The role of calcium and cellular membrane dysfunction in experimental trauma and subarachnoid hemorrhage

1985 ◽  
Vol 62 (5) ◽  
pp. 698-703 ◽  
Author(s):  
Otakar R. Hubschmann ◽  
Douglas C. Nathanson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cellular Membrane ◽  
Membrane Injury ◽  
Content Type ◽  
Experimental Trauma ◽  
Acute Subarachnoid Hemorrhage ◽  
A Chain ◽  
The Moment ◽  
Large Vessels

✓ Acute subarachnoid hemorrhage (SAH) and intraparenchymal hematoma (IPH) in cats are accompanied by massive cellular depolarization. This depolarization, characterized by potassium (K+) efflux and calcium (Ca++) influx, results in membrane destabilization, osmotic imbalance, and a decrease in electrical conduction. The Ca++ influx appears to initiate a chain reaction that, in some instances, may result in delayed cell destruction. The ionic dysequilibrium probably contributes to both brain engorgement and spasm in large vessels. The cellular depolarization and calcium-induced cell membrane injury at the moment of impact may play a greater role in the pathophysiology of head trauma than previously thought.

Social capital in the theory and research of LIS professionals in the light of the literature on the subject. Review of current knowledge

2021 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Maja Dorota Wojciechowska
Keyword(s):  
Social Capital ◽  
Current Knowledge ◽  
Future Research ◽  
Content Type ◽  
Individual Social Capital ◽  
Rural Libraries ◽  
The Subject ◽  
The Moment ◽  
The Impact

Purpose The purpose of the paper is to present the latest scholarly trends in the field of social capital in libraries, to review research concepts published by LIS professionals and to suggest further research possibilities in this area. Design/methodology/approach This paper presents a review and critical analysis of literature associated with research on social capital in libraries to highlight its importance for the development of LIS and its impact on the functioning of environments linked with various types of libraries. The goal of literature analysis was to determine the current condition of research on social capital in libraries. The main trends were identified and the need for further qualitative analyses, which are missing at the moment, was confirmed. Findings It was determined that, so far, LIS professionals have focussed mainly on the role of municipal libraries in developing social capital, the problem of building trust, especially in immigrant circles and the impact of libraries on promoting a civil society. Academic libraries, rural libraries, organisational capital in libraries and individual social capital of librarians were a much less frequent subject of research. The role of libraries in developing social capital in educational (primary and secondary education) and professional (non-university professionals) circles is practically non-existent in research, and it will require in-depth studies and analyses in the coming years. Originality/value This paper constitutes a synthetic review of the latest research concepts concerning social capital in libraries. It identifies the most important research trends and areas that so far have not been explored and suggests research methods to help LIS professionals design future research in this area more effectively.

Chronic subdural hematoma presenting as spontaneous subarachnoid hemorrhage

1985 ◽  
Vol 63 (5) ◽  
pp. 691-692 ◽  
Author(s):  
Zbigniew Kotwica ◽  
Jerzy Brzeziński
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Clinical Findings ◽  
Content Type ◽  
Acute Subarachnoid Hemorrhage ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ Six cases of chronic subdural hematoma presenting with the clinical findings of acute subarachnoid hemorrhage are reported. No systemic or focal cause for the bleeding was found, and possible mechanisms are discussed.

Detection of soluble E-selectin, ICAM-1, VCAM-1, and L-selectin in the cerebrospinal fluid of patients after subarachnoid hemorrhage

1998 ◽  
Vol 89 (4) ◽  
pp. 559-567 ◽  
Author(s):  
Richard S. Polin ◽  
Murad Bavbek ◽  
Mark E. Shaffrey ◽  
Kevin Billups ◽  
Christopher A. Bogaev ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Content Type ◽  
Vascular Adhesion Molecules ◽  
And Migration ◽  
Vascular Adhesion ◽  
Fine Print

