Explore the vast range of titles available.

The measurement of rock resistivity currently mainly adopts the method of reducing saturation, which requires the rock sample to reach complete saturation during measurement. In response to the accuracy issue of measuring rock electrical parameters using desaturation methods for unsaturated or incompletely saturated rock samples, the influence of saturation degree on the measurement results of rock electrical parameters and the root causes of the influence were analyzed, and a feasible correction method was established. The results indicate that the saturation degree of rock samples first affects the measurement of porosity, calculation of water saturation, and initial resistivity measurement of saturated saline rock samples, and further transmits to geological factors, cementation index, and lithology coefficient, while the saturation index is not affected by them. After correcting the porosity, water saturation, initial water saturation, and initial resistivity of the rock sample using saturation degree values, a one-to-one correspondence between water saturation and resistivity data was achieved. The base value for calculating the resistivity increase rate is more in line with reality, and the final rock electrical parameters obtained are more reasonable.

Capillary number, understood as the ratio of viscous force to capillary force, is one of the most important parameters in enhanced oil recovery (EOR). It continues to attract the interest of scientists and engineers, because the nature and quantification of macroscopic capillary forces remain controversial. At least 41 different capillary numbers have been collected here from the literature. The ratio of viscous and capillary force enters crucially into capillary desaturation experiments. Although the ratio is length scale dependent, not all definitions of capillary number depend on length scale, indicating potential inconsistencies between various applications and publications. Recently, new numbers have appeared and the subject continues to be actively discussed. Therefore, a short review seems appropriate and pertinent.

Background Oxygen desaturation during exercise is mainly observed in severe cases of chronic obstructive pulmonary disease (COPD) and is associated with a worse prognosis, but little is known about the type of desaturation that causes the greatest risk of mortality. Material and Methods We studied all of the 6-min walk tests performed periodically at a tertiary hospital over a period of 12 years in patients with moderate or severe COPD. We classified patients as non-desaturators if they did not suffer a drop in oxygen saturation (SpO2 < 88%) during the test, early desaturators if the time until desaturation was < 1 min, and non-early desaturators if it was longer than 1 min. The average length of follow-up per patient was 5.6 years. Results Of the 319 patients analyzed, 126 non-desaturators, 91 non-early desaturators and 102 early desaturators were identified. The mortality analysis showed that early desaturators had a mortality of 73%, while it was 38% for non-early desaturators and 28% for non-desaturators, with a survival of 5.9 years compared to 7.5 years and 9.6 years, respectively (hazard ratio of 3.50; 95% CI 2.3–5.3; p  < 0.0001). Conclusions The early desaturation seen in patients with chronic obstructive pulmonary disease is associated with greater mortality and is likely responsible for the poor prognosis shown globally in patients who desaturate. The survival of patients with early desaturation is almost 4 years less with respect to non-desaturators, and they, thus, require closer observation.

High‐altitude indoctrination (HAI) trains individuals to recognize symptoms of hypoxia by simulating high‐altitude conditions using normobaric (NH) or hypobaric (HH) hypoxia. Previous studies suggest that despite equivalent inspired oxygen levels, physiological differences could exist between these conditions. In particular, differences in neurophysiological responses to these conditions are not clear. Our study aimed to investigate correlations between oxygen saturation (SpO2) and neural responses in NH and HH. We recorded 5‐min of resting‐state eyes‐open electroencephalogram (EEG) and SpO2 during control, NH, and HH conditions from 13 participants. We applied a multivariate framework to characterize correlations between SpO2 and EEG measures (spectral power and multiscale entropy [MSE]), within each participant and at the group level. Participants were desaturating during the first 150 s of NH versus steadily desaturated in HH. We considered the entire time interval, first and second half intervals, separately. All the conditions were characterized by statistically significant participant‐specific patterns of EEG–SpO2 correlations. However, at the group level, the desaturation period expressed a robust pattern of these correlations across frequencies and brain locations. Specifically, the first 150 s of NH during desaturation differed significantly from the other conditions with negative absolute alpha power–SpO2 correlations and positive MSE–SpO2 correlations. Once steadily desaturated, NH and HH had no significant differences in EEG–SpO2 correlations. Our findings indicate that the desaturating phase of hypoxia is a critical period in HAI courses, which would require developing strategies for mitigating the hypoxic stimulus in a real‐world situation. It is still unknown whether there are differences in neurophysiological responses to normobaric and hypobaric hypoxia, as normobaric hypoxia is often used as a proxy for hypobaric hypoxia during research and hypoxia awareness courses. We collected 5‐min of eyes‐open resting‐state data with an electroencephalogram (EEG) and oxygen saturation (SpO2) monitor from 13 participants during normobaric hypoxia, hypobaric hypoxia, and normobaric normoxia. We found that there is less variability in the spatiotemporal patterns of EEG–SpO2 correlations during the desaturation phase of normabric hypoxia when compared to a stable desaturated phase.

