The role of central nervous system on hypoglycemia and the feasibility of the brain theory in traditional Chinese medicine on treatment of diabetes mellitus

2014 ◽  
Vol 12 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Hai-li Jiang ◽  
Jing-jing Niu ◽  
Wei-fei Zhang ◽  
Wen-jin Huang ◽  
Ming-yue Zhou ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Central Nervous System ◽  
Nervous System ◽  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Treatment Of Diabetes ◽  
Brain Theory ◽  
The Brain

scholarly journals Analysis of the Role of Neurospecific Proteins in the Diagnosis of Cognitive Dysfunction in Patients with Type 1 Diabetes Mellitus

2014 ◽  
Vol 17 (2) ◽  
pp. 83-90 ◽  
Author(s):  
Yulia Gennad'evna Samoylova ◽  
Maria Vladimirovna Novoselova ◽  
Natalya Grigor'evna Zhukova ◽  
Olga Sergeevna Tonkikh
Keyword(s):  
Diabetes Mellitus ◽  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Dysfunction ◽  
Structural Changes ◽  
Neurospecific Proteins ◽  
The Central Nervous System ◽  
The Brain

Background. Impairment of the central nervous system manifested as cognitive dysfunction caused by metabolic or structural changes is a severe progressive vascular complication of type 1 diabetes mellitus (T1DM). Significant difficulties in the diagnosis of cognitive dysfunction are associated with subjective diagnostic techniques. Objective. To identify the role of neurospecific markers in the diagnosis of cognitive dysfunction in patients with T1DM. Materials and Methods. A total of 58 patients with T1DM aged 16?30 years were included in this study. The control group included 29 healthy young adults matched by gender and age. The survey included clinical and laboratory examinations, psychological testing and magnetic resonance imaging (MRI) of the brain. The Montreal Cognitive Assessment (MoCA) was used to screen for cognitive impairment. The levels of neurospecific proteins (S100, glial fibrillary acidic protein and myelin basic protein) were determined to identify early markers of cognitive impairment. MRI of the brain was performed using a Siemens Magnetom 1.0 T system to assess structural changes in the central nervous system. Results. The study revealed increased levels of all neurospecific proteins, which correlated with parameters of hyperglycaemia and cognitive deficit (MoCA scores of

scholarly journals Activation of central 5-HT2A receptor in brain inhibited the seizure-induced respiratory arrest in the DBA/1 mouse SUDEP model

2020 ◽  
Author(s):  
Yue Shen ◽  
HaiXiang Ma ◽  
XiTing Lian ◽  
LeYuan Gu ◽  
Qian Yu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Drug Resistance ◽  
Nervous System ◽  
Underlying Mechanism ◽  
Respiratory Arrest ◽  
Acoustic Stimulation ◽  
Unexpected Death ◽  
Anti Epileptic Drug ◽  
The Brain

AbstractSudden unexpected death in epilepsy (SUDEP) is the fatal cause leading to the death of epilepsy patients with anti-epileptic drug resistance. However, the underlying mechanism of SUDEP remains to be elusive. Our previous study demonstrated that enhancement of serotonin (5-HT) synthesis by intraperitoneal (IP) injection of 5-hydroxytryptophan in brain significantly reduced the incidence of seizure-induced respiratory arrest (S-IRA) in DBA/1 mice SUDEP models. Given that 5-HT2A receptor (5-HT2AR) acts an important role in mediating respiration system in brain, we hypothesized that 5-HT2AR is of great significance to modulate S-IRA and SUDEP. To test this hypothesis, we examined whether the decreased incidence S-IRA evoked by either acoustic stimulation or PTZ by blocking 5-HT2AR by administration with ketanserin (KET), a selective antagonist of 5HT2AR, in DBA/1 mice SUDEP models to test the role of 5-HT2AR modulating S-IRA. Our results suggested that the decreased incidence of S-IRA by 5-Hydroxytryptophan (5-HTP), a precursor for central nervous system (CNS) serotonin (5-HT) synthesis, was significantly reversed by IP and intracerebroventricularly (ICV) injection of ketanserin in our models. Thus, our data suggested that 5-HT2AR in the brain may be a potential and specific target to prevent SUDEP.

