Assessment of in-shoe pressure: development of a clinical user guide based on a DELPHI-derived consensus

The Foot ◽  
2021 ◽  
pp. 101892
Author(s):  
Joshua Palaya ◽  
Christopher MacKenzie ◽  
Sue Pearson ◽  
Linda Murray ◽  
Chloe Katsanos
Keyword(s):  
Pressure Development

scholarly journals The Messinian Salinity Crisis as a trigger for high pore pressure development in the Western Mediterranean

2021 ◽  
Author(s):  
Michael S. Dale ◽  
Héctor Marín‐Moreno ◽  
Ismael Himar Falcon‐Suarez ◽  
Carlos Grattoni ◽  
Jonathan M. Bull ◽  
...  
Keyword(s):  
Pore Pressure ◽  
Western Mediterranean ◽  
Messinian Salinity Crisis ◽  
Pressure Development

scholarly journals Calculation Of Pressure Rise And Energy Of Hot Gases Due To High Energy Arcing Faults In The Metal-clad Switchgear

2017 ◽  
Vol 4 (2) ◽  
pp. 116-119
Author(s):  
M. Iwata ◽  
T. Miyagi ◽  
Y. Goda ◽  
K. Shirai
Keyword(s):  
Thermal Effect ◽  
Pressure Rise ◽  
High Energy ◽  
Arcing Faults ◽  
Pressure Development ◽  
Calculation Results ◽  
Roof Panel

This paper presents the 3-D CFD calculation results of the pressure rise due to the High Energy Arcing Faults (HEAFs) in the metal-clad switchgears. The calculations were performed considering the came-off of the roof panel that was observed in the arc tests. The calculated pressure development approximately agreed with the measured one. Furthermore, the energy of hot gases exhausted from the broken roof panel was calculated to investigate the thermal effect of hot gases.

scholarly journals Sex-related effects on diabetes-induced alterations in calcium release in the rat heart

2007 ◽  
Vol 293 (6) ◽  
pp. H3584-H3592 ◽  
Author(s):  
Nazmi Yaras ◽  
Erkan Tuncay ◽  
Nuhan Purali ◽  
Babur Sahinoglu ◽  
Guy Vassort ◽  
...  
Keyword(s):  
Calcium Release ◽  
Binding Protein ◽  
Ryanodine Receptors ◽  
Left Ventricular ◽  
Adult Rats ◽  
Fk506 Binding Protein ◽  
Pressure Development ◽  
Spatiotemporal Parameters ◽  
Intracellular Ca ◽  
Developed Pressure

The present study was designed to determine whether the properties of local Ca2+ release and its related regulatory mechanisms might provide insight into the role of sex differences in heart functions of control and streptozotocin-induced diabetic adult rats. Left ventricular developed pressure, the rates of pressure development and decay (±dP/d t), basal intracellular Ca2+ level ([Ca2+]i), and spatiotemporal parameters of [Ca2+]i transients were found to be similar in male and female control rats. However, spatiotemporal parameters of Ca2+ sparks in cardiomyocytes isolated from control females were significantly larger and slower than those in control males. Diabetes reduced left ventricular developed pressure to a lower extent in females than in males, and the diabetes-induced depressions in both +dP/d t and −dP/d t were less in females than in males. Diabetes elicited a smaller reduction in the amplitude of [Ca2+]i transients in females than in males, a smaller reduction in sarcoplasmic reticulum-Ca2+ load, and less increase in basal [Ca2+]i. Similarly, the elementary Ca2+ events and their control proteins were clearly different in both sexes, and these differences were more marked in diabetes. Diabetes-induced depression of the Ca2+ spark amplitude was significantly less in females than in matched males. Levels of cardiac ryanodine receptors (RyR2) and FK506-binding protein 12.6 in control females were significantly higher than those shown in control males. Diabetes induced less RyR2 phosphorylation and FK506-binding protein 12.6 unbinding in females. Moreover, total and free sulfhydryl groups were significantly less reduced, and PKC levels were less increased, in diabetic females than in diabetic males. The present data related to local Ca2+ release and its related proteins describe some of the mechanisms that may underlie sex-related differences accounting for females to have less frequent development of cardiac diseases.

Investigation of liquefaction and pore water pressure development in layered sands

2008 ◽  
Vol 7 (1) ◽  
pp. 199-219 ◽  
Author(s):  
Pelin Tohumcu Özener ◽  
Kutay Özaydın ◽  
Mehmet M. Berilgen
Keyword(s):  
Pore Water ◽  
Pore Water Pressure ◽  
Water Pressure ◽  
Pressure Development

scholarly journals Cardiovascular and cerebrovascular risk with nonsteroidal anti-inflammatory drugs and cyclooxygenase 2 inhibitors: latest evidence and clinical implications

2017 ◽  
Vol 8 (6) ◽  
pp. 173-182 ◽  
Author(s):  
Andrea Fanelli ◽  
Daniela Ghisi ◽  
Pierangelo Lora Aprile ◽  
Francesco Lapi
Keyword(s):  
Term Treatment ◽  
Cyclooxygenase 2 ◽  
Thrombotic Risk ◽  
Long Term Treatment ◽  
Pressure Development ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
High Doses ◽  
The Right ◽  
Meta Analyses

Observational studies and meta-analyses have shown that the administration of nonsteroidal anti-inflammatory drugs (NSAIDs), especially when prescribed at high doses for long periods of time, can potentially increase the risk of cardiovascular diseases. The increased thrombotic risk related to the use of NSAIDs is mainly due to their cyclooxygenase 2 selectivity. The dosage use, the formulation selected and the duration of the therapy are other factors that can significantly impact on the cardiovascular risk. In order to minimize the risk, prescription of the right drug based on the patient’s features and the different safety profiles of several NSAIDs that are available on the market is key for their appropriate administration. Despite the baseline cardiovascular and gastrointestinal risk of each patient, monitoring of patients is suggested for increases in blood pressure, development of edema, deterioration of renal function, or gastrointestinal bleeding during long-term treatment with NSAIDs.