Biological membranes, primarily composed of lipids, envelop each living cell. The intricate composition and organization of membrane lipids, including the variety of fatty acids they encompass, serve a dynamic role in sustaining cellular structural integrity and functionality. Typically, modifications in lipid composition coincide with consequential alterations in universally significant signaling pathways. Exploring the various fatty acids, which serve as the foundational building blocks of membrane lipids, provides crucial insights into the underlying mechanisms governing a myriad of cellular processes, such as membrane fluidity, protein trafficking, signal transduction, intercellular communication, and the etiology of certain metabolic disorders. Furthermore, comprehending how alterations in the lipid composition, especially concerning the fatty acid profile, either contribute to or prevent the onset of pathological conditions stands as a compelling area of research. Hence, this review aims to meticulously introduce the intricacies of membrane lipids and their constituent fatty acids in a healthy organism, thereby illuminating their remarkable diversity and profound influence on cellular function. Furthermore, this review aspires to highlight some potential therapeutic targets for various pathological conditions that may be ameliorated through dietary fatty acid supplements. The initial section of this review expounds on the eukaryotic biomembranes and their complex lipids. Subsequent sections provide insights into the synthesis, membrane incorporation, and distribution of fatty acids across various fractions of membrane lipids. The last section highlights the functional significance of membrane-associated fatty acids and their innate capacity to shape the various cellular physiological responses.

Interleukin-10 (IL-10) is a key anti-inflammatory cytokine that can limit immune cell activation and cytokine production in innate immune cell types 1 . Loss of IL-10 signalling results in life-threatening inflammatory bowel disease in humans and mice—however, the exact mechanism by which IL-10 signalling subdues inflammation remains unclear 2 – 5 . Here we find that increased saturated very long chain (VLC) ceramides are critical for the heightened inflammatory gene expression that is a hallmark of IL-10 deficiency. Accordingly, genetic deletion of ceramide synthase 2 (encoded by Cers2 ), the enzyme responsible for VLC ceramide production, limited the exacerbated inflammatory gene expression programme associated with IL-10 deficiency both in vitro and in vivo. The accumulation of saturated VLC ceramides was regulated by a decrease in metabolic flux through the de novo mono-unsaturated fatty acid synthesis pathway. Restoring mono-unsaturated fatty acid availability to cells deficient in IL-10 signalling limited saturated VLC ceramide production and the associated inflammation. Mechanistically, we find that persistent inflammation mediated by VLC ceramides is largely dependent on sustained activity of REL, an immuno-modulatory transcription factor. Together, these data indicate that an IL-10-driven fatty acid desaturation programme rewires VLC ceramide accumulation and aberrant activation of REL. These studies support the idea that fatty acid homeostasis in innate immune cells serves as a key regulatory node to control pathologic inflammation and suggests that ‘metabolic correction’ of VLC homeostasis could be an important strategy to normalize dysregulated inflammation caused by the absence of IL-10. IL-10 exerts its anti-inflammatory activity in macrophages by increasing the expression of enzymes that promote fatty acid desaturation and downstream regulation of the transcription factor REL.

Dietary interventions can change metabolite levels in the tumour microenvironment, which might then affect cancer cell metabolism to alter tumour growth 1 – 5 . Although caloric restriction (CR) and a ketogenic diet (KD) are often thought to limit tumour progression by lowering blood glucose and insulin levels 6 – 8 , we found that only CR inhibits the growth of select tumour allografts in mice, suggesting that other mechanisms contribute to tumour growth inhibition. A change in nutrient availability observed with CR, but not with KD, is lower lipid levels in the plasma and tumours. Upregulation of stearoyl-CoA desaturase (SCD), which synthesises monounsaturated fatty acids, is required for cancer cells to proliferate in a lipid-depleted environment, and CR also impairs tumour SCD activity to cause an imbalance between unsaturated and saturated fatty acids to slow tumour growth. Enforcing cancer cell SCD expression or raising circulating lipid levels through a higher-fat CR diet confers resistance to the effects of CR. By contrast, although KD also impairs tumour SCD activity, KD-driven increases in lipid availability maintain the unsaturated to saturated fatty acid ratios in tumours, and changing the KD fat composition to increase tumour saturated fatty acid levels cooperates with decreased tumour SCD activity to slow tumour growth. These data suggest that diet-induced mismatches between tumour fatty acid desaturation activity and the availability of specific fatty acid species determine whether low glycaemic diets impair tumour growth. Lien et al. show that low glycemic diets can reduce tumour growth by deregulating lipid metabolism.

