Simple asymptotic potential model for finding weakly bound negative ions

The primary force of muscle contraction is thought to involve a change in the myosin head whilst attached to actin, the energy coming from ATP hydrolysis. This change in attached state could either be a conformational change in the head or an alteration in the binding angle made with actin. A considerable amount is known about one bound state, the so-called strongly attached state, which occurs in the presence of ADP or in the absence of nucleotide. In this state, which probably corresponds to the last attached state of the force-producing cycle, the angle between the long axis myosin head and the actin filament is roughly 45°. Details of other attached states before and during power production have been difficult to obtain because, even at very high protein concentration, the complex is almost completely dissociated by ATP. Electron micrographs of the complex in the presence of ATP have therefore been obtained only after chemically cross-linking myosin subfragment-1 (S1) to actin filaments to prevent dissociation. But it is unclear then whether the variability in attachment angle observed is due merely to the cross-link acting as a hinge.We have recently found low ionic-strength conditions under which, without resorting to cross-linking, a high fraction of S1 is bound to actin during steady state ATP hydrolysis. The structure of this complex is being studied by cryo-electron microscopy of hydrated specimens. Most advantages of frozen specimens over ambient temperature methods such as negative staining have already been documented. These include improved preservation and fixation rates and the ability to observe protein directly rather than a surrounding stain envelope. In the present experiments, hydrated specimens have the additional benefit that it is feasible to use protein concentrations roughly two orders of magnitude higher than in conventional specimens, thereby reducing dissociation of weakly bound complexes.

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Spectral characteristics of the weakly bound electron species in methanol as determined from a hybrid solvation model

Journal de Chimie Physique ◽

10.1051/jcp/1996930182 ◽

1996 ◽

Vol 93 ◽

pp. 182-187 ◽

Cited By ~ 4

Author(s):

C Pépin ◽

T Goulet ◽

D Houde ◽

JP Jay-Gerin

Keyword(s):

Spectral Characteristics ◽

Solvation Model ◽

Weakly Bound ◽

Bound Electron

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ELECTRICAL FIELD STRENGTH ON THE POSITIVE CORONA ELECTRODE WITH THE COUNTERFLOW OF NEGATIVE IONS

Le Journal de Physique Colloques ◽

10.1051/jphyscol:19797178 ◽

1979 ◽

Vol 40 (C7) ◽

pp. C7-361-C7-362

Author(s):

N. B. Bogdanova ◽

B. G. Pevchev ◽

V. I. Popkov

Keyword(s):

Field Strength ◽

Negative Ions ◽

Electrical Field ◽

Electrical Field Strength ◽

Corona Electrode

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BALB-Abcb4 mice lacking the hepatobiliary phospholipid transporter represent a potential model of hepatic osteodystrophy

Zeitschrift für Gastroenterologie ◽

10.1055/s-0029-1241569 ◽

2009 ◽

Vol 47 (09) ◽

Author(s):

K Hochrath ◽

B Rathkolb ◽

K Butuzova ◽

W Hans ◽

H Fuchs ◽

...

Keyword(s):

Potential Model ◽

Hepatic Osteodystrophy

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RELATIVE CONTRIBUTIONS OF FIBROSIS AND CONNEXIN CHANGES TOTHE ATRIAL FIBRILLATION SUBSTRATE DURING THE DEVELOPMENT AND REVERSAL OF CONGESTIVEHEART FAILURE

Clinical & Investigative Medicine ◽

10.25011/cim.v31i4.4793 ◽

2008 ◽

Vol 31 (4) ◽

pp. 5

Author(s):

Brett Burstein ◽

Kunihiro Nishida ◽

Philippe Comtois ◽

Louis Villenuve ◽

Yung-Hsin Yeh ◽

...

Keyword(s):

Atrial Fibrillation ◽

Potential Model ◽

Diastolic Pressure ◽

Recovery Period ◽

Left Ventricular ◽

Muscle Bundle ◽

Protein Ratio ◽

Conduction Disturbances ◽

Conduction Abnormalities ◽

Mrna And Protein Expression

Background: Connexin alterations occur in various atrial fibrillation (AF) paradigms, but their functional significance remains unclear. No data are available regarding the effects of CHF on atrial connexin expression and phosphorylation. We therefore analyzed connexin changes and their contribution to the AF substrate during the development and reversal ofCHF. Methods and Results: Dogs were allocated to three groups: CHF induced by 2-week ventricular tachypacing (CHF, n=15); CHF dogs allowed to recover for 4 weeks after 2-week tachypacing (REC, n=15) and non-paced shams (CTL, n=11). Left ventricular end-diastolic pressure increased with CHF (14.5±1.0*** vs.3.7±0.7, ***P < 0.001 vs. CTL) and normalized upon CHF recovery (5.1±1.0^†††, ^††† P < 0.001 vs. CHF). Real-time PCR and Western-blot analyses revealed connexin43 (Cx43) and connexin40 (Cx40) mRNA and protein expression to be unchanged by CHF and REC. However, CHF caused Cx43 dephosphorylation(by ~73%***) and increased Cx40/Cx43 protein ratio (by ~35%***), with both alterations completely reversing in REC. Immunofluorescent confocal microscopy confirmed connexin protein trends, with a reduction in phosphorylated Cx43 (by ~68%*** in CHF) that returned to control in REC. CHF caused conduction abnormalities (phasedelay-range and heterogeneity index, both P < 0.01) and burst pacing-induced AF prolongation (CTL 22±7s, CHF 1100±171s***, REC 884±220s***) which persisted in the recovery period, along with residual fibrosis (CTL 3.6±0.7%, CHF 14.7±1.5%***, REC13.3±2.3%***). Fibrosis physically interrupted muscle bundle continuity and anionically-based action potential model of canine atrium showed that fibrosiswas able to account for the observed conduction abnormalities. Conclusions: CHF causes connexin-dephosphorylation and Cx40/Cx43ratio increases. With CHF reversal, atrial connexin alterations recover completely, but tissue fibrosis, conduction abnormalities and a substrate forAF remain with fibrosis accounting for conduction abnormalities. Thus, althougha trial connexin changes occur with CHF, they are not essential for conduction disturbances and AF promotion, which appear rather to be related primarily tofibrotic interruption of muscle-bundle continuity.

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