Biotransport to the Cerebral Tissues Related to the Vascular Diseases

2008 ◽  
Author(s):  
Kazuo Tanishita ◽  
Kazuto Masamoto ◽  
Iwao Kanno ◽  
Hirosuke Kobayashi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Oxygen Transport ◽  
Consumption Rate ◽  
Vascular Diseases ◽  
Selective Vulnerability ◽  
Whole Body ◽  
Sensorimotor Function ◽  
Irreversible Damage

Brain is a highly oxidative organ and its consumption rate of oxygen accounts for 20 percent of that of the whole body. This large consumption rate must be met by continuous supply of oxygen, because lack of oxygen rapidly causes irreversible damage to central nervous system. Acute hypoxic episodes cause a certain pattern of regional damage. Cerebral cortex (e.g., layers III, V, and VI) is one of the most susceptible regions to hypoxia, and damage to sensorimotor function is particularly severe in humans that survive hypoxic/ischemic episodes. However, little is known about whether oxygen transport in intracortical regions relates to such selective vulnerability to hypoxia.

I. Environmental Contamination and Biochemical Relationships

1975 ◽  
Vol 38 (5) ◽  
pp. 285-300 ◽  
Author(s):  
A. G. HUGUNIN ◽  
R. L. BRADLEY
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Methyl Mercury ◽  
Sea Water ◽  
Inorganic Mercury ◽  
Whole Body ◽  
Irreversible Damage ◽  
Mercury Compounds ◽  
The Central Nervous System ◽  
Pass Through

Mercury is naturally concentrated in geographical belts, but geological cycling has distributed the element in all strata of the earth. Natural concentrations of mercury are approximately 100 ppb in soil, 0.06 ppb in fresh water, 0.01–0.30 ppb in sea water, and 0.003–0.009 μg/m3 in air. Concentrations vary, being highest near mineral deposits. The concentration of mercury in some areas has been significantly increased by human carelessness. An epidemic among Japanese fishing families, death of Swedish wildlife, and discovery of elevated mercury levels in American fish focused attention on this problem. The discovery that certain species are capable of methylating inorganic mercury indicates pollution with any chemical form of mercury is dangerous. Alkylmercurials are the most dangerous form of mercury in the environment. Alkylmercurials are absorbed from the gastrointestinal tract, diffuse across the blood-brain carrier, and pass through the placental membrane in significantly higher proportions than other mercury compounds. The whole body half-life of methyl mercury in humans is 76 ± 3 days compared to half-lives of 37 ± 3 days for men and 48 ± 5 days for women observed for mercuric salts. Not readily broken down, sufficient concentrations of methyl mercury can cause irreversible damage to the central nervous system. Renal damage usually results from high levels of aryl- or alkoxyalkylmercurials and inorganic mercury; however, vapors of elemented mercury can damage the central nervous system. Organic mercury compounds cause chromosome changes, but the medical implications resulting from levels of mercury in food are unknown. The concentration of mercury in red blood cells and hair is indicative of the exposure to alkylmercurials. On a group basis, blood and urine concentrations of mercury may corrrelate with recent exposure to mercury.

Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

1995 ◽  
Vol 53 ◽  
pp. 958-959
Author(s):  
S.S. Spicer ◽  
B.A. Schulte
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Peripheral Nervous System ◽  
Sensory Neurons ◽  
Sensory Nerves ◽  
Tissue Antigens ◽  
The Central Nervous System ◽  
The Brain ◽  
Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

Synthesis and Evaluation of 18F-INER-1577-3 as a Central Nervous System (CNS) Histone Deacetylase Imaging Agent

2020 ◽  
Vol 16 (8) ◽  
pp. 978-990
Author(s):  
Ming-Hsin Li ◽  
Han-Chih Chang ◽  
Chun-Fang Feng ◽  
Hung-Wen Yu ◽  
Chyng-Yann Shiue
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Histone Deacetylases ◽  
Authentic Sample ◽  
Cancer Cell Line ◽  
Radiochemical Yield ◽  
Imaging Agent ◽  
Whole Body ◽  
Imaging Agents ◽  
Synthesis Time

