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At least 19 recordsLinked to original sources
PubMed1977

Influence of systemic factors on hyperbaric oxygen toxicity in the rat visual system.

The electroretinogram (ERG) was measured in lightly anaesthetised rats exposed to 4-7 atm O2 until death. An initial increase and later decrease in amplitude with increase in latency was seen which, although not consistently related to the appearance of seizures characteristically seen above 4.5 atm 02, appeared closely linked to systemic factors. A fall in respiration rate always preceded the fall of the ERG, and apnoea preceded ERG extinction. When blood pressure and ERG were measured in two comparable groups of rats exposed to 5.76 atm O2, both records showed similar time courses. The cerebral visual evoked response (VER) was measured at 5.76 atm O2 simultaneously with the ERG. The later VER waves showed a degree of enhancement at the time of seizures, but otherwise amplitude and waveform were maintained until late in toxicity. EEG spiking gave the earliest indication of toxicity, and it is concluded that the primary projection to the rat visual cortex is comparatively resistant to high-pressure oxygen.

Animals↗
PubMed2025

Systems Factors Contributing to Racial/Ethnic Disparities in Maternal Health: A Systematic Review.

INTRODUCTION: Despite ongoing efforts to reduce adverse maternal outcomes, including maternal mortality and severe maternal morbidity, racial/ethnic disparities in outcomes persist in high-income countries, including the United States (US) and Canada. Limited research has examined hospital-level factors that may drive disparities and contribute to adverse outcomes. This systematic review summarizes factors within the health system contributing to adverse outcomes and racial/ethnic disparities in the US and Canada to inform future policies and practices. METHOD: We searched SCOPUS, PubMed, EBSCOhost, and ProQuest Healthcare Administration for studies that reported hospital-level factors contributing to adverse maternal outcomes and racial/ethnic disparities. The review followed a two-stage screening process. The risk of bias of the included studies was evaluated using the Mixed Methods Appraisal Tool. The System Engineering Initiative for Patient Safety (SEIPS) 2.0 framework guided the identification and categorization of factors. RESULTS: Of 2441 studies retrieved, 30 met the inclusion criteria. Twenty-eight studies were conducted in the US, and 2 were conducted in Canada. The review included 16 qualitative, 11 quantitative, and 3 mixed-methods studies. We identified 60 factors associated with different system components, including person(s) (12%), tasks (28%), tools and technology (7%), internal environment (10%), organization (28%), and external environment (15%). Shortage of resources, including staffing, poor care coordination, and discriminatory organizational practices, were key factors described in the studies. CONCLUSION: Addressing health system factors in addition to broader societal factors is important to reduce adverse outcomes and promote equity for all women and birthing persons.

Humans↗
PubMed1976

Associated systemic factors in cerebrovascular ischemia.

Systemic disorders (eg, cardiac, hematologic) are commonly recognized as predisposing and sometimes actual precipitating events in cerebral ischemia. From available studies, the incidence of precipitation is not clear. To determine this, we undertook a comprehensive investigation of all patients with ischemic brain disease for a one-year period. Results reveal that brain ischemia is more commonly precipitated by systemic illness than usually supposed, particularly transient ischemic attacks of the vertebrobasilar circulation and completed infarcts in the carotid distribution. Cardiac disorders outnumber all other precipitating events. As they are more amenable to therapy than atherosclerosis, a diligent search for such precipitating events is warranted in patients with ischemic symptoms.

Aged↗
PubMed1979

Molecular assembly in the contact phase of the Hageman factor system.