Object. The goal of this study was to explore whether the levels of soluble adhesion molecules were elevated in cerebrospinal fluid (CSF) after subarachnoid hemorrhage (SAH). This association was suggested by the known inflammatory response in vasospasm and the role of vascular adhesion molecules in regulating leukocytic adhesion to, and migration across, vascular endothelium. Methods. A prospective analysis was performed on CSF samples obtained in 17 patients who had suffered a recent aneurysmal SAH and in 16 control patients by using quantitative enzyme-linked immunosorbent assays for E-selectin, intercellular adhesion molecule—1 (ICAM—1), vascular adhesion molecule—1 (VCAM-1), and L-selectin. Levels of soluble forms of E-selectin (p = 0.0013), ICAM-1 (p = 0.0001), and VCAM-1 (p = 0.048) were found to be elevated in the CSF of patients after SAH compared with levels in the CSF of normal controls, patients with unruptured aneurysms, and patients tested months after SAH occurred. In addition, individual patients tested at the time of their initial ictus demonstrated a fall in adhesion molecule levels over time. Levels of E-selectin (p = 0.044) were highest in patients who later developed moderate or severe vasospasm. Conclusions. Adhesion molecules are known to be involved in white cell adherence to the endothelium and subsequent diapedesis and migration in which a role in initiation of tissue damage is postulated. The authors have demonstrated the elevation of three adhesion molecules, with severely elevated levels of E-selectin seen in patients who later develop vasospasm. A correlation with a role of vascular adhesion molecules in the pathogenesis of cerebral vasospasm is suggested.

Subarachnoid hemorrhage following chymopapain chemonucleolysis

1987 ◽  
Vol 66 (5) ◽  
pp. 775-778 ◽  
Author(s):  
Joseph F. Cusick ◽  
Khang-Cheng Ho ◽  
Jay F. Schamberg
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Vessel Wall ◽  
Neurological Complications ◽  
Causative Role ◽  
Content Type ◽  
Frequent Finding ◽  
Histological Abnormality ◽  
Upper Cervical ◽  
Cervical Level

✓ Subarachnoid hemorrhage is a frequent finding in patients who have incurred neurological complications following chymopapain chemonucleolysis, but the basis for this occurrence remains controversial. The authors report the clinical and postmortem findings in a 42-year-old man who died 5 days after chemonucleolysis at the L4–5 and L5–S1 disc spaces. The predominant histological abnormality was a severe inflammatory arteritis of a medium-sized artery at the upper cervical level with disruption of the vessel wall. The potential causative role of chymopapain in this situation and the correlation of a vascular basis for many of the complications found after inadvertent intrathecal chymopapain injection are discussed.

Failure of a Heifetz aneurysm clip

1982 ◽  
Vol 57 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Ram Kossowsky ◽  
Manuel Dujovny ◽  
Nir Kossovsky ◽  
Yves Keravel
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Stress Corrosion ◽  
Fracture Mechanism ◽  
Intergranular Corrosion ◽  
Content Type ◽  
Aneurysm Clip ◽  
Stress Load ◽  
Highly Sensitive ◽  
Acute Subarachnoid Hemorrhage ◽  
Fine Print

✓ A 16-year-old girl died from an acute subarachnoid hemorrhage following the fracture of a blade of a Heifetz aneurysm clip. The clip was manufactured from 17-7PH steel, which on metallurgical testing was found to be highly sensitive to intergranular corrosion. The fracture mechanism was stress corrosion, brought on by the combination of a stress load, an electrolytic environment, and a susceptible steel.

Neuropeptide Y in the primate model of subarachnoid hemorrhage

1992 ◽  
Vol 77 (3) ◽  
pp. 417-423 ◽  
Author(s):  
Ryszard M. Pluta ◽  
Anna Deka-Starosta ◽  
Alois Zauner ◽  
Jay K. Morgan ◽  
Karin M. Muraszko ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Neuropeptide Y ◽  
Cerebral Vasospasm ◽  
Primate Model ◽  
Content Type ◽  
Peripheral Plasma ◽  
Delayed Cerebral Vasospasm ◽  
Arterial Plasma ◽  
Fine Print

✓ The cause of cerebral vasospasm after subarachnoid hemorrhage (SAH) remains unknown. Recently, an association between the potent vasoconstricting peptide, neuropeptide Y, and delayed cerebral vasospasm after SAH has been postulated. This was based on the findings of increased neuropeptide Y levels in the cerebrospinal fluid (CSF) and plasma after SAH in animals and humans. For this study, the primate model of SAH was used to assess the possible role of neuropeptide Y in delayed vasospasm after SAH. Fifteen cynomolgus monkeys underwent placement of a clot of either whole blood or red blood cells in the subarachnoid space around the middle cerebral artery (MCA). Sequential arteriography for assessment of MCA diameter and sampling of blood and CSF for neuropeptide Y were performed: before SAH (Day 0); 7 days after SAH, when signs of delayed cerebral vasospasm peak in this model and in humans; 12 days after SAH; and 28 days after SAH. Subarachnoid hemorrhage did not evoke changes in CSF or plasma levels of neuropeptide Y. Nine monkeys had arteriographic evidence of vasospasm on Day 7, but no change in neuropeptide Y levels occurred in plasma or CSF. In addition, neuropeptide Y levels did not change, even after resolution of vasospasm on Day 12 or Day 28. Neuropeptide Y levels were substantially higher in CSF than in arterial plasma (p < 0.003 at each interval). No correlation was found between neuropeptide Y levels in CSF and in plasma. These results do not confirm a relationship between neuropeptide Y levels in the CSF or peripheral plasma and delayed cerebral vasospasm in SAH.