Background:: Epigenetic dysfunction is implicated in many neurologic, psychiatric and oncologic diseases. Consequently, histone deacetylases (HDACs) inhibitors have been developed as therapeutic and imaging agents for these diseases. However, only a few radiotracers have been developed as HDACs imaging agents for the central nervous system (CNS). We report herein the synthesis and evaluation of [18F]INER-1577-3 ([18F]5) as an HDACs imaging agent for CNS. Methods:: [18F]INER-1577-3 ([18F]5) was synthesized by two methods: one-step (A) and two-step (B) methods. Briefly, radiofluorination of the corresponding precursors (11, 12) with K[18F]/K2.2.2 followed by purifications with HPLC gave ([18F]5). The quality of [18F]INER- 1577-3 synthesized by these methods was verified by HPLC and TLC as compared to an authentic sample. The inhibitions of [18F]INER-1577-3 and related HDACs inhibitors on tumor cells growth were carried out with breast cancer cell line 4T1 and MCF-7. The whole-body and brain uptake of [18F]INER-1577-3 in rats and AD mice were determined using a micro-PET scanner and the data was analyzed using PMOD. Results: : The radiochemical yield of [18F]INER-1577-3 synthesized by these two methods was 1.4 % (Method A) and 8.8% (Method B) (EOB), respectively. The synthesis time was 115 min and 100 min, respectively, from EOB. The inhibition studies showed that INER-1577-3 has a significant inhibitory effect in HDAC6 and HDAC8 but not HDAC2. PET studies in rats and AD mice showed a maximum at about 15 min postinjection for the whole brain of a rat (0.47 ± 0.03 %ID/g), SAMP8 mice (5.63 ± 1.09 %ID/g) and SAMR1 mice (7.23 ± 1.21 %ID/g). Conclusion:: This study showed that INER-1577-3 can inhibit tumor cell growth and is one of a few HDACs inhibitors that can penetrate the blood-brain barrier (BBB) and monitor HDAC activities in AD mice. Thus, [18F]INER-1577-3 may be a potent HDACs imaging agent, especially for CNS.

Bone-brain crosstalk and potential associated diseases

2016 ◽  
Vol 28 (2) ◽  
Author(s):  
Audrey Rousseaud ◽  
Stephanie Moriceau ◽  
Mariana Ramos-Brossier ◽  
Franck Oury
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Development ◽  
Cognitive Functions ◽  
Intimate Relationship ◽  
Whole Body ◽  
Reciprocal Relationships ◽  
Skeletal Homeostasis ◽  
The Central Nervous System ◽  
The Brain

AbstractReciprocal relationships between organs are essential to maintain whole body homeostasis. An exciting interplay between two apparently unrelated organs, the bone and the brain, has emerged recently. Indeed, it is now well established that the brain is a powerful regulator of skeletal homeostasis via a complex network of numerous players and pathways. In turn, bone via a bone-derived molecule, osteocalcin, appears as an important factor influencing the central nervous system by regulating brain development and several cognitive functions. In this paper we will discuss this complex and intimate relationship, as well as several pathologic conditions that may reinforce their potential interdependence.

scholarly journals An overlooked cause of longitudinally extensive spinal cord lesions: Primary central nervous system lymphoma

2020 ◽  
Author(s):  
Meng Wang ◽  
Baochang Qi ◽  
Jinming Han ◽  
Chunjie Guo ◽  
Limei Qu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Lymphoma ◽  
High Dose Chemotherapy ◽  
Lower Limbs ◽  
Whole Body ◽  
Sensory Loss ◽  
High Dose ◽  
Spinal Cord Lesions