Сellular and Molecular Mechanisms of Proinflammatory Monocytes Participation in the Pathogenesis of Mental Disorders. Part 3

Psychiatry ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 125-134
Author(s):  
E. F. Vasilyeva ◽  
O. S. Brusov
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mental Disorders ◽  
Molecular Mechanisms ◽  
Microglial Cells ◽  
Inflammatory Reactions ◽  
Mental Diseases ◽  
The Central Nervous System ◽  
The Brain

Background: at present, the important role of the monocyte-macrophage link of immunity in the pathogenesis of mental diseases has been determined. In the first and second parts of our review, the cellular and molecular mechanisms of activation of monocytes/macrophages, which secreting proinflammatory CD16 receptors, cytokines, chemokines and receptors to them, in the development of systemic immune inflammation in the pathogenesis of somatic diseases and mental disorders, including schizophrenia, bipolar affective disorder (BAD) and depression were analyzed. The association of high levels of proinflammatory activity of monocytes/macrophages in patients with mental disorders with somatic comorbidity, including immune system diseases, is shown. It is known that proinflammatory monocytes of peripheral blood, as a result of violation of the integrity of the hematoencephalic barrier can migrate to the central nervous system and activate the resident brain cells — microglia, causing its activation. Activation of microglia can lead to the development of neuroinammation and neurodegenerative processes in the brain and, as a result, to cognitive disorders. The aim of review: to analyze the results of the main scientific studies concerning the role of cellular and molecular mechanisms of peripheral blood monocytes interaction with microglial cells and platelets in the development of neuroinflammation in the pathogenesis of mental disorders, including Alzheimer’s disease (AD). Material and methods: keywords “mental disorders, AD, proinflammatory monocytes, microglia, neuroinflammation, cytokines, chemokines, cell adhesion molecules, platelets, microvesicles” were used to search for articles of domestic and foreign authors published over the past 30 years in the databases PubMed, eLibrary, Science Direct and EMBASE. Conclusion: this review analyzes the results of studies which show that monocytes/macrophages and microglia have similar gene expression profiles in schizophrenia, BAD, depression, and AD and also perform similar functions: phagocytosis and inflammatory responses. Monocytes recruited to the central nervous system stimulate the increased production of proinflammatory cytokines IL-1, IL-6, tumor necrosis factor alpha (TNF-α), chemokines, for example, MCP-1 (Monocyte chemotactic protein-1) by microglial cells. This promotes the recruitment of microglial cells to the sites of neuronal damage, and also enhances the formation of the brain protein beta-amyloid (Aβ). The results of modern studies are presented, indicating that platelets are involved in systemic inflammatory reactions, where they interact with monocytes to form monocyte-platelet aggregates (MTA), which induce the activation of monocytes with a pro inflammatory phenotype. In the last decade, it has been established that activated platelets and other cells of the immune system, including monocytes, detached microvesicles (MV) from the membrane. It has been shown that MV are involved as messengers in the transport of biologically active lipids, cytokines, complement, and other molecules that can cause exacerbation of systemic inflammatory reactions. The presented review allows us to expand our knowledge about the cellular and molecular aspects of the interaction of monocytes/macrophages with microglial cells and platelets in the development of neuroinflammation and cognitive decline in the pathogenesis of mental diseases and in AD, and also helps in the search for specific biomarkers of the clinical severity of mental disorder in patients and the prospects for their response to treatment.

Neuropsychiatry of neurometabolic, neuroendocrine, and mitochondrial disorders

2020 ◽  
pp. 309-322
Author(s):  
Mark Walterfang ◽  
Ramon Mocellin ◽  
Dennis Velakoulis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Psychiatric Illness ◽  
Mitochondrial Disorders ◽  
Endocrine Function ◽  
Endocrine Disorders ◽  
Endocrine Tumours ◽  
Neurometabolic Disorders ◽  
The Brain

This chapter examines the role of neurometabolic, neuroendocrine, and mitochondrial disorders in causing neuropsychiatric syndromes. It examines how disorders of cellular metabolic processes, particularly those that affect the brain, can result in major psychiatric syndromes and the over-representation of some neurometabolic disorders in psychiatric illness. It also discusses a range of endocrine disorders, particularly disorders of increased or reduced endocrine function and endocrine tumours, in producing psychiatric syndromes. The chapter also reviews the role of mitochondrial disorders in disrupting central nervous system processes and metabolism, and how some mitochondrial disorders result in psychiatric illness.

scholarly journals High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives

2019 ◽  
Vol 20 (24) ◽  
pp. 6258 ◽  
Author(s):  
Biscetti ◽  
Rando ◽  
Nardella ◽  
Cecchini ◽  
Pecorini ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Central Nervous System ◽  
Nervous System ◽  
Nuclear Protein ◽  
State Of The Art ◽  
High Mobility ◽  
High Mobility Group ◽  
Future Perspectives ◽  
Vascular Bed

Diabetes mellitus (DM) is an endemic disease, with growing health and social costs. The complications of diabetes can affect potentially all parts of the human body, from the heart to the kidneys, peripheral and central nervous system, and the vascular bed. Although many mechanisms have been studied, not all players responsible for these complications have been defined yet. High Mobility Group Box-1 (HMGB1) is a non-histone nuclear protein that has been implicated in many pathological processes, from sepsis to ischemia. The purpose of this review is to take stock of all the most recent data available on the role of HMGB1 in the complications of DM.

scholarly journals A sart1 Zebrafish Mutant Results in Developmental Defects in the Central Nervous System