Natriuretic peptide system and endothelin in aneurysmal subarachnoid hemorrhage

1997 ◽  
Vol 87 (2) ◽  
pp. 275-280 ◽  
Author(s):  
Eelco F. M. Wijdicks ◽  
Wouter I. Schievink ◽  
John C. Burnett
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Natriuretic Peptide ◽  
Cerebral Vasospasm ◽  
Fluid Balance ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Peptide System ◽  
Natriuretic Peptide System ◽  
Fine Print

✓ The natriuretic peptide system consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The system is implicated in the control of body fluid homeostasis, causes natriuresis and diuresis (ANP and BNP), and regulates vascular tone (CNP). A reciprocal relationship between ANP and endothelin (ET) has been suggested, and earlier studies have documented a possible role of ET in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The authors studied plasma ANP, BNP, CNP, and ET for 6 consecutive days in 13 patients with SAH by using radioimmunoassay. The median admission values for ANP were 31.5 pg/ml (range 16.8–323 pg/ml [normal 15 ± 7 pg/ml]); for BNP, 45.3 pg/ml (range 2.2–80.2 pg/ml [normal 12 ± 9 pg/ml]); for CNP, 7.7 pg/ml (range < 2–20 pg/ml [normal 5.2 ± 3 pg/ml]); and for ET, 11 pg/ml (range 6.5–25.1 pg/ml [normal 7.2 ± 4 pg/ml]). Additional increases (defined as > 100% increase on two consecutive measurements) were noted in ANP (11 patients), BNP (10 patients), and CNP (three patients), and resulted in a negative fluid balance in 10 of the 13 patients. The CNP increased in three of four patients with cerebral vasospasm and in one of nine patients without cerebral vasospasm (Fisher's exact test, p = 0.2). No major fluctuations in plasma ET were noted. In seven patients, the plasma ET level did not increase beyond 10 pg/ml during the days of measurement. In six patients, only an occasional sample showed an increase to a maximum of 25 pg/ml. Changes in BNP, ANP, and CNP were independent of each other. The authors conclude that both plasma ANP and BNP increase after SAH and often result in a negative fluid balance. Plasma ANP and BNP seem differentially regulated in the presence of SAH but not by the level of the plasma ET. The possible role of CNP as a regulatory response to cerebral vasospasm needs further exploration.

scholarly journals Nautilus-assisted coil embolization for a complex AcomA wide-necked aneurysm in the setting of acute subarachnoid hemorrhage

2021 ◽  
pp. neurintsurg-2021-017670
Author(s):  
Alexander Sirakov ◽  
Svetozar Matanov ◽  
Pervinder Bhogal ◽  
Stanimir Sirakov
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Coil Embolization ◽  
Cerebral Aneurysms ◽  
Anterior Communicating Artery ◽  
New Approach ◽  
Content Type ◽  
Acute Subarachnoid Hemorrhage ◽  
Inner Diameter ◽  
Aneurysmal Neck ◽  
Video Player

Numerous devices and sophisticated strategies have been developed to further increase the number of aneurysms amenable to endovascular treatment.1–4 Despite the superfluity of available neurovascular armamentarium, wide-necked bifurcation aneurysms can still pose a significant technical challenge to the treating clinician.5–7 Neck bridging is a conceptually new approach, which provides increased occlusion rates with lower recurrence and complications rates.8–10 The Nautilus (EndoStream Medical) is an intrasaccular bridging device intended to assist in coil embolization of wide-necked cerebral aneurysms. This CE-marked device, available in various sizes, consists of flexible-layers, and is a nitinol-based, detachable implant. The device is delivered through a standard microcatheter with a minimal 0.0165" inner diameter and is fully radiopaque and completely resheathable.Owing to its unique ‘tornado’ like shape the device entirely reconstructs the aneurysmal neck, which facilitates the following coil embolization. In this video 1, we demonstrate the use of Nautilus - assisted coil embolization for a complex anterior communicating artery (AcomA) wide-necked aneurysm in the setting of acute subarachnoid hemorrhage.Video 1

