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Query: UMLS:C0036341 (
schizophrenia
)
60,220
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Intracellular free calcium concentrations ([Ca(2+)](1)) were measured in platelets from healthy volunteers before and after adding
thrombin
, chlorpromazine, haloperidol and/or lithium, and in platelets from DSM-III-R diagnosed schizophrenic patients receiving neuroleptic medication.
Thrombin
increased [Ca(2+)]( 1) in a dose- dependent fashion. Chlorpromazine and haloperidol also mobilized Ca(2+) in a dose-dependent fashion, and augmented the response to low doses of
thrombin
without changing the maximal response to
thrombin
. The effects of all three drugs were not additive, suggesting that they affected the same intraplatelet calcium pool; most likely the dense tubular system. Lithium also increased [Ca(2+) ] but without affecting the response to
thrombin
, chlorpromazine or haloperidol. The effects of the latter three drugs were additive to that of lithium, suggesting that lithium was acting on a different calcium pool. The response to
thrombin
was significantly lower in platelets from schizophrenic patients than in platelets from healthy volunteers. Further studies are required to explore potential causes for this observation. Such causes include
schizophrenia
per se and chronic neuroleptic treatment.
...
PMID:Calcium mobilization in platelets from schizophrenic and healthy subjects. Regulation by lithium and neuroleptics. 2229 85
Blood platelets are considered to be a peripheral marker in
schizophrenia
and other psychiatric disorders. Oxidative stress in
schizophrenia
may be responsible for changes in platelet metabolism and function; therefore, the aim of this study was to examine and compare the generation of superoxide anions and activity of an antioxidant enzyme (glutathione peroxidase [GPx]) in blood platelets in patients with
schizophrenia
and healthy subjects. The level of superoxide anions generated in platelets after
thrombin
and platelet-activating factor stimulation and activity of GPx in patients with
schizophrenia
and healthy volunteers was estimated. The results obtained from the study indicate that the generation of superoxide anions in platelets as a response of platelets in patients with
schizophrenia
to such activating factors as
thrombin
or platelet-activating factor is higher than in the response of platelets of healthy subjects. In platelets from schizophrenic patients, suppressed GPx activity of about 67% was observed.
...
PMID:Generation of superoxide anion radicals and platelet glutathione peroxidase activity in patients with schizophrenia. 2483 3
Heparin cofactor II (HCII) belongs to serpin superfamily and it acts as a thrombin inhibitor in the coagulation cascade, in a glycosaminoglycan-dependent pathway using the release of a sequestered hirudin-like N-terminal tail for interaction with
thrombin
. This serpin belongs to multiple member group V2 of vertebrate serpin classification. However, there is no comprehensive study illustrating the exact phylogenetic history of HCII, to date. Herein, we explored phylogenetic traits of HCII genes. Structures of HCII gene from selected ray-finned fishes and lamprey varied in exon I and II with insertions of novel introns of which one in core domain for ray-finned fishes in exon II at the position 241c. We found HCII remain nested in the largest intron of phosphatidylinositol (PI) 4-kinase (PIK4CA) gene (genetic variants of this gene cause
schizophrenia
) at the origin of vertebrates, dated about 500MY old. We found that sequence features such as two acidic repeats (AR1-II), GAG-binding helix-D, three serpin motifs and inhibitory reactive center loop (RCL) of HCII protein are highly conserved in 55 vertebrates analyzed. We identified 985 HCII variants by analysis of 1092 human genomes with top three variation classes belongs to SNPs (84.3%), insertion (7.1%) and deletion (5.0%). We identified 37 deleterious mutations in the human HCII protein and we have described these mutations in relation to HCII sequence-structure-function relationships. These understandings may have clinical and medical importance as well.
...
