A review of psychosocial factors and stroke: A new public health problem.

The role of psychosocial factors (PSF) in increased risk of stroke is a novel public health challenge, but unclear definitions for PSF and the multiple stroke subtypes have led to inconsistent reports. A review of this issue is therefore warranted. METHODS: Several databases were used for this narrative systematic review (Medline, Embase and Cochrane Library). Two independent reviewers evaluated articles from between 2001 and 2018 on the themes of PSF and stroke/transient ischemic attack (TIA). PSF criteria were job strain, psychological interpersonal and behavioral stress, and social deprivation. Ischemic and hemorrhagic stroke and TIA subtypes were also identified. RESULTS: Forty-five cohorts, five case-control studies and two meta-analyses were included. Despite mixed results, PSF were associated with an increased risk of ischemic and hemorrhagic stroke in populations of all ages, and more predominantly in women. CONCLUSION: This broad review shows that the presence of PSF is associated with an increased risk stroke and TIA. As such, PSF must figure in both public health policy and stroke prevention programs, similar to other established metabolic and environmental factors.

Air pollution and stroke. A new modifiable risk factor is in the air.

Evidence from epidemiological studies has demonstrated that outdoor air pollution is now a well-known major problem of public health, mainly in low and middle income countries. Contrasting with myocardial infarction, there are few data on the association of air pollution and stroke. METHODS: We propose a narrative literature review of the effects and the underlying biological mechanisms of short- and long-term exposure to air pollutants on stroke risk and mortality, using the following key-words: stroke, cerebrovascular events, ischemic and haemorrhage stroke, transient ischaemic attack, mortality, air pollution and air pollutants. RESULTS: Twenty-one papers were selected. Air pollution, of which whose small particulate matter are the most toxic, contributes to about one-third of the global burden of stroke. We can identify vulnerable patients with classical neuro-vascular risk factors or a prior history of stroke or transient ischemic attack or persons living in low-income countries. Biological mechanisms of this new morbid association are discussed. CONCLUSION: Air pollution should be recognized as a silent killer inducing stroke whose mortality rates remain elevated by its role as a new modifiable neurovascular risk factor, needing public health policies.

[Acute management of spontaneous intracerebral hemorrhage]. / Prise en charge aiguë des hémorragies intracérébrales spontanées.

Intracerebral hemorrhage accounts for approximately 15% of the 115,000 strokes occurring each year in France. Although therapeutic strategies are more limited than for ischemic stroke, major points in the management of intracerebral hemorrhage can reduce short term morbidity and mortality by limiting the expansion of the hematoma and the occurrence of early complications, and long term patients' outcome by reducing the risk of recurrence. This article aims to update the key elements that contribute to improve of the prognosis of intracerebral hemorrhage patients.

[Management of ischemic stroke in the acute phase]. / Prise en charge de l'infarctus cérébral à la phase initiale.

Ischemic stroke accounts for 80% of overall stroke, and is one of the leading causes of death, disability and dementia in worldwide. Management of patients with acute ischemic stroke dramatically improved over time with the implementation of intensive care stroke units, the development of acute recanalization strategies, the optimization of the management of post-stroke complications, and the prevention of early stroke recurrence. The objective of this article is to provide a general overview of the current management of patients with acute ischemic stroke aiming at improving post-stroke outcome.

An examination of the soluble oligomeric complexes extracted from the red cell membrane and their relation to the membrane cytoskeleton.

