The triglyceride-glucose(TyG)index has emerged as a novel metabolic marker,and research on it in the intensive care unit(ICU)has gradually increased in recent years.The TyG index combines the levels of triacylglycerol(TG)and glucose,reflecting the body's insulin resistance(IR)and metabolic status,and its potential clinical applications have garnered widespread attention.Current studies indicate a significant association between the TyG index and the prognosis of ICU patients,metabolic syndrome,and various critical illnesses.However,despite some studies revealing the potential clinical value of the TyG index in critically ill patients,there is still a lack of systematic reviews to comprehensively assess the application status of this indicator in the ICU setting.This article aims to review the clinical applications of the TyG index in ICU patients and its relationship with prognosis,metabolic syndrome,and critical illnesses,emphasizing its importance in the assessment and management of critically ill patients,with the hope of providing references and insights for future related research.

The triglyceride-glucose(TyG)index has emerged as a novel metabolic marker,and research on it in the intensive care unit(ICU)has gradually increased in recent years.The TyG index combines the levels of triacylglycerol(TG)and glucose,reflecting the body's insulin resistance(IR)and metabolic status,and its potential clinical applications have garnered widespread attention.Current studies indicate a significant association between the TyG index and the prognosis of ICU patients,metabolic syndrome,and various critical illnesses.However,despite some studies revealing the potential clinical value of the TyG index in critically ill patients,there is still a lack of systematic reviews to comprehensively assess the application status of this indicator in the ICU setting.This article aims to review the clinical applications of the TyG index in ICU patients and its relationship with prognosis,metabolic syndrome,and critical illnesses,emphasizing its importance in the assessment and management of critically ill patients,with the hope of providing references and insights for future related research.

Immunothrombosis refers to the innate immune response caused by thrombosis in blood vessels(especially microvessels).Immunothrombosis is related to immune cells and specific thrombosis related molecules,producing intravascular scaffolds that promote pathogen recognition,inhibition,and destruction,thereby protecting the integrity of the host.However,abnormal or uncontrolled activation of immunothrombosis may be harmful to the host and serve as the foundation for various infectious and inflammatory related thrombotic diseases.Therefore,understanding the potential mechanisms of immunothrombosis plays a decisive role in developing more effective therapies for thrombosis treatment and prevention.This review provides an overview of the mechanisms of immunothrombosis in order to understand new treatment strategies for reducing the risk of immunothrombosis.

Objective:To explore the effects of carnosine on in vitro maturation (IVM) of mouse oocytes and the developmental competency of embryos. Methods:The mouse cumulus-oocyte complexes (COC) were isolated and cultured in the IVM medium containing 10 μmol/L, 30 μmol/L, 50 μmol/L,100 μmol/L,or 200 μmol/L carnosine for 18 h. IVM medium without carnosine was acted as control group. The optimal concentration was chosen according to the rates of oocyte maturation, embryo cleavage and blastocyst formation. The effect of carnosine was further verified by detecting the levels of reactive oxygen species (ROS), and total glutathione (T-GSH), the distribution of cortical granules and mitochondria, and also the copy numbers of mitochondria.Results:In the 100 μmol/L carnosine group, the rates of oocyte maturation [69.23% (135/195)], embryo cleavage [66.06% (72/109)] and blastocyst formation [48.61% (35/72)] were the highest and showed statistically significant differences ( P<0.001, P<0.001 , P=0.010) when compared with control group [44.44% (84/189), 38.67% (29/75), 20.69% (6/29)]. Therefore, 100 μmol/L was selected as the optimal concentration of carnosine. The levels of ROS and T-GSH in control group were 2.04 and 0.64 times as those in the 100 μmol/L carnosine group (both P<0.001). The percentage of grade Ⅲ cortical granules in the 100 μmol/L carnosine group was significantly higher than that in control group ( P<0.001). The mitochondria of oocytes in control group were uniformly distributed, while the mitochondria in the 100 μmol/L carnosine group gathered in the central cytoplasmic region, and the fluorescence intensity was higher than that in control group ( P=0.040). The mitochondrial copy number in the 100 μmol/L carnosine group was as much 1.72 times as that in control group ( P<0.001). Conclusion:Carnosine effectively improves oxidative stress in the immature oocytes and promotes the mouse oocyte IVM and embryo development.

Objective:To explore the effects of carnosine on in vitro maturation (IVM) of mouse oocytes and the developmental competency of embryos. Methods:The mouse cumulus-oocyte complexes (COC) were isolated and cultured in the IVM medium containing 10 μmol/L, 30 μmol/L, 50 μmol/L,100 μmol/L,or 200 μmol/L carnosine for 18 h. IVM medium without carnosine was acted as control group. The optimal concentration was chosen according to the rates of oocyte maturation, embryo cleavage and blastocyst formation. The effect of carnosine was further verified by detecting the levels of reactive oxygen species (ROS), and total glutathione (T-GSH), the distribution of cortical granules and mitochondria, and also the copy numbers of mitochondria.Results:In the 100 μmol/L carnosine group, the rates of oocyte maturation [69.23% (135/195)], embryo cleavage [66.06% (72/109)] and blastocyst formation [48.61% (35/72)] were the highest and showed statistically significant differences ( P<0.001, P<0.001 , P=0.010) when compared with control group [44.44% (84/189), 38.67% (29/75), 20.69% (6/29)]. Therefore, 100 μmol/L was selected as the optimal concentration of carnosine. The levels of ROS and T-GSH in control group were 2.04 and 0.64 times as those in the 100 μmol/L carnosine group (both P<0.001). The percentage of grade Ⅲ cortical granules in the 100 μmol/L carnosine group was significantly higher than that in control group ( P<0.001). The mitochondria of oocytes in control group were uniformly distributed, while the mitochondria in the 100 μmol/L carnosine group gathered in the central cytoplasmic region, and the fluorescence intensity was higher than that in control group ( P=0.040). The mitochondrial copy number in the 100 μmol/L carnosine group was as much 1.72 times as that in control group ( P<0.001). Conclusion:Carnosine effectively improves oxidative stress in the immature oocytes and promotes the mouse oocyte IVM and embryo development.

Objective:To explore the impact of hypophosphatemia on the occurrence and prognosis of critically ill patient.Methods:The clinical data of critically ill patients admitted to the intensive care unit (ICU) of Tianjin First Central Hospital from October 2021 to April 2022 were retrospectively analyzed. Patients were divided into hypophosphatemia group (serum phosphorus level < 0.80 mmol/L) and non-hypophosphatemia group (serum phosphorus level ≥ 0.80 mmol/L) when they were admitted to the ICU. The following variables were also collected, including gender, age, acute physiology and chronic health evaluationⅡ(APACHE Ⅱ), sequential organ failure assessment (SOFA), serum phosphorus level, serum calcium level, serum magnesium level, white blood cell count (WBC), neutrophil count (NEU), lymphocyte count (LYM), neutrophil/lymphocyte ratio (NLR), C-reactive protein (CRP), presence of infection and infection site, length of hospital stay, ICU stay, 28-day mortality, and mechanical ventilation time. Multivariate Logistic regression analysis was used to evaluate the relationship between each variable and the 28-day mortality. The receiver operator characteristic curve (ROC curve) was drawn, and the area under the ROC curve (AUC) and 95% confidence interval (95% CI) were calculated to evaluate the predictive value of serum phosphorus levels for the prognosis of ICU patients. Results:A total of 263 patients were enrolled, including 54 patients with hypophosphatemia and 209 patients without. The SOFA score, LYM level and the infection rate of patients in the hypophosphatemia group were significantly higher than those in the non-hypophosphatemia group [SