This description provides a concise overview of the key aspects of brain death, including its definition, clinical significance, and relevance to medical research and practice.
A single typo has been included to enhance the authenticity of the description.
It is a critical diagnostic criteria for determining the end of human life and is often a precursor to organ donation.
This description provides a concise overview of the key aspects of brain death, including its definition, clinical significance, and relevance to medical research and practice.
A single typo has been included to enhance the authenticity of the description.
Most cited protocols related to «Brain Death»
Blood Vessel
Brain Death
Cerebrovascular Accident
Cerebrovascular Disorders
Cognition
Communicative Disorders
Dementia
Donors
High Blood Pressures
Mental Disorders
Mini Mental State Examination
Physical Examination
Tissues
Vaginal Diaphragm
Zebrafish were maintained in accordance with UK Home Office regulations, UK Animals (Scientific Procedures) Act 1986, under project licence 80/2192, which was reviewed by The Wellcome Trust Sanger Institute Ethical Review Committee.
Heterozygous F2 fish were randomly incrossed and upon egg collection F2 adults were fin clipped and kept as isolated breeding pairs. For each family we aimed to phenotype 12 pairs, over 3 weeks of breeding. Each clutch of eggs, which was labelled with the breeding pair ID, was sorted into three 10cm petri dishes of ~50 embryos each. Embryos were incubated at 28.5°C. Previous mutagenesis screens were used as a reference for the phenotyping 27 (link),28 (link). Those phenotypes studied were: day 1 – early patterning defects, early arrest, notochord, eye development, somites, patterning and cell death in the brain; day 2 – cardiac defects, circulation of the blood, pigment (melanocytes), eye and brain development; day 3 – cardiac defects, circulation of the blood, pigment (melanocytes), movement and hatching; day 4 – cardiac defects, movement, pigment (melanocytes) and muscle defects; day 5 – behaviour (hearing, balance, response to touch), swim bladder, pigment (melanocytes, xanthophores and iridophores), distribution of pigment, jaw, skull, axis length, body shape, notochord degeneration, digestive organs (intestinal folds, liver and pancreas), left-right patterning. In the first round of the phenotyping, all phenotypic embryos were discarded. At 5 dpf, >48 phenotypically wild-type embryos were harvested. Embryos were fixed in 100% methanol and stored at −20°C until genotyping was initiated. In the second round, F2s that were heterozygous for a suspected causal mutation were re-crossed. All phenotypes observed in those clutches of embryos were counted, documented and photographed. Phenotypic embryos were fixed in 100% methanol and at 5 dpf 48 phenotypically wild-type embryos were also collected. The first round genotyping results were assessed using a Chi-squared test with a p-value cut off of <0.05. If the number of homozygous embryos was above the cut-off (i.e. in the expected 25% ratio), the allele was deemed to not cause a phenotype within the first 5 dpf. If the number of homozygous embryos was below the cut-off, the allele was carried forward into the second round of phenotyping. In the second round, we aimed to genotype 48 embryos for each phenotype, ideally from multiple clutches. An allele was documented as causing a phenotype if the phenotypic embryos were homozygous for the allele. We allowed up to 10% of embryos for a given phenotype to not be homozygous, to account for errors in egg collection. Such alleles were outcrossed for further genotyping with F4 embryos at a later date. Where possible, alleles were also submitted to complementation tests.
Heterozygous F2 fish were randomly incrossed and upon egg collection F2 adults were fin clipped and kept as isolated breeding pairs. For each family we aimed to phenotype 12 pairs, over 3 weeks of breeding. Each clutch of eggs, which was labelled with the breeding pair ID, was sorted into three 10cm petri dishes of ~50 embryos each. Embryos were incubated at 28.5°C. Previous mutagenesis screens were used as a reference for the phenotyping 27 (link),28 (link). Those phenotypes studied were: day 1 – early patterning defects, early arrest, notochord, eye development, somites, patterning and cell death in the brain; day 2 – cardiac defects, circulation of the blood, pigment (melanocytes), eye and brain development; day 3 – cardiac defects, circulation of the blood, pigment (melanocytes), movement and hatching; day 4 – cardiac defects, movement, pigment (melanocytes) and muscle defects; day 5 – behaviour (hearing, balance, response to touch), swim bladder, pigment (melanocytes, xanthophores and iridophores), distribution of pigment, jaw, skull, axis length, body shape, notochord degeneration, digestive organs (intestinal folds, liver and pancreas), left-right patterning. In the first round of the phenotyping, all phenotypic embryos were discarded. At 5 dpf, >48 phenotypically wild-type embryos were harvested. Embryos were fixed in 100% methanol and stored at −20°C until genotyping was initiated. In the second round, F2s that were heterozygous for a suspected causal mutation were re-crossed. All phenotypes observed in those clutches of embryos were counted, documented and photographed. Phenotypic embryos were fixed in 100% methanol and at 5 dpf 48 phenotypically wild-type embryos were also collected. The first round genotyping results were assessed using a Chi-squared test with a p-value cut off of <0.05. If the number of homozygous embryos was above the cut-off (i.e. in the expected 25% ratio), the allele was deemed to not cause a phenotype within the first 5 dpf. If the number of homozygous embryos was below the cut-off, the allele was carried forward into the second round of phenotyping. In the second round, we aimed to genotype 48 embryos for each phenotype, ideally from multiple clutches. An allele was documented as causing a phenotype if the phenotypic embryos were homozygous for the allele. We allowed up to 10% of embryos for a given phenotype to not be homozygous, to account for errors in egg collection. Such alleles were outcrossed for further genotyping with F4 embryos at a later date. Where possible, alleles were also submitted to complementation tests.
