Aggregation of blood platelets by adrenaline and its uptake

Barthel, Wolfgang; Markwardt, Fritz

doi:10.1016/0006-2952(75)90415-3

Cited by 27 publications

(17 citation statements)

References 13 publications

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“…Kayser-Fleischer ring is seen in some patients during ophthalmological examinations. Between one- and two-thirds of patients report psychiatric symptoms at initial presentation [56-58]. Psychiatric signs are present in almost 50% of patients at any one time [59], and present before motor signs in 20% of cases; up to half of patients may be seen initially by a psychiatrist [60].…”

Section: Resultsmentioning

confidence: 99%

“…Four main psychiatric symptom clusters have been identified: mood and affective change; behavior and personality change; psychosis and; cognitive impairment [61]. Personality changes are very common, particularly irritability and aggression [56,62]. Mood disturbance, including both depression and mania, is the most common formal neuropsychiatric illness [63-67].…”

Section: Resultsmentioning

confidence: 99%

“…Mood disturbance, including both depression and mania, is the most common formal neuropsychiatric illness [63-67]. Psychosis, delusional states and catatonia, while less frequent in WD, can be extremely disabling [56,57,60,61,68]. Schizophrenia-like symptoms were reported to be present in up to 10% of patients [63], but were less prevalent in one case series (2.4%) [69].…”

Section: Resultsmentioning

confidence: 99%

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Diagnostic and treatment implications of psychosis secondary to treatable metabolic disorders in adults: a systematic review

Bonnot

Klünemann

Sedel

et al. 2014

Orphanet Journal of Rare Diseases

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ObjectiveIt is important for psychiatrists to be aware of certain inborn errors of metabolism (IEMs) as these rare disorders can present as psychosis, and because definitive treatments may be available for treating the underlying metabolic cause. A systematic review was conducted to examine IEMs that often present with schizophrenia-like symptoms.Data sourcesPublished literature on MEDLINE was assessed regarding diseases of homocysteine metabolism (DHM; cystathionine beta-synthase deficiency [CbS-D] and homocysteinemia due to methyltetrahydrofolate reductase deficiency [MTHFR-D]), urea cycle disorders (UCD), acute porphyria (POR), Wilson disease (WD), cerebrotendinous-xanthomatosis (CTX) and Niemann-Pick disease type C (NP-C).Study selectionCase reports, case series or reviews with original data regarding psychiatric manifestations and cognitive impairment published between January 1967 and June 2012 were included based on a standardized four-step selection process.Data extractionAll selected articles were evaluated for descriptions of psychiatric signs (type, severity, natural history and treatment) in addition to key disease features.ResultsA total of 611 records were identified. Information from CbS-D (n = 2), MTHFR-D (n = 3), UCD (n = 8), POR (n = 12), WD (n = 11), CTX (n = 14) and NP-C publications (n = 9) were evaluated. Six non-systematic literature review publications were also included. In general, published reports did not provide explicit descriptions of psychiatric symptoms. The literature search findings are presented with a didactic perspective, showing key features for each disease and psychiatric signs that should trigger psychiatrists to suspect that psychotic symptoms may be secondary to an IEM.ConclusionIEMs with a psychiatric presentation and a lack of, or sub-clinical, neurological signs are rare, but should be considered in patients with atypical psychiatric symptoms.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Diagnostic and treatment implications of psychosis secondary to treatable metabolic disorders in adults: a systematic review

Bonnot

Klünemann

Sedel

et al. 2014

Orphanet Journal of Rare Diseases

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“…Apart from high-potency block of Sur1-Trpm4 channels (EC50 = 48 nM) [21,23], glibenclamide also blocks Sur1-regulated KATP channels in pancreatic β cells [62]. However, at the doses used in CNS ischemia and trauma, the potential consequence of block of pancreatic KATP channels – hypoglycemia – is not observed; infusion of 200 ng/hr of glibenclamide in rats has a minimal effect on serum glucose [4,63,64]. Sur2-regulated KATP channels in cardiac and smooth muscle cells are less sensitive to block by glibenclamide, by a factor of 10 times or more [62,65].…”

Section: Progressive Hemorrhagic Necrosis – Role Of the Sur1-trpm4 Chmentioning

confidence: 99%

“…Constant subcutaneous infusion of glibenclamide was used in the preclinical studies as a convenient alternative to constant IV infusion, as is used with injectable glibenclamide (RP-1127) in clinical trials for other CNS indications (ClinicalTrials.gov identifiers: NCT01454154; NCT01268683; NCT01794182). In the animal studies, no clinically relevant hypoglycemia or other toxicity has been detected with infusions of 200 ng/hr [4,63,64] or 400 ng/hr [68]. In a Phase I trial of RP-1127 in 16 normal subjects (ClinicalTrials.gov identifier: NCT01132703), a 3-day IV infusion (125 μg/hr) produced no clinically significant hypoglycemia or other serious adverse event (S. Jacobson, personal communication).…”

Section: Progressive Hemorrhagic Necrosis – Role Of the Sur1-trpm4 Chmentioning

confidence: 99%

The Sur1-Trpm4 Channel in Spinal Cord Injury

Simard¹,

Woo

Aarabi

et al. 2013

J Spine

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Spinal cord injury (SCI) is a major unsolved challenge in medicine. Impact trauma to the spinal cord shears blood vessels, causing an immediate ‘primary hemorrhage’. During the hours following trauma, the region of hemorrhage enlarges progressively, with delayed or ‘secondary hemorrhage’ adding to the primary hemorrhage, and effectively doubling its volume. The process responsible for the secondary hemorrhage that results in early expansion of the hemorrhagic lesion is termed ‘progressive hemorrhagic necrosis’ (PHN). PHN is a dynamic process of auto destruction whose molecular underpinnings are only now beginning to be elucidated. PHN results from the delayed, progressive, catastrophic failure of the structural integrity of capillaries. The resulting ‘capillary fragmentation’ is a unique, pathognomonic feature of PHN. Recent work has implicated the Sur1-Trpm4 channel that is newly upregulated in penumbral microvessels as being required for the development of PHN. Targeting the Sur1-Trpm4 channel by gene deletion, gene suppression, or pharmacological inhibition of either of the two channel subunits, Sur1 or Trpm4, yields exactly the same effects histologically and functionally, and exactly the same unique, pathognomonic phenotype – the prevention of capillary fragmentation. The potential advantage of inhibiting Sur1-Trpm4 channels using glibenclamide is a highly promising strategy for ameliorating the devastating sequelae of spinal cord trauma in humans.

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Physiology of Vascular Homeostasis

Sanchorawala¹,

Keaney²

1997

Developments in Cardiovascular Medicine

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Aggregation of blood platelets by adrenaline and its uptake

Cited by 27 publications

References 13 publications

Diagnostic and treatment implications of psychosis secondary to treatable metabolic disorders in adults: a systematic review

Diagnostic and treatment implications of psychosis secondary to treatable metabolic disorders in adults: a systematic review

The Sur1-Trpm4 Channel in Spinal Cord Injury

Physiology of Vascular Homeostasis

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