Normalization constraint for variational bounds on fluid permeability

1985 ◽  
Vol 83 (2) ◽  
pp. 754-760 ◽  
Author(s):  
James G. Berryman ◽  
Graeme W. Milton
2000 ◽  
Vol 63 (3) ◽  
pp. 353-364
Author(s):  
A. G. Donchev ◽  
N. N. Kolesnikov ◽  
V. I. Tarasov

1996 ◽  
Vol 17 (2) ◽  
pp. 222-230 ◽  
Author(s):  
Sridhar Ranganathan ◽  
Frederick R. Phelan ◽  
Suresh G. Advani

2008 ◽  
Vol 79 (3) ◽  
pp. 189-204
Author(s):  
H. Brito-Santana ◽  
R. Rodríguez-Ramos ◽  
R. Guinovart-Díaz ◽  
J. Bravo-Castillero ◽  
F. J. Sabina ◽  
...  

1990 ◽  
Vol 258 (3) ◽  
pp. G391-G394 ◽  
Author(s):  
A. T. McKie ◽  
W. Powrie ◽  
R. J. Naftalin

The hydrostatic pressure required to reduce the water content of rabbit feces in an odometer from greater than 80 to less than 65% was approximately 5 atm. This pressure was unaffected by raising the temperature from 20 to 37 degrees C. It became progressively more difficult to dehydrate feces as consolidation occurred, as is evident from the significant (P less than 0.001) reduction in the fecal consolidation coefficient (Co) from 1.76 +/- 0.25 X 10(-6) (n = 4) to 1.35 +/- 0.093 X 10(-7) m2/s (n = 4) and the fecal fluid permeability coefficient (k) from 4.10 +/- 0.51 X 10(-8) (n = 4) to 1.42 +/- 0.12 X 10(-10) m/s (n = 4), concomitant with the reduction in fecal water content. The results suggest that rabbit hard feces are unlikely to be produced, under physiological conditions, by mechanical pressure exerted by the wall of the colon or by a prolonged retention time of hard feces by the distal colon. The hypertonic absorbate (1,000 mosmol/kg) produced by rabbit descending colon is of sufficient magnitude to overcome the fecal resistance to dehydration.


2018 ◽  
Vol 40 (5-6) ◽  
pp. 586-600 ◽  
Author(s):  
Charlotte Holme Nielsen ◽  
Anne Bladt Brandt ◽  
Thomas Thymann ◽  
Karina Obelitz-Ryom ◽  
Pingping Jiang ◽  
...  

Preterm birth interrupts intrauterine brain growth and maturation and may induce a delay in postnatal neurodevelopment. Such developmental delays can result from the reduced fetal age at birth, together with the clinical compli­cations of preterm birth (e.g., hypoxia, ischemia, and inflammation). We hypothesized that late preterm birth, inducing only mild clinical complications, has minimal effects on brain-related outcomes such as motor function and behavior. Using the pig as a model for late preterm infants, piglets were cesarean delivered preterm (90%, 106 days gestation) or at full term, reared by identical procedures, and euthanized for tissue collection at birth or after 11 days (e.g., term-corrected age for preterm pigs). Clinical variables and both structural and functional brain endpoints were assessed. The preterm pigs were slow to get on their feet, gained less weight (–30%), and had a higher cerebral hydration level and blood-to-cerebrospinal fluid permeability than the term pigs. At term-corrected age (11 days), the absolute weight of the brain and the weights of its regions were similar between 11-day-old preterm and newborn term pigs, and both were lower than in 11-day-old term pigs. Postnatally, physical activity and movements in an open field were similar, except that preterm pigs showed a reduced normalized stride length and increased normalized maximum stride height. Perinatal brain growth is closely associated with advancing postconceptional age in pigs, and late preterm birth is initially associated with impaired brain growth and physical activity. Postnatally, neuromuscular functions mature rapidly and become similar to those in term pigs, even before term-corrected age. Neuromuscular functions and behavior may show rapid postnatal adaptation to late preterm birth in both pigs and infants.


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