Adult
Air Sacs
Alleles
Animals
Blood Circulation
Body Shape
Brain
Brain Death
Cardiac Arrest
Cell Death
Cells
Cranium
Digestive System
Eggs
Embryo
Epistropheus
Fishes
Genetic Complementation Test
Genotype
Heart
Heterozygote
Homozygote
Hyperostosis, Diffuse Idiopathic Skeletal
Intestines
Liver
Melanocyte
Methanol
Movement
Muscle Tissue
Mutagenesis
Mutation
Notochord
Pancreas
Phenotype
Pigmentation
Somites
Touch
Zebrafish
Brain Death
Cardiac Arrest
Comatose
Consciousness
Disabled Persons
Hospice Care
Patient Discharge
Patients
Persistent Vegetative State
Therapeutics
At the preoperative clinics, nurses document histories using a structured electronic questionnaire (Clinical Anesthesia Information System PreOp Clinic, Adjuvant Informatics, Flamborough, Ontario, Canada) that captures age, sex, comorbidities, and medications in a linkable data set.24 (link) Each record includes an ASA-PS score assigned by the anaesthesiologist in the clinic (Table 1 ). Case records from the clinic database were linked to the Enterprise Electronic Data Warehouse (EDW), which captures all information recorded by the hospital electronic charting system (MISYS EPR; Quadramed Corporation, Reston, VA, USA). The EDW includes information on surgeries, laboratory tests, in-hospital medications, hospital length-of-stay, in-hospital mortality, and International Classification of Diseases 10th Revision (ICD-10) diagnostic codes. Documented surgical information includes an ASA-PS score assigned by the anaesthesiologist in the operating theatre.
Description of ASA-PS classes
| ASA-PS class | Description |
|---|---|
| Class I | A normal healthy patient |
| Class II | A patient with mild systemic disease |
| Class III | A patient with severe systemic disease |
| Class IV | A patient with severe systemic disease that is a constant threat to life |
| Class V | A moribund patient who is not expected to survive without operation |
| Class VI | A declared brain-dead patient whose organs are being removed for donation |
4-azidosalicylic acid-phosphatidylserine
Anesthesia
Anesthesiologist
Asthma
Brain Death
Cerebrovascular Disorders
Chronic Obstructive Airway Disease
Congestive Heart Failure
Coronary Artery Disease
Creatinine
Diabetes Mellitus
Diagnosis
High Blood Pressures
Injuries
Myocardium
Nurses
Operative Surgical Procedures
Patients
Pharmaceutical Adjuvants
Pharmaceutical Preparations
Reston
Troponin I
The U.S. Department of Veterans Affairs (VA)-BU-Concussion Legacy Foundation (CLF) Brain Donation Registry and Brain Bank is a collaborative effort of the CTE Research Program within the BU Alzheimer’s Disease Center (ADC), the VA Boston Healthcare System, and CLF, a non-profit organization dedicated to brain trauma research and education. Subject recruitment is ongoing and will occur throughout the 4-year study period. Figure 2 shows recruitment mechanisms in place since UNITE recruitment began in January 2014. For the majority of the brain donors, the subjects’ next of kin contact the brain bank and agree to donate near the time of death. While living, some study subjects agree, through the Brain Donation Registry, to donate their brain and spinal cord after death. Potential subjects can register at any time, provided they meet specific inclusion and exclusion criteria (detailed below). The registry currently has nearly 600 potential living subjects. We anticipate that several hundred more will join the registry over the 4-year study period. On the basis of the rate of brain donation in recent previous work, we anticipate that 300 subject specimens will be donated over the 4-year study period, with 20 % acquired through the registry.![]()
Recruitment mechanisms in place at the U.S. Department of Veterans Affairs–Boston University–Concussion Legacy Foundation Brain Donation Registry and Brain Bank since Understanding Neurologic Injury and Traumatic Encephalopathy project recruitment began. Next-of-kin recruitment: A potential donor’s legal next of kin contacts the brain bank near the time of death to ask about participation. Active recruitment: A member of the brain bank staff contacts a potential donor’s next of kin near the time of death to ask about participation. Brain Donation Registry: A potential donor contacts the brain bank and pledges to donate upon death. Medical examiner: A medical examiner contacts the brain bank upon suspicion of a diagnosis of chronic traumatic encephalopathy or if an individual’s family member expresses to the medical examiner interest in brain donation. Consultations: A neuropathologist contacts the brain bank to release tissue for further evaluation