Abstract Background: Primary central nervous system lymphoma (PCNSL ) is a rare and aggressive malignant tumor. It is easy to be misdiagnosed due to its low incidence and unspecific presentations in clinical practice. PCNSL mainly occurs intracranially in the brain while spinal cord is rarely involved. Case presentation: Here we report a 76-year-old woman who had a suspicious tumor history and presented retardant paralysis, bladder dysfunction and sensory loss of the lower limbs. Magnetic resonance imaging (MRI) of the thoracic spine disclosed longitudinally extensive lesions extending from thoracic 4 (T4) to lumbar 1 (L1) vertebral level with an enhanced nodular lesion noting at levels of T10 and T11 . In order to further identify the cause, the whole body 18 F-fluorodeoxyglucose ( 18 F-FDG) positron emission tomography (PET)/computed tomography (CT) was performed and showed a hypermetabolic nodule corresponded to MRI enhancing lesions, which further suggesting the possibility of a tumor. The patient then underwent a surgical resection and spinal cord biopsy confirmed the diagnosis of non-Hodgkin's lymphoma (diffuse large B-cell type). The patient then received a high-dose chemotherapy based on methotrexate combined with Rituximab. Unfortunately, the symptoms of this patient have not been improved significantly after three rounds of chemotherapy. Conclusion: Our case indicates that PCNSL may also serve as a possible cause for longitudinally extensive spinal cord lesions, especially the patients who had a suspicious tumor history, MRI enhancing lesion s in the spinal cord corresponded to hypermetabolic nodules on 18 F-FDG- PET/CT at the same level.

Vascular Diseases of the Central Nervous System: Percutaneous Approach

2002 ◽  
pp. 1115-1153
Author(s):  
Peter J. Mitchell ◽  
Randall T. Higashida ◽  
Christopher F. Dowd ◽  
Van V. Halbach
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vascular Diseases ◽  
Percutaneous Approach ◽  
The Central Nervous System

Developmental Overview of Central Neuroanatomy

2017 ◽  
Author(s):  
Peggy Mason
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Neural Tube ◽  
The Central Nervous System ◽  
Dorsal Telencephalon ◽  
Adult Spinal Cord ◽  
The Brain

The central nervous system develops from a proliferating tube of cells and retains a tubular organization in the adult spinal cord and brain, including the forebrain. Failure of the neural tube to close at the front is lethal, whereas failure to close the tube at the back end produces spina bifida, a serious neural tube defect. Swellings in the neural tube develop into the hindbrain, midbrain, diencephalon, and telencephalon. The diencephalon sends an outpouching out of the cranium to form the retina, providing an accessible window onto the brain. The dorsal telencephalon forms the cerebral cortex, which in humans is enormously expanded by growth in every direction. Running through the embryonic neural tube is an internal lumen that becomes the cerebrospinal fluid–containing ventricular system. The effects of damage to the spinal cord and forebrain are compared with respect to impact on self and potential for improvement.

scholarly journals Region-specific irradiation system with heavy-ion microbeam for active individuals of Caenorhabditis elegans

2017 ◽  
Vol 58 (6) ◽  
pp. 881-886 ◽  
Author(s):  
Michiyo Suzuki ◽  
Yuya Hattori ◽  
Tetsuya Sakashita ◽  
Yuichiro Yokota ◽  
Yasuhiko Kobayashi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Microfluidic Channel ◽  
Muscle Cells ◽  
Heavy Ion ◽  
Whole Body ◽  
Carbon Ions ◽  
Tail Region ◽  
The Central Nervous System

Abstract Radiation may affect essential functions and behaviors such as locomotion, feeding, learning and memory. Although whole-body irradiation has been shown to reduce motility in the nematode Caenorhabditis elegans, the detailed mechanism responsible for this effect remains unknown. Targeted irradiation of the nerve ring responsible for sensory integration and information processing would allow us to determine whether the reduction of motility following whole-body irradiation reflects effects on the central nervous system or on the muscle cells themselves. We therefore addressed this issue using a collimating microbeam system. However, radiation targeting requires the animal to be immobilized, and previous studies have anesthetized animals to prevent their movement, thus making it impossible to assess their locomotion immediately after irradiation. We developed a method in which the animal was enclosed in a straight, microfluidic channel in a polydimethylsiloxane chip to inhibit free motion during irradiation, thus allowing locomotion to be observed immediately after irradiation. The head region (including the central nervous system), mid region around the intestine and uterus, and tail region were targeted independently. Each region was irradiated with 12 000 carbon ions (12C; 18.3 MeV/u; linear energy transfer = 106.4 keV/μm), corresponding to 500 Gy at a φ20 μm region. Motility was significantly decreased by whole-body irradiation, but not by irradiation of any of the individual regions, including the central nervous system. This suggests that radiation inhibits locomotion by a whole-body mechanism, potentially involving motoneurons and/or body-wall muscle cells, rather than affecting motor control via the central nervous system and the stimulation response.

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