An homogeneous model for adiabatic capillary tubes

1998 ◽  
Vol 18 (3-4) ◽  
pp. 207-219 ◽  
Author(s):  
P.K. Bansal ◽  
A.S. Rupasinghe
Author(s):  
Hugo Augusto ◽  
Felipe Silva ◽  
Caio Vinicios Juvencio da Silva ◽  
Maycon Ferreira Silva ◽  
Leonardo José Cavalcante Vasconcelos

2018 ◽  
Vol 11 (1) ◽  
pp. 7
Author(s):  
Latif Ngudi Wibawanto ◽  
Budi Santoso ◽  
Wibawa Endra Juwana

This research was conducted to find out the flow characteristic of two phases through the channel with sudden expansion in the form of change of flow pattern and pressure recovery. The test was carried out with variation of superficial velocity of water 0.2-1.3 m / s and superficial air velocity of 0.2-1.9 m / s resulting in pattern of three flow patterns ie bubble, plug, and slug. The expansion channel resulted in some changes to the flow pattern that originally plugs in the upstream channel into bubble in the downstream channel and the slug becomes plug. Pressure recovery experimental results compared with the homogeneous model flow equation and Wadle correlation, both correlations have predictions with standard deviation values of 0.32 and 0.43.


2010 ◽  
Vol 75 (3) ◽  
pp. 971-995
Author(s):  
Karen Lange

AbstractWe say a countable model has a 0-basis if the types realized in are uniformly computable. We say has a (d-)decidable copy if there exists a model ≅ such that the elementary diagram of is (d-)computable. Goncharov, Millar, and Peretyat'kin independently showed there exists a homogeneous model with a 0-basis but no decidable copy. We extend this result here. Let d ≤ 0′ be any low2 degree. We show that there exists a homogeneous model with a 0-basis but no d-decidable copy. A degree d is 0-basis homogeneous bounding if any homogenous with a 0-basis has a d-decidable copy. In previous work, we showed that the non low2 Δ20 degrees are 0-basis homogeneous bounding. The result of this paper shows that this is an exact characterization of the 0-basis homogeneous bounding Δ20 degrees.


Pharmaceutics ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 738
Author(s):  
Sasikarn Looprasertkul ◽  
Amornpun Sereemaspun ◽  
Nakarin Kitkumthorn ◽  
Kanidta Sooklert ◽  
Tewarit Sarachana ◽  
...  

Gold nanoparticles (AuNPs) are used for diagnostic and therapeutic purposes, especially antiangiogenesis, which are accomplished via inhibition of endothelial cell proliferation, migration, and tube formation. However, no research has been performed on the effects of AuNPs in pericytes, which play vital roles in endothelial cell functions and capillary tube formation during physiological and pathological processes. Therefore, the effects of AuNPs on the morphology and functions of pericytes need to be elucidated. This study treated human placental pericytes in monoculture with 20 nm AuNPs at a concentration of 30 ppm. Ki-67 and platelet-derived growth factor receptor-β (PDGFR-β) mRNA expression was measured using real-time reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell migration was assessed by Transwell migration assay. The fine structures of pericytes were observed by transmission electron microscopy. In addition, 30 ppm AuNP-treated pericytes and intact human umbilical vein endothelial cells were cocultured on Matrigel to form three-dimensional (3D) capillary tubes. The results demonstrated that AuNPs significantly inhibited proliferation, reduced PDGFR-β mRNA expression, and decreased migration in pericytes. Ultrastructural analysis of pericytes revealed AuNPs in late endosomes, autolysosomes, and mitochondria. Remarkably, many mitochondria were swollen or damaged. Additionally, capillary tube formation was reduced. We found that numerous pericytes on 3D capillary tubes were round and did not extend their processes along the tubes, which resulted in more incomplete tube formation in the treatment group compared with the control group. In summary, AuNPs can affect pericyte proliferation, PDGFR-β mRNA expression, migration, morphology, and capillary tube formation. The findings highlight the possible application of AuNPs in pericyte-targeted therapy for antiangiogenesis.


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