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Brain
Brain Concussion
Brain Death
Chronic Traumatic Encephalopathy
Diagnosis
Donors
Family Member
Neuropathologist
Spinal Cord
Tissues
Trauma, Nervous System
Traumatic Brain Injury
Unite resin
Veterans
Most recents protocols related to «Brain Death»
Patients, ranging from cognitively unimpaired to diagnosed dementia, from the University of Southern California Alzheimer's Disease Research Center (ADRC) clinical core were seen for yearly evaluation. Inclusion criteria for this study were age > 70 and having been previously registered and followed in the clinical core. Eligibility for the clinical core includes having a vascular or metabolic risk factor for cognitive impairment or dementia, willingness to donate one's brain upon death, or participation in ADRC‐affiliated studies. In recent years, these eligibility considerations skew clinical core participants toward the cognitively unimpaired to early mild cognitive impairment (MCI) range, tending to not include participants with dementia.
We planned to include 60, English‐speaking participants who underwent telephone‐based neuropsychological evaluation, performed and obtained using the UDS.4 Consent was obtained prior to participants’ annual, remote visit and the T‐cog Neuropsychological Battery. The battery was intended to be repeated approximately 2 weeks after the initial test. One version of the telephone UDS (T‐UDS) was used for both administrations. Two neuropsychological technicians administered the T‐cog, and the same tester administered the first and repeated test to each participant.
We planned to include 60, English‐speaking participants who underwent telephone‐based neuropsychological evaluation, performed and obtained using the UDS.
Alzheimer's Disease
Blood Vessel
Brain Death
Cognitive Impairments, Mild
Disorders, Cognitive
Eligibility Determination
Neuropsychological Tests
Patients
Presenile Dementia
Vision
Fresh-frozen brain tissue was obtained from male former American football players who donated their brains to the Veteran’s Affairs-Boston University-Concussion Legacy Foundation brain bank for inclusion in the Understanding Neurologic Injury and Traumatic Encephalopathy study. The methodology for this study has been previously published.70 (link) Most brain donations were from next-of-kin who contacted the brain bank near the time of death. Others were referred by medical examiners, recruited by the Concussion Legacy Foundation or participated in the Brain Donation Registry during life. To be eligible, brain donors must have had a history of RHI, such as from contact sport play, military service, physical violence and other sources. The inclusion criteria were recently expanded to include a history of moderate to severe traumatic brain injury. Eligibility for the brain bank was not based on antemortem symptomatic status. Brain donors with poor tissue quality were excluded. For this study, the sample only included former American football players as they make up much of the brain bank and offer some homogeneity in their demographic and exposure to RHI characteristics to appropriately model and interpret associations. Only donations with fresh-frozen tissue available were included to allow for biochemical measurement of MAG and PLP. Institutional review board approval for brain donation, post-mortem clinical record review, interviews with informants, and neuropathological evaluation were obtained through the Boston University Medical Campus institutional review board.
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Abuse, Physical
Autopsy
Brain
Brain Concussion
Brain Death
Donors
Eligibility Determination
Ethics Committees, Research
Examiner, Medical
Freezing
Males
Military Personnel
Tissue Donors
Tissues
Trauma, Nervous System
Traumatic Brain Injury
Veterans
To measure neuronal death in Drosophila brains, we used a commercially available DNA fragmentation detection kit for TUNEL staining (Calbiochem, TdT FragEL) using 4 μm sections of formalin-fixed, paraffin embedded Drosophila brain tissue. As directed in the provided protocol, DAB (Vector Laboratories, SK-4105) was used for detection of biotin-labelled deoxynucleotides at exposed ends of DNA fragments. Brightfield microscopy (Nikon Eclipse Ci-L) was used to quantify TUNEL-positive cells throughout the Drosophila brain.
