On the stability of the exact solutions of the dual-phase lagging model of heat conduction

The dual-phase lagging (DPL) model has been considered as one of the most promising theoretical approaches to generalize the classical Fourier law for heat conduction involving short time and space scales. Its applicability, potential, equivalences, and possible drawbacks have been discussed in the current literature. In this study, the implications of solving the exact DPL model of heat conduction in a three-dimensional bounded domain solution are explored. Based on the principle of causality, it is shown that the temperature gradient must be always the cause and the heat flux must be the effect in the process of heat transfer under the dual-phase model. This fact establishes explicitly that the single- and DPL models with different physical origins are mathematically equivalent. In addition, taking into account the properties of the Lambert W function and by requiring that the temperature remains stable, in such a way that it does not go to infinity when the time increases, it is shown that the DPL model in its exact form cannot provide a general description of the heat conduction phenomena

A new heat propagation velocity prevails over Brownian particle velocities in determining the thermal conductivities of nanofluids

An alternative insight is presented concerning heat propagation velocity scales in predicting the effective thermal conductivities of nanofluids. The widely applied Brownian particle velocities in published literature are often found too slow to describe the relatively higher nanofluid conductivities. In contrast, the present model proposes a faster heat transfer velocity at the same order as the speed of sound, rooted in a modified kinetic principle. In addition, this model accounts for both nanoparticle heat dissipation as well as coagulation effects. This novel model of effective thermal conductivities of nanofluids agrees well with an extended range of experimental data

Plasma soluble thrombomodulin levels are associated with mortality in the acute respiratory distress syndrome

OBJECTIVE: Thombomodulin (TM) is an activator of protein C and a biomarker for endothelial injury. We hypothesized that (1) elevated plasma levels would be associated with clinical outcomes and (2) polymorphisms in the TM gene would be associated with plasma levels. PATIENTS: We studied 449 patients enrolled in the Fluid and Catheter Treatment Trial (FACTT) for whom both plasma and DNA were available. We used logistic regression and receiver operator curves (ROC) to test for associations between soluble TM (sTM) and mortality at 60 days. MEASUREMENTS AND RESULTS: Plasma sTM levels were higher in non-survivors than survivors at baseline [median 147 (IQR, 95–218) vs. 89 (56–129) ng/mL, p < 0.0001] and on day 3 after study enrollment [205 (146–302) vs. 127 (85–189), p < 0.0001]. The odds of death increased by 2.4 (95 %CI 1.5–3.8, p < 0.001), and by 2.8 (1.7–4.7, P < 0.001) for every log increase in baseline and day 3 sTM levels, respectively, after adjustment for age, race, gender, severity of illness, fluid management strategy, baseline creatinine, and non-pulmonary sepsis as the primary cause of ARDS. By ROC analysis, plasma sTM levels discriminated between non-survivors and survivors [AUC = 72 % (66–78 %) vs. AUC = 54 % for severity based on Berlin criteria). Addition of sTM improved discrimination based on APACHE III from 77 to 80 % (P < 0.03). sTM levels at baseline were not statistically different among subjects stratified by genotypes of tag SNPs in the TM gene. CONCLUSIONS: Higher plasma sTM levels are associated with increased mortality in ARDS. The lack of association between the sTM levels and genetic variants suggests that the increased levels of sTM may reflect severity of endothelial damage rather than genetic heterogeneity. These findings underscore the importance of endothelial injury in ARDS pathogenesis and suggest that, in combination with clinical markers, sTM could contribute to risk stratification