scholarly journals What is the trigger mechanism for the reversal of electron flow in oxygen-tolerant [NiFe] hydrogenases?

2015 ◽  
Vol 6 (2) ◽  
pp. 1433-1443 ◽  
Author(s):  
Ian Dance

A new mechanistic model is developed for the sequence of events by which oxygen-tolerant [NiFe] hydrogenase enzymes respond to O2.

2017 ◽  
Vol 25 (4) ◽  
pp. 396-407 ◽  
Author(s):  
F. Wania ◽  
M.J. Binnington ◽  
M.S. Curren

Indigenous Arctic populations experience elevated exposures to many environmental contaminants compared with groups residing in southern Canada. This is largely due to consumption of traditional foods, some of which (ringed seals, beluga whales, narwhals, etc.) have relatively high concentrations of persistent organic pollutants. Models of contaminant fate, transport, and bioaccumulation represent powerful tools to explore this exposure issue, wherein combined models can be used to mechanistically and dynamically describe the entire sequence of events linking chemical emissions into the environment to ultimate contaminant concentrations in indigenous Arctic populations. In this review, various approaches adapted and applied to understanding indigenous Arctic contaminant exposure are explored, including early models describing body burdens in single traditional food species to more recent approaches holistically examining uptake and bioaccumulation in entire food chains. The applications of these models are also discussed, including attempts to (i) identify chemical properties favouring transport to, and bioaccumulation in, the Arctic; (ii) clarify the main determinants of temporal trends observed in indigenous Arctic biomonitoring; (iii) explore the impacts of permanent and temporary dietary transitions on current and future indigenous Arctic contaminant exposures; and (iv) correlate modeled early-life pollutant exposures with measured health impacts. The review demonstrates the effectiveness of mechanistic model approaches in investigating indigenous Arctic contaminant exposure, and confirms their utility in continued improvements to understanding associated risk in this unique population context.


Author(s):  
K. Kovacs ◽  
E. Horvath ◽  
J. M. Bilbao ◽  
F. A. Laszlo ◽  
I. Domokos

Electrolytic lesions of the pituitary stalk in rats interrupt adenohypophysial blood flow and result in massive infarction of the anterior lobe. In order to obtain a deeper insight into the morphogenesis of tissue injury and to reveal the sequence of events, a fine structural investigation was undertaken on adenohypophyses of rats at various intervals following destruction of the pituitary stalk.The pituitary stalk was destroyed electrolytically, with a Horsley-Clarke apparatus on 27 male rats of the R-Amsterdam strain, weighing 180-200 g. Thirty minutes, 1,2,4,6 and 24 hours after surgery the animals were perfused with a glutaraldehyde-formalin solution. The skulls were then opened and the pituitary glands removed. The anterior lobes were fixed in glutaraldehyde-formalin solution, postfixed in osmium tetroxide and embedded in Durcupan. Ultrathin sections were stained with uranyl acetate and lead citrate and investigated with a Philips 300 electron microscope.


Author(s):  
L.X. Oakford ◽  
S.D. Dimitrijevich ◽  
R. Gracy

In intact skin the epidermal layer is a dynamic tissue component which is maintained by a basal layer of mitotically active cells. The protective upper epidermis, the stratum corneum, is generated by differentiation of the suprabasal keratinocytes which eventually desquamate as anuclear comeocytes. A similar sequence of events is observed in vitro in the non-contracting human skin equivalent (HSE) which was developed in this lab (1). As a part of the definition process for this model of living skin we are examining its ultrastructural features. Since desmosomes are important in maintaining cell-cell interactions in stratified epithelia their distribution in HSE was examined.


Author(s):  
L. J. Brenner ◽  
D. G. Osborne ◽  
B. L. Schumaker

Exposure of the ciliate, Tetrahymena pyriformis, strain WH6, to normal human or rabbit sera or mouse ascites fluids induces the formation of large cytoplasmic bodies. By electron microscopy these (LB) are observed to be membrane-bounded structures, generally spherical and varying in size (Fig. 1), which do not resemble the food vacuoles of cells grown in proteinaceous broth. The possibility exists that the large bodies represent endocytic vacuoles containing material concentrated from the highly nutritive proteins and lipoproteins of the sera or ascites fluids. Tetrahymena mixed with bovine serum albumin or ovalbumin solutions having about the same protein concentration (7g/100 ml) as serum form endocytic vacuoles which bear little resemblance to the serum-induced LB. The albumin-induced structures (Fig. 2) are irregular in shape, rarely spherical, and have contents which vary in density and consistency. In this paper an attempt is made to formulate the sequence of events which might occur in the formation of the albumin-induced vacuoles.


2014 ◽  
Vol 56 ◽  
pp. 99-110 ◽  
Author(s):  
David Allsop ◽  
Jennifer Mayes

One of the hallmarks of AD (Alzheimer's disease) is the formation of senile plaques in the brain, which contain fibrils composed of Aβ (amyloid β-peptide). According to the ‘amyloid cascade’ hypothesis, the aggregation of Aβ initiates a sequence of events leading to the formation of neurofibrillary tangles, neurodegeneration, and on to the main symptom of dementia. However, emphasis has now shifted away from fibrillar forms of Aβ and towards smaller and more soluble ‘oligomers’ as the main culprit in AD. The present chapter commences with a brief introduction to the disease and its current treatment, and then focuses on the formation of Aβ from the APP (amyloid precursor protein), the genetics of early-onset AD, which has provided strong support for the amyloid cascade hypothesis, and then on the development of new drugs aimed at reducing the load of cerebral Aβ, which is still the main hope for providing a more effective treatment for AD in the future.


1977 ◽  
Vol 38 (02) ◽  
pp. 0399-0406 ◽  
Author(s):  
Peter N. Walsh ◽  
Richard E. Goldberg ◽  
Richard L. Tax ◽  
Larry E. Magargal

SummaryTo determine whether platelets play a role in the pathogenesis of retinal vein occlusion (RVO), platelets and coagulation were evaluated in 28 patients with RVO. Platelet coagulant activities concerned with the initiation and early stages of intrinsic coagulation were 2–4 fold increased in 9 patients with acute primary RVO but not in patients with acute secondary (10 patients) or chronic (9 patients) RVO. Platelet factor 3 activity, platelet aggregation, serotonin release by platelets and plasma coagulation were normal in all patients. Platelets may provide a trigger mechanism for venous thrombosis in the eye when local conditions permit.


1964 ◽  
Vol 12 (02) ◽  
pp. 471-483 ◽  
Author(s):  
F Rodríguez-Erdmann

SummaryThe rôle of the clotting system in the pathogenesis of the generalized Shwartzman reaction (gSr) has been stressed in recent years. The clotting system is activated ubiquitously and as a result of it, fibrin is deposited intravascularly and a haemorrhagic diathesis develops. Evidence is presented herein, that endotoxin does not activate purified prothrombin, nor does endotoxin influence the convertion of prothrombin when it is activated in the presence of purified platelet-factor 3 (or caephalin) purified Ac-G (factor V) and Ca-ions.The trigger mechanism of the gSr also seems to be in the so-called prephase of clotting mechanism. Data are presented, which show that endotoxin activates the Hageman factor in vitro. The importance of this clotting factor and of platelet-factor 3 is discussed. Also the rôle played by the RES and cardiodynamic and vascular components are taken in consideration in the discussion.


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