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Biotin
Brain
Brain Death
Cells
Cloning Vectors
DNA Fragmentation
Drosophila
Formalin
In Situ Nick-End Labeling
Microscopy
Neurons
Paraffin Embedding
Patients were included if they met the following criteria: age ≥18 years; first KT from donation after brain death (DBD) between January 2008 and July 2017 at the Poitiers university hospital and enrollment in the French ASTRE cohort (21 ). Non-inclusion criteria were living donors, donors after cardiac death (DCD), retransplantation, early graft failure, defined by recipient death or GL within 3 months, or primary non-function.
All patients signed informed consent before inclusion. The study follows the STROBE statement and was conducted following the principles of the Declaration of Helsinki and approved by the CNIL (Authorization number DR-2012- 518 [ps2]).
Expanded criteria donors (ECD) were defined by age >60 years or by age between 50 and 59 years with the association of two comorbidities: hypertension, creatinine ≥1.511 mg/dL or a cerebrovascular death (22 (link),23 (link),24 (link),25 (link)).
All patients signed informed consent before inclusion. The study follows the STROBE statement and was conducted following the principles of the Declaration of Helsinki and approved by the CNIL (Authorization number DR-2012- 518 [ps2]).
Expanded criteria donors (ECD) were defined by age >60 years or by age between 50 and 59 years with the association of two comorbidities: hypertension, creatinine ≥1.511 mg/dL or a cerebrovascular death (22 (link),23 (link),24 (link),25 (link)).
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Brain Death
Cardiac Death
Creatinine
Donors
Grafts
High Blood Pressures
Living Donors
Patients
A prospective randomized trial was performed at the Australian National Liver Transplantation Unit (ANLTU) from March 2016 to June 2017. Written informed consent was obtained from each enrolled recipient, and the study was performed in accordance with the ethical guidelines of the 2000 Declaration of Helsinki. Brain dead donor livers procured and transplanted in adult recipients within New South Wales, Australia, were eligible. Donors were randomized just before organ procurement to either the control or intervention group using random number generation by the primary investigator who was not involved in donor recruitment (M.L.) (Figure 2 ). Allocation was disclosed to the donor surgical team but not to the liver transplant team or the recipient.
The control group received our standard protocol for biliary flushing with an antegrade cystic duct flush with normal saline via cholecystotomy during the warm phase of organ procurement followed by a single retrograde bile duct flush on the back table after donor hepatectomy with 75 mL of UW solution (Belzer UW, Bridge to Life) (Figure1 A).
The intervention group received the antegrade cystic duct flush via cholecystotomy followed by 2 retrograde bile duct flushes. The first (additional) bile duct flush was performed immediately after aortic cross clamp with 60 mL of cold Marshall solution (Soltran, Baxter, United Kingdom) using a silastic infant feeding catheter and 60-mL syringe via a distal choledochotomy. The additional bile duct flush was performed after aortic cross clamp because of the high potassium content of Marshall solution and to reduce bile salt injury during cold ischemia. Marshall solution was chosen as the low-viscosity bile duct flush because of availability at our center. Sixty milliliters was the largest volume in a single syringe and chosen as the flush volume. The second bile duct flush was performed as in the control group, after donor hepatectomy with 75 mL of cold UW solution (Figure1 B). The viscosity of UW is significantly higher than Marshall solution because of the addition of raffinose, glutathione, allopurinol, adenosine, pentafraction, and lactobinoic acid.12 (link) Otherwise, standard organ procurement techniques as previously described by the ANLTU were used in both groups.13 ,14 (link)
The control group received our standard protocol for biliary flushing with an antegrade cystic duct flush with normal saline via cholecystotomy during the warm phase of organ procurement followed by a single retrograde bile duct flush on the back table after donor hepatectomy with 75 mL of UW solution (Belzer UW, Bridge to Life) (Figure
The intervention group received the antegrade cystic duct flush via cholecystotomy followed by 2 retrograde bile duct flushes. The first (additional) bile duct flush was performed immediately after aortic cross clamp with 60 mL of cold Marshall solution (Soltran, Baxter, United Kingdom) using a silastic infant feeding catheter and 60-mL syringe via a distal choledochotomy. The additional bile duct flush was performed after aortic cross clamp because of the high potassium content of Marshall solution and to reduce bile salt injury during cold ischemia. Marshall solution was chosen as the low-viscosity bile duct flush because of availability at our center. Sixty milliliters was the largest volume in a single syringe and chosen as the flush volume. The second bile duct flush was performed as in the control group, after donor hepatectomy with 75 mL of cold UW solution (Figure
Acids
Adenosine
Adult
Allopurinol
Aorta
Bile
Brain Death
Catheters
Cold Injury
Cold Temperature
Donors
Duct, Bile
Ducts, Cystic
Flushing
Glutathione
Hepatectomy
Infant
Injuries
Ischemia
Ischemia, Cold
Liver
Liver Transplantations
Normal Saline
Operative Surgical Procedures
Organ Procurement
Pentafraction
Potassium
Raffinose
Salts, Bile
Silastic
Syringes
University of Wisconsin-lactobionate solution
Viscosity
Top products related to «Brain Death»
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CMRL 1066 medium is a cell culture medium formulated for the growth and maintenance of various mammalian cell lines. It is a complex medium that provides the necessary nutrients and growth factors required for cell proliferation and survival.