Background A significant association between muscular tissue oxygen saturation (SmtO 2 ), measured by near-infrared spectroscopy (NIRS), and postoperative complications has been observed in patients undergoing major surgery. However, the association between muscular tissue desaturation and acute kidney injury (AKI) has not yet been reported in patients following surgery for acute type A aortic dissection. Method One hundred seventy-four adult patients who underwent total aortic arch replacement (TAAR) under cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) for acute type A aortic dissection were retrospectively analyzed. Muscular tissue oxygen saturation (SmtO 2 ) in the gastrocnemius muscle region and regional cerebral oxygen saturation (rScO 2 ) on the bilateral forehead were measured using near-infrared spectroscopy (NIRS).The thresholds defining muscular tissue desaturation were SmtO 2  < 80%, < 85%, and < 90% of baseline (relative changes compared to the baseline) and < 55% and < 50% (absolute values). Cerebral desaturation was defined as rScO 2  < 55%, < 50%, and < 80% baseline, on either the left or right side. The baseline, minimum, and mean values of SmtO 2 and rScO 2 were also extracted for analysis. The primary objective of this study was to investigate the association between muscular tissue desaturation and AKI. Result AKI occurred in 71 (40.80%) of the 174 patients underwent TAAR under CPB and DHCA. SmtO 2  < 80% of baseline was associated with an increased risk of AKI (odds ratio [OR], 1.021; 95% confidence interval [CI], 1.001–1.041; P  = 0.034). A receiver operating characteristic curve showed that the optimal cutoff for SmtO 2  < 80% baseline duration was 33.5 min in predicting AKI (sensitivity, 70.00%; specificity, 77.80%). The durations of SmtO 2  < 85% baseline (OR, 1.009; 95% CI, 0.996–1.021; P  = 0.195) and < 90% baseline (OR,1.007; 95% CI, 0.996–1.018; P  = 0.208) were not significantly associated with AKI. There were no significant differences in the durations of absolute SmtO 2 values < 55% and < 50% or in the minimum SmtO 2 between the two cohorts. Durations of left and right rScO 2  < 55%, < 50%, and < 80% baseline were not associated with AKI. Patients with AKI experienced significantly higher in-hospital mortality and more postoperative complications compared with non-AKI patients. Conclusion Muscular tissue desaturation, defined as SmtO 2  < 80% of baseline monitored on the lower leg, was significantly associated with an increased risk of AKI in patients who underwent TAAR under CPB and DHCA. Cerebral desaturation, defined as absolute rScO 2  < 55% or < 50%, or < 80% baseline was not associated with AKI.

Colonization of new ecological niches has triggered large adaptive radiations. Although some lineages have made use of such opportunities, not all do so.The factors causing this variation among lineages are largely unknown. Here, we show that deficiency in docosahexaenoic acid (DHA), an essential ω-3 fatty acid, can constrain freshwater colonization by marine fishes. Our genomic analyses revealed multiple independent duplications of the fatty acid desaturase gene Fads2 in stickleback lineages that subsequently colonized and radiated in freshwater habitats, but not in close relatives that failed to colonize.Transgenic manipulation of Fads2 in marine stickleback increased their ability to synthesize DHA and survive on DHA-deficient diets. Multiple freshwater ray-finned fishes also show a convergent increase in Fads2 copies, indicating its key role in freshwater colonization.

Most tumours have an aberrantly activated lipid metabolism 1 , 2 that enables them to synthesize, elongate and desaturate fatty acids to support proliferation. However, only particular subsets of cancer cells are sensitive to approaches that target fatty acid metabolism and, in particular, fatty acid desaturation 3 . This suggests that many cancer cells contain an unexplored plasticity in their fatty acid metabolism. Here we show that some cancer cells can exploit an alternative fatty acid desaturation pathway. We identify various cancer cell lines, mouse hepatocellular carcinomas, and primary human liver and lung carcinomas that desaturate palmitate to the unusual fatty acid sapienate to support membrane biosynthesis during proliferation. Accordingly, we found that sapienate biosynthesis enables cancer cells to bypass the known fatty acid desaturation pathway that is dependent on stearoyl-CoA desaturase. Thus, only by targeting both desaturation pathways is the in vitro and in vivo proliferation of cancer cells that synthesize sapienate impaired. Our discovery explains metabolic plasticity in fatty acid desaturation and constitutes an unexplored metabolic rewiring in cancers. In several human and mouse cancer cell lines and carcinomas, a sapienate biosynthesis pathway underpins metabolic plasticity by allowing these cells to bypass stearoyl-CoA desaturase-dependent fatty acid desaturation.