PMID:Genetic variants and evolutionary analyses of heparin cofactor II. 2495 Jun 23
Recent studies implicate extracellular proteases in synaptic plasticity, learning, and memory. The data are especially strong for such serine proteases as
thrombin
, tissue plasminogen activator, neurotrypsin, and neuropsin as well as matrix metalloproteinases, MMP-9 in particular. The role of those enzymes in the aforementioned phenomena is supported by the experimental results on the expression patterns (at the gene expression and protein and enzymatic activity levels) and functional studies, including knockout mice, specific inhibitors, etc. Counterintuitively, the studies have shown that the extracellular proteolysis is not responsible mainly for an overall degradation of the extracellular matrix (ECM) and loosening perisynaptic structures, but rather allows for releasing signaling molecules from the ECM, transsynaptic proteins, and latent form of growth factors. Notably, there are also indications implying those enzymes in the major neuropsychiatric disorders, probably by contributing to synaptic aberrations underlying such diseases as
schizophrenia
, bipolar, autism spectrum disorders, and drug addiction.
...
PMID:Neural ECM proteases in learning and synaptic plasticity. 2541 Mar 56
Calcium signalling has long been implicated in bipolar disorder, especially by reports of altered intracellular calcium ion concentrations ([Ca
2+
]). However, the evidence has not been appraised critically. We carried out a systematic review and meta-analysis of studies of cellular calcium indices in bipolar disorder. 2281 records were identified and 117 screened, of which 32 were eligible and 21 were suitable for meta-analyses. The latter each involved up to 642 patients and 404 control subjects. We found that basal free intracellular [Ca
2+
] is increased in bipolar disorder, both in platelets and in lymphocytes. The effect size is 0.55, with an estimated elevation of 29%. It is observed in medication-free patients. It is present in mania and bipolar depression, but data are equivocal for euthymia. Cells from bipolar disorder individuals also show an enhanced [Ca
2+
] response to stimulation with 5-HT or
thrombin
, by an estimated 25%, with an effect size of 0.63. In studies which included other diagnoses, intracellular basal [Ca
2+
] was higher in bipolar disorder than in unipolar depression, but not significantly different from
schizophrenia
. Functional parameters of cellular Ca
2+
(e.g. calcium transients), and neuronal [Ca
2+
], have been much less investigated, and no firm conclusions can be drawn. In summary, there is a robust, medium effect size elevation of basal and stimulated free intracellular [Ca
2+
] in bipolar disorder. The results suggest altered calcium functioning in the disorder, and encourage further investigations into the underlying mechanisms, and the implications for pathophysiology and therapeutics.
...
PMID:Cellular calcium in bipolar disorder: systematic review and meta-analysis. 3180 67
Introduction
: The revised Ghent nosology presents the classical features of Marfan syndrome. However, behind its familiar face, Marfan syndrome hides less well-known features.
Areas covered
: The German Marfan Organization listed unusual symptoms and clinical experts reviewed the literature on clinical features of Marfan syndrome not listed in the Ghent nosology. Thereby we identified the following features: (1) bicuspid aortic valve, mitral valve prolapse, pulmonary valve prolapse, tricuspid valve prolapse, (2) heart failure and cardiomyopathy, (3) supraventricular arrhythmia, ventricular arrhythmia, and abnormal repolarization, (4) spontaneous coronary artery dissection, anomalous coronary arteries, and atherosclerotic coronary artery disease, tortuosity-, aneurysm-, and dissection of large and medium-sized arteries, (5) restrictive lung disease, parenchymal lung disease, and airway disorders, (6) obstructive- and central sleep apnea, (7) liver and kidney cysts, biliary tract disease, diaphragmatic hernia, and adiposity, (8) premature labor, and urinary incontinence, (9) myopathy, reduced bone mineral density, and craniofacial manifestations, (10) atrophic scars, (11) caries, and craniomandibular dysfunction, (12) headache from migraine and spontaneous cerebrospinal fluid leakage, (13) cognitive dysfunction,
schizophrenia
, depression, fatigue, and pain, (14) and activated fibrinolysis,
thrombin
, platelets, acquired von Willebrand disease, and platelet dysfunction.
Expert commentary
: Future research, nosologies, and guidelines may consider less well-known features of Marfan syndrome.
...
PMID:Features of Marfan syndrome not listed in the Ghent nosology - the dark side of the disease. 3182 51
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