Direct measurement of flow from the posterior lymph hearts of hydrated and dehydrated toads (Bufo marinus).

1997 ◽  
Vol 200 (11) ◽  
pp. 1695-1702 ◽  
Author(s):  
J M Jones ◽  
A K Gamperl ◽  
A P Farrell ◽  
D P Toews
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Systolic Pressure ◽  
Lymph Flow ◽  
Bufo Marinus ◽  
Experimental Chamber ◽  
Doppler Flow ◽  
Simultaneous Measurements ◽  
Pressure Development ◽  
Lymph Heart

Flow from the posterior lymph hearts of Bufo marinus was measured using Doppler flow probes. These probes were placed on the posterior vertebral vein and recorded flow as lymph was ejected from the heart. In resting, hydrated toads, mean lymph flow from one of the paired posterior lymph hearts was 25.9 +/- 4.9 ml kg-1 h-1, stroke volume was 8.9 +/- 1.4 microL kg-1 and lymph heart rate was 47.5 +/- 3.7 beats min-1. We estimate that, together, the paired posterior lymph hearts are capable of generating flows that are approximately one-sixtieth of the resting cardiac output. Mean peak systolic pressure developed by the posterior lymph hearts was 1.62 +/- 0.08 kPa. Simultaneous measurements of lymph heart pressure development and flow revealed that the outflow pore of the heart opened at a pressure of 0.71 +/- 0.04 kPa, approximately 113 +/- 5 ms into systole. When toads were moderately disturbed, stroke volume increased by as much as fourfold with little change in lymph heart rate (< 5 beats min-1). When toads were dehydrated, lymph flow decreased by 70% at 12h and by 80% and 24h. Since there was only a modest non-significant decrease in lymph heart rate (30%), this reduction in flow was attributed to decreases in stroke volume (approximately 80%). Lymph heart flow and stroke volume returned to control values 30 min after adding water back into the experimental chamber. Stroke volume was clearly more important in regulating lymph flow than lymph heart rate under these conditions in Bufo marinus.

Effect of Multidirectional Shaking on Pore Pressure Development in Sands

1978 ◽  
Vol 104 (1) ◽  
pp. 27-44 ◽  
Author(s):  
H. Bolton Seed ◽  
Geoffrey R. Martin ◽  
Robert M. Pyke
Keyword(s):  
Pore Pressure ◽  
Pressure Development

Transgenic overexpression of cardiac A1adenosine receptors mimics ischemic preconditioning

2000 ◽  
Vol 279 (3) ◽  
pp. H1071-H1078 ◽  
Author(s):  
R. Ray Morrison ◽  
Rachael Jones ◽  
Anne M. Byford ◽  
Alyssa R. Stell ◽  
Jason Peart ◽  
...  
Keyword(s):  
Infarct Size ◽  
Functional Recovery ◽  
Ischemic Preconditioning ◽  
Adenosine Receptors ◽  
Myocardial Function ◽  
Wild Type ◽  
Beneficial Effects ◽  
Pressure Development ◽  
Ldh Release

The role of A1adenosine receptors (A1AR) in ischemic preconditioning was investigated in isolated crystalloid-perfused wild-type and transgenic mouse hearts with increased A1AR. The effect of preconditioning on postischemic myocardial function, lactate dehydrogenase (LDH) release, and infarct size was examined. Functional recovery was greater in transgenic versus wild-type hearts (44.8 ± 3.4% baseline vs. 25.6 ± 1.7%). Preconditioning improved functional recovery in wild-type hearts from 25.6 ± 1.7% to 37.4 ± 2.2% but did not change recovery in transgenic hearts (44.8 ± 3.4% vs. 44.5 ± 3.9%). In isovolumically contracting hearts, pretreatment with selective A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine attenuated the improved functional recovery in both wild-type preconditioned (74.2 ± 7.3% baseline rate of pressure development over time untreated vs. 29.7 ± 7.3% treated) and transgenic hearts (84.1 ± 12.8% untreated vs. 42.1 ± 6.8% treated). Preconditioning wild-type hearts reduced LDH release (from 7,012 ± 1,451 to 1,691 ± 1,256 U · l−1 · g−1 · min−1) and infarct size (from 62.6 ± 5.1% to 32.3 ± 11.5%). Preconditioning did not affect LDH release or infarct size in hearts overexpressing A1AR. Compared with wild-type hearts, A1AR overexpression markedly reduced LDH release (from 7,012 ± 1,451 to 917 ± 1,123 U · l−1 · g−1 · min−1) and infarct size (from 62.6 ± 5.1% to 6.5 ± 2.1%). These data demonstrate that murine preconditioning involves endogenous activation of A1AR. The beneficial effects of preconditioning and A1AR overexpression are not additive. Taken with the observation that A1AR blockade equally eliminates the functional protection resulting from both preconditioning and transgenic A1AR overexpression, we conclude that the two interventions affect cardioprotection via common mechanisms or pathways.

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