Data obtained in the past few years have defined the molecular mechanisms of contact activation of the Hageman factor pathways of plasma, i.e., the kinin-forming, intrinsic clotting and fibrinolytic systems. Involved are four molecules: Hageman factor, high molecular weight (MW) kininogen, prekallikrein and factor XI. High MW kininogen serves as a surface cofactor to assemble prekallikrein or factor XI in proximity to surface-bound Hageman factor. Reciprocal proteolytic activation of Hageman factor and prekallikrein represents an essential step in the rapid activation of the contact phase. Although Hageman factor does undergo cleavage and activation in the absence of prekallikrein or high MW kininogen, the rate is approximately 50 and 100 times slower than when these molecules are present. Once Hageman factor is activated on the surface, it cleaves and activates clotting factor XI. Activated Hageman factor (HFa) exhibits two molecular forms. One of these, alpha HFa, activates prekallikrein and factor XI, and the intrinsic clotting system on the surface. alpha HFa and clotting factor XI remain surface bound. The other form of activated Hageman factor, beta HFa, leaves the surface, going into solution where it readily activates additional prekallikrein but not factor XI. Of perhaps even greater importance, kallikrein rapidly dissociates from the surface. Thus the formation of bradykinin and fibrinolysis is disseminated whereas clotting via the intrinsic system remains localized. Reviewed here is the molecular mechanism of contact activation of the Hageman factor pathways and discussed in the interaction of Hageman factor with the negatively charged surface, prekallikrein, factor XI and high MW kininogen. The multiple forms of activated Hageman factor and their potential biologic significance are also discussed.

Blood Coagulation↗
PubMed1978

Epileptic brain damage: the role of systemic factors that modify cerebral energy metabolism.

The possible role of systemic physiological changes (occurring secondarily during status epilepticus) in the causation of epileptic brain damage has been evaluated in rats. Animals were anaesthetized, paralysed and mechanically ventilated; sustained electrocortical seizure discharges were induced by the intravenous injection of bicuculline, 1.2 mg/kg. After two hours of seizure activity brains were fixed by perfusion for histology. Physiological variables were maintained within certain limits from the end of the initial seizure phase (approximate duration twenty minutes) until two hours after onset of seizure to provide six groups: (1) Standard: mean arterial pressure above 120 mmHg, no hypoxia or hypoglycaemia, rectal temperature close to 37 degrees C. (2) Moderate Hypotension: mean arterial pressure at 70-75 mmHg. (3) Severe Hypotension: mean arterial pressure at 50 mmHg. (4) Hypoxia: arterial oxygen tension at 50 mmHg. (5) Hypoglycaemia: non-fed animals, with blood glucose close to 3.0 mumol/g. (6) Hyperthermia: rectal temperature at 40 degrees C. Microvacuolation and ischaemic cell change were identified by light microscopy in scattered neurons in the cortex (principally in the outer layers) in animals in three groups (Standard, Severe Hypotension and Hyperthermia). Similar neuronal changes were seen in the hippocampus (predominantly in the h1 or Sommer sector) in the Standard and Hyperthermia Groups. It is tentatively proposed that neuronal damage in animals with unrestricted cerebral oxygen and glucose availability is due to oxidative mechanisms in cells with excessively enhanced neuronal activity and that lesions caused by failing energy production do not appear until severe degrees of hypoxia are reached.

Animals↗
PubMed1978

Systemic factors contributory to retinal vein occlusion.

This study was undertaken in 79 patients with retinal vein occlusion to assess the different systemic mechanisms contributing to the occlusion, namely, intrinsic vessel disease and abnormalities of the blood constituents and blood viscosity. In 55 patients older than 50 years of age, important associations were hypertension, abnormal results on glucose tolerance test, hyperlipidemia, chronic lung disease, and elevated serum IgA levels. In the 24 patients younger than 50 years of age, male incidence was high and important associations were head injuries, hyperlipidemia, and the use of estrogen-containing preparations. Hyperviscosity and cryofibrinogenemia were prominent in both groups. The pathogenesis of retinal venous occlusion is complex involving interaction between the vessel wall and blood constituents.

Adult↗
PubMed1976

Purification and some properties of factor D of the human properdin system.

Factor D has been purified by gel and ion exchange chromatographies, and by ultrafiltration through different membranes. The final preparation appeared pure in various analytical tests. The molecular weight of human D is 21,500 according to gel chromatography, the isoelectric point was found at pH 7.8. Factor D is an active esterolytic enzyme, it cleaves N-alpha-acetyl-L-lysine methyl ester and N-alpha-acetyl-L-glycyl-L-lysine methyl ester. Both peptide esters inhibit the hydrolytic activation of factor B by D in the presence of cobra venom factor. D is also inhibited by diisopropyl-fluorophosphate and by penylmethyl-sulfonyl-flouride.

Humans↗