The metabolic rate could be one of the factors affecting the salinity tolerance capacity of fish. Experiment I tested whether metabolic rates correlate with the upper salinity tolerance limit among individual grass carp by daily increasing salinity (1 g kg⁻¹ day⁻¹). The feeding dropped sharply as the salinity reached 10 g kg⁻¹ and ceased when salinities exceeded 11 g kg⁻¹. The ventilation frequency decreased weakly as salinity increased from 0 to 12 g kg⁻¹ and then increased rapidly as salinity reached 14 g kg⁻¹. The fish survived at salinities lower than 14 g kg⁻¹, and all fish died when salinity reached 17 g kg⁻¹. The upper salinity tolerance limit was not correlated with metabolic rates. Therefore, a lower metabolic rate may not necessarily allow for better salinity tolerance capacity. Experiment II tested how different salinities (0, 0.375, 0.75, 1.5, 3, and 6 g kg⁻¹ for 2 weeks) affect the metabolic parameters of grass carp. The changes in the resting metabolic rate with increasing salinity could be explained by the relative changes in interlamellar cell mass and protruding lamellae. The maximum metabolic rate remained constant, suggesting that the salinity-induced changes in the gill surface had a minor effect on oxygen uptake capacity.

The surface area (SA) of organs and cells may vary with temperature, which changes the SA exchange limitation on metabolic flows as well as the influence of temperature on metabolic scaling. The effect of SA change can intensify (when the effect is the same as that of temperature) or compensate for (when the effect is the opposite of that of temperature) the negative effects of temperature on metabolic scaling, which can result in multiple patterns of metabolic scaling with temperature among species. The present study aimed to examine whether metabolic scaling in black carp changes with temperature and to identify the link between metabolic scaling and SA at the organ and cellular levels at different temperatures. The resting metabolic rate (RMR), gill surface area (GSA) and red blood cell (RBC) size of black carp with different body masses were measured at 10 °C and 25 °C, and the scaling exponents of these parameters were compared. The results showed that both body mass and temperature independently affected the RMR, GSA and RBC size of black carp. A consistent scaling exponent of RMR (0.764, 95% CI [0.718–0.809]) was obtained for both temperatures. The RMR at 25 °C was 2.7 times higher than that at 10 °C. At both temperatures, the GSA scaled consistently with body mass by an exponent of 0.802 (95% CI [0.759–0.846]), while RBC size scaled consistently with body mass by an exponent of 0.042 (95% CI [0.010–0.075]). The constant GSA scaling can explain the constant metabolic scaling as temperature increases, as metabolism may be constrained by fluxes across surfaces. The GSA at 10 °C was 1.2 times higher than that at 25 °C, which suggests that the constraints of GSA on the metabolism of black carp is induced by the higher temperature. The RBC size at 10 °C was 1.1 times higher than that at 25 °C. The smaller RBC size (a larger surface-to-volume ratio) at higher temperature suggests an enhanced oxygen supply and a reduced surface boundary limit onb_R, which offset the negative effect of temperature onb_R.

Renal cell cancer is associated with the coagulation system. Long non-coding RNA (lncRNA) expression is closely associated with the development of clear cell renal cell carcinoma (ccRCC). The aim of this study was to build a novel lncRNA model to predict the prognosis and immunological state of ccRCC. The transcriptomic data and clinical data of ccRCC were retrieved from TCGA database, subsequently, the lasso regression and lambda spectra were used to filter prognostic lncRNAs. ROC curves and the C-index were used to confirm the predictive effectiveness of this model. We also explored the difference in immune infiltration, immune checkpoints, tumor mutation burden (TMB) and drug sensitivity between the high- and low-risk groups. We created an 8 lncRNA model for predicting the outcome of ccRCC. Multivariate Cox regression analysis showed that age, tumor grade, and risk score are independent prognostic factors for ccRCC patients. ROC curve and C-index revealed the model had a good performance in predicting prognosis of ccRCC. GO and KEGG analysis showed that coagulation related genes were related to immune response. In addition, high risk group had greater TMB level and higher immune checkpoints expression. Sorafenib, Imatinib, Pazopanib, and etoposide had higher half maximal inhibitory concentration (IC₅₀₎ in the high risk group whereas Sunitinib and Bosutinib had lower IC₅₀. This novel coagulation-related long noncoding RNAs model could predict the prognosis of patients with ccRCC, and coagulation-related lncRNA may be connected to the tumor microenvironment and gene mutation of ccRCC.