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1.
Metab Brain Dis ; 35(4): 559-578, 2020 04.
Article in English | MEDLINE | ID: mdl-32146658

ABSTRACT

Hepatic encephalopathy (HE) may occur in patients with liver failure. The most critical pathophysiologic mechanism of HE is cerebral edema following systemic hyperammonemia. The dysfunctional liver cannot eliminate circulatory ammonia, so its plasma and brain levels rise sharply. Astrocytes, the only cells that are responsible for ammonia detoxification in the brain, are dynamic cells with unique phenotypic properties that enable them to respond to small changes in their environment. Any pathological changes in astrocytes may cause neurological disturbances such as HE. Astrocyte swelling is the leading cause of cerebral edema, which may cause brain herniation and death by increasing intracranial pressure. Various factors may have a role in astrocyte swelling. However, the exact molecular mechanism of astrocyte swelling is not fully understood. This article discusses the possible mechanisms of astrocyte swelling which related to hyperammonia, including the possible roles of molecules like glutamine, lactate, aquaporin-4 water channel, 18 KDa translocator protein, glial fibrillary acidic protein, alanine, glutathione, toll-like receptor 4, epidermal growth factor receptor, glutamate, and manganese, as well as inflammation, oxidative stress, mitochondrial permeability transition, ATP depletion, and astrocyte senescence. All these agents and factors may be targeted in therapeutic approaches to HE.


Subject(s)
Astrocytes/metabolism , Brain Edema/metabolism , Hepatic Encephalopathy/metabolism , Hyperammonemia/metabolism , Ammonia/metabolism , Astrocytes/pathology , Brain/metabolism , Brain/pathology , Brain Edema/pathology , Cell Size , Hepatic Encephalopathy/pathology , Humans , Hyperammonemia/pathology , Oxidative Stress/physiology
2.
Biomedicine (Taipei) ; 8(2): 9, 2018 Jun.
Article in English | MEDLINE | ID: mdl-29806587

ABSTRACT

BACKGROUND: The incidence of kidney cancer from different areas of Iran was reported. Nevertheless, there is no available systematic reviews in this regard. Therefore, the present systematic review carried out to estimate the incidence rate of kidney cancer among Iranian people. METHOD: This systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) in September 2017. A search was concluded using Medline/ PubMed, Scopus, ScienceDirect, and Google scholar for international papers and four national databases (Scientific Information Database, MagIran, IranMedex, and IranDoc) for Persian papers. The incidence rate of kidney cancer was calculated using random effect model. RESULT: An aggregate of 159 papers were retrieved in the primary search of the databases. Further screening and advanced refinement of the retrieved studies produced 15 studies totally. The age-standardized rate (ASR) of kidney cancer was 1.94, 95% CI (1.62-2.55) and 1.36, 95 % CI (1.09-1.62) in males and females, respectively. CONCLUSION: In comparison to other parts of the world, the incidence of kidney cancer was lower in Iran. Afterwards, further studies are necessary to outline the exact incidence rate and the trend of kidney cancer in Iran.

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