The role of hotel restaurants in gastronomic place branding

2016 ◽  
Vol 10 (1) ◽  
pp. 81-90 ◽  
Author(s):  
Valery Gordin ◽  
Julia Trabskaya ◽  
Elena Zelenskaya
Keyword(s):  
Place Branding ◽  
Content Type ◽  
Saint Petersburg ◽  
Settlement Type ◽  
A Chain ◽  
Hotel Managers ◽  
The City ◽  
Practical Implications

Purpose – This paper aims to display the role of hotel restaurants in gastronomic place branding. The authors view hotel restaurants as having a great potential in the promotion of local gastronomy. Design/methodology/approach – The research was done in several stages. First, the authors selected six destinations (Lapland, Catalonia, Saint Petersburg, Marseille, Parma and Munich) according to the classification of gastronomic brands based on the settlement type. Second, the authors studied conceptions of hotel restaurants located in these destinations to see how they reflect local gastronomic brands. For this purpose, restaurant menus, verbal descriptions of interiors and names of establishments were analyzed using elements of content analysis. Finally, the authors conducted several interviews with hotel managers in one of the destinations to distinguish the challenges of gastronomic branding within hotel restaurants. Findings – The results allowed defining the role of hotel restaurants in gastronomic branding depending on the following factors: hotel’s affiliation with a chain, hotel’s star rating and destination type. Practical implications – The authors argue that gastronomic branding raises attractiveness of hotels, its restaurants and destination on the whole. This research was presented to the Tourism Committee of St Petersburg, resulting in increased attention to gastronomic branding among the city authorities. Originality/value – The role of hotel restaurants in gastronomic branding has not been studied previously. However, hotel restaurants differ from other actors of gastronomic branding due to the necessity to comply with hotel’s conception, brand and standards.

The role of the prostacyclin-thromboxane system in cerebral vasospasm following induced subarachnoid hemorrhage in the rabbit

1984 ◽  
Vol 61 (6) ◽  
pp. 1120-1128 ◽  
Author(s):  
Richard C. Chan ◽  
Felix A. Durity ◽  
Gordon B. Thompson ◽  
Robert A. Nugent ◽  
Marie Kendall
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Platelet Aggregation ◽  
Clinical Status ◽  
Control Group ◽  
Content Type ◽  
Arterial Blood ◽  
Or Groups ◽  
Significant Difference ◽  
Potent Vasoconstrictor

✓ Subarachnoid hemorrhage (SAH) was induced in 50 rabbits by injecting 1.25 cc/kg of autologous, well heparinized, fresh arterial blood into the cisterna magna, followed by suspending the animals in a head-down position at 30° for 15 minutes. The animals were evenly divided into five groups: a control group, or groups receiving post-SAH prostacyclin (PGI2), carbacyclin, thromboxane A2 (TXA2) synthetase inhibitor (OKY-1581), or nutralipid. Radiographic vertebrobasilar arterial spasm was demonstrated on the 3rd day post-SAH in the control animals. This was decreased in the prostacyclin and the carbacyclin groups and was absent in the OKY-1581 and the nutralipid groups. Cerebral blood flow (CBF) measurements on the 4th day post-SAH using the xenon-133 technique failed to reveal any significant difference between the prostacyclin, the carbacyclin, and the control groups, but flows in the nutralipid and the OKY-1581 groups were significantly higher. There was a good correlation between the clinical status and the CBF. Intracytoplasmic vacuolation and detachment of the vascular endothelium, seen ultrastructurally, may account for the impaired synthesis of prostacyclin. Exogenous prostacyclin and carbacyclin decreased vasospasm but failed to improve cerebral perfusion. OKY-1581 blocked the synthesis of the potent vasoconstrictor, TXA2, which is not only formed during platelet aggregation but also induces platelet aggregation. Nutralipid contains linolenic acid, a precursor of eicosapentaenoic acid (EPA), which is more potent in inhibiting platelet aggregation and in blocking TXA2 production. The various fatty acid constituents of nutralipid bind to albumin and thereby shorten the half-life of TXA2.

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