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2340
Author(s):  
Hannah E. Henson ◽  
Michael R. Taylor
Keyword(s):  
Central Nervous System ◽  
Cell Death ◽  
Nervous System ◽  
Developmental Defects ◽  
Whole Exome ◽  
The Central Nervous System ◽  
And Function ◽  
Upregulated Genes ◽  
The Brain

The spliceosome consists of accessory proteins and small nuclear ribonucleoproteins (snRNPs) that remove introns from RNA. As splicing defects are associated with degenerative conditions, a better understanding of spliceosome formation and function is essential. We provide insight into the role of a spliceosome protein U4/U6.U5 tri-snRNP-associated protein 1, or Squamous cell carcinoma antigen recognized by T-cells (Sart1). Sart1 recruits the U4.U6/U5 tri-snRNP complex to nuclear RNA. The complex then associates with U1 and U2 snRNPs to form the spliceosome. A forward genetic screen identifying defects in choroid plexus development and whole-exome sequencing (WES) identified a point mutation in exon 12 of sart1 in Danio rerio (zebrafish). This mutation caused an up-regulation of sart1. Using RNA-Seq analysis, we identified additional upregulated genes, including those involved in apoptosis. We also observed increased activated caspase 3 in the brain and eye and down-regulation of vision-related genes. Although splicing occurs in numerous cells types, sart1 expression in zebrafish was restricted to the brain. By identifying sart1 expression in the brain and cell death within the central nervous system (CNS), we provide additional insights into the role of sart1 in specific tissues. We also characterized sart1’s involvement in cell death and vision-related pathways.

Understanding and Treatment of Diabetes Mellitus by Traditional Chinese Medicine

1981 ◽  
Vol 09 (01) ◽  
pp. 93-94 ◽  
Author(s):  
Keji Chen
Keyword(s):  
Diabetes Mellitus ◽  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Treatment Of Diabetes ◽  
Ancient Times ◽  
Medical Books

This paper reviews the understanding and treatment of diabetes mellitus in traditional Chinese medicine from ancient times to the present day. The most valuable ancient medical books and the most commonly used plants are enumerated in this paper.

scholarly journals Heterotopic ossification after central nervous system injuries: understanding of pathogenesis

2018 ◽  
Vol 25 (3-4) ◽  
pp. 119-124
Author(s):  
I. F Gareev ◽  
O. A Beylerli ◽  
A. K Vakhitov
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Heterotopic Ossification ◽  
Genetic Factors ◽  
Cellular Interactions ◽  
Heterotopic Ossifications ◽  
The Brain

Available data on the pathogenesis, cellular interactions, role of inflammation, humoral and genetic factors in the formation of heterotopic ossifications resulting from injuries of the brain or spinal cord are presented.

scholarly journals Glymphatics: A Transformative Development in Medical Neuroscience Relevant to Injuries in Military Central Nervous System

2021 ◽  
Author(s):  
James Meyerhoff ◽  
Nabarun Chakraborty ◽  
Rasha Hammamieh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Sleep Deprivation ◽  
Brain Edema ◽  
Critical Role ◽  
Spatial Relationship ◽  
Military Operations ◽  
Glymphatic System ◽  
The Brain

ABSTRACT Introduction The glia-operated glymphatic system, analogous to but separate from the lymphatics in the periphery, is unique to brain and retina, where it is very closely aligned with the arteriolar system. This intimate relationship leads to a “blood vessel like” distribution pattern of glymphatic vessels in the brain. The spatial relationship of glymphatics, including their essential component aquaporin-4 with vascular pericytes of brain arterioles is critical to functionality and is termed “polarization”. Materials and Methods We review the available literature on the factors affecting the resting state of glymphatics under normal conditions, including the important role of sleep in supporting normal glymphatic function (including waste removal) as well as the critical role of “polarization” under normal conditions. We then examine the effects of traumatic brain injury (TBI) or seizures on the glymphatic system and its state of “polarization”. Results Injury, such as TBI, can disrupt polarization resulting in “depolarization” leading to brain edema. Conclusion Damage to the glymphatic system might explain the brain edema so often seen following TBI or other insult. Moreover, similar damage should be expected in response to seizures, which can often be associated with chemical exposures as well as with TBI. Military operations, whether night operations or continuous operations, quite often impose limitations on sleep. As glymphatic function is sleep-dependent, sleep deprivation alone could compromise glymphatic function, as well, and might in addition, explain some of the well-known performance deficits associated with sleep deprivation. Possible effects of submarine and diving operations, chemical agents (including seizures), as well as high altitude exposure and other threats should be considered. In addition to the brain, the retina is also served and protected by the glymphatic system. Accordingly, the effect of military-related risks (e.g., exposure to laser or other threats) to retinal glymphatic function should also be considered. An intact glymphatic system is absolutely essential to support normal central nervous system functionality, including cognition. This effects a broad range of military threats on brain and retinal glymphatics should be explored. Possible preventive and therapeutic measures should be proposed and evaluated, as well.

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