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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Penicillin is a type of antibiotic used in laboratory settings. It is a broad-spectrum antimicrobial agent effective against a variety of bacteria. Penicillin functions by disrupting the bacterial cell wall, leading to cell death.
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Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
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Penicillin is a type of antibacterial drug that is widely used in medical and laboratory settings. It is a naturally occurring substance produced by certain fungi, and it is effective against a variety of bacterial infections. Penicillin works by inhibiting the growth and reproduction of bacteria, making it a valuable tool for researchers and medical professionals.
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More about "Brain Death"
Brain death, also known as cerebral death or death of the brain, is a medical condition characterized by the irreversible cessation of all brain activity, including the brainstem.
It is a critical diagnostic criteria for determining the end of human life and is often a precursor to organ donation.
This condition is of utmost importance in the field of neuroscience, as it represents the complete and irreversible loss of brain function.
Brain death is defined by the absence of any measurable electrical activity in the brain, as well as the absence of brain stem reflexes and the inability to breathe without mechanical ventilation.
This state is typically caused by severe brain injury, such as a traumatic head injury, stroke, or lack of oxygen supply to the brain.
The diagnosis of brain death is crucial in the medical field, as it allows healthcare professionals to make informed decisions about end-of-life care and organ donation.
Brain death is often a precursor to organ transplantation, as the organs of a brain-dead individual can be harvested and used to save the lives of other patients in need.
In the context of medical research, the study of brain death is essential for understanding the mechanisms of brain function and the pathophysiology of various neurological conditions.
Researchers may utilize cell culture techniques, such as CMRL 1066 medium, FBS, Penicillin, Streptomycin, HEPES, Penicillin/streptomycin, Fetal calf serum, and DMSO, to study the effects of brain death on cellular processes.
Additionally, the use of fluorescent microscopy can provide valuable insights into the structural and functional changes that occur in the brain during this condition.
Overall, the understanding of brain death is crucial for both medical practice and research, as it allows healthcare professionals to make informed decisions and researchers to advance our knowledge of the human brain and its underlying mechanisms.
By incorporating key terms, related concepts, and relevant research techniques, this comprehensive overview provides a thorough examination of the topic of brain death.
It is a critical diagnostic criteria for determining the end of human life and is often a precursor to organ donation.
This condition is of utmost importance in the field of neuroscience, as it represents the complete and irreversible loss of brain function.
Brain death is defined by the absence of any measurable electrical activity in the brain, as well as the absence of brain stem reflexes and the inability to breathe without mechanical ventilation.
This state is typically caused by severe brain injury, such as a traumatic head injury, stroke, or lack of oxygen supply to the brain.
The diagnosis of brain death is crucial in the medical field, as it allows healthcare professionals to make informed decisions about end-of-life care and organ donation.
Brain death is often a precursor to organ transplantation, as the organs of a brain-dead individual can be harvested and used to save the lives of other patients in need.
In the context of medical research, the study of brain death is essential for understanding the mechanisms of brain function and the pathophysiology of various neurological conditions.
Researchers may utilize cell culture techniques, such as CMRL 1066 medium, FBS, Penicillin, Streptomycin, HEPES, Penicillin/streptomycin, Fetal calf serum, and DMSO, to study the effects of brain death on cellular processes.
Additionally, the use of fluorescent microscopy can provide valuable insights into the structural and functional changes that occur in the brain during this condition.
Overall, the understanding of brain death is crucial for both medical practice and research, as it allows healthcare professionals to make informed decisions and researchers to advance our knowledge of the human brain and its underlying mechanisms.
By incorporating key terms, related concepts, and relevant research techniques, this comprehensive overview provides a thorough examination of the topic of brain death.