A part of the spectrin extracted from red cell membranes at low ionic strength occurs in the form of a high-molecular weight oligomeric complex with actin and proteins 4.1 and 4.9. When the extraction is performed at 35 degrees, the spectrin is present in this complex as the dimer, all higher forms being dissociated. We have been unable to establish any correlation between the fraction of the spectrin thus complexed and the metabolic state of the cell. At least a large part of the complex appears to be a defined monodisperse species, sedimenting at 31S. The actin is present as short protofilaments. The average number of spectrin molecules associated with each molecule of complex has been studied by cytochalasin binding and electron microscopy. The complexes present the appearance in the electron microscope of spiders, in which the legs are spectrin dimers, attached to a globular element, containing by inference, actin and proteins 4.1 and 4.9; they are active in nucleating the polymerization of G-actin. The complexes are extremely stable, being resistant to dissociation under the conditions of the deoxyribonuclease assay, even after treatment with trypsin to degrade the actin-associated proteins. It is suggested that the complexes represent intact junctions of the membrane cytoskeletal network. Relevant structural features of the network are revealed by electron microscopy. The results lead to inferences concerning the mechanism of dissociation of the network from the membrane.

Octapeptide analogues of somatostatin inhibit the clonal growth and vasoactive intestinal peptide-stimulated cyclic AMP formation in human small cell lung cancer cells.

Two endocrinologically active octapeptide analogues (BIM-23014 C and BIM-23034) of somatostatin (SRIF) containing either an N- or C-terminal 3-(2-naphthyl)-D-Ala residue were examined for their ability to inhibit the in vitro receptor binding, clonal growth, and vasoactive intestinal peptide (VIP)-stimulated cyclic AMP formation in human small cell lung cancer cell (SCLC) line NCI-H345. Both SRIF peptides inhibited [125I]SRIF(Tyr11)-14 binding with IC50 values in the low nM range. Colony formation in the in vitro SCLC growth assay was also inhibited in the same concentration range, as was VIP-stimulated cyclic AMP formation. Therefore, octapeptide analogues of SRIF function as SCLC SRIF receptor agonists.

Subcellular redistribution of Pit-2 P(i) transporter/amphotropic leukemia virus (A-MuLV) receptor in A-MuLV-infected NIH 3T3 fibroblasts: involvement in superinfection interference.

Amphotropic murine leukemia virus (A-MuLV) utilizes the Pit-2 sodium-dependent phosphate transporter as a cell surface receptor to infect mammalian cells. Previous studies established that infection of cells with A-MuLV resulted in the specific down-modulation of phosphate uptake mediated by Pit-2 and in resistance to superinfection with A-MuLV. To study the mechanisms underlying these phenomena, we constructed plasmids capable of efficiently expressing epsilon epitope- and green fluorescent protein (GFP)-tagged human Pit-2 proteins in mammalian cells. Overexpression of epsilon-epitope-tagged Pit-2 transporters in NIH 3T3 cells resulted in a marked increase in sodium-dependent P(i) uptake. This increase in P(i) uptake was specifically blocked by A-MuLV infection but not by infection with ecotropic MuLV (E-MuLV) (which utilizes a cationic amino acid transporter, not Pit-2, as a cell surface receptor). These data, together with the finding that the tagged Pit-2 transporters retained their A-MuLV receptor function, indicate that the insertion of epitope tags does not affect either retrovirus receptor or P(i) transporter function. The overexpressed epitope-tagged transporters were detected in cell lysates, by Western blot analysis using both epsilon-epitope- and GFP-specific antibodies as well as with Pit-2 antiserum. Both the epitope- and GFP-tagged transporters showed almost exclusive plasma membrane localization when expressed in NIH 3T3 cells, as determined by laser scanning confocal microscopy. Importantly, when NIH 3T3 cells expressing these proteins were productively infected with A-MuLV, the tagged transporters and receptors were no longer detected in the plasma membrane but rather were localized to a punctate structure within the cytosolic compartment distinct from Golgi, endoplasmic reticulum, endosomes, lysosomes, and mitochondria. The intracellular Pit-2 pool colocalized with the virus in A-MuLV-infected cells. A similar redistribution of the tagged Pit-2 proteins was not observed following infection with E-MuLV, indicating that the redistribution of Pit-2 is not directly attributable to general effects associated with retroviral infection but rather is a specific consequence of A-MuLV-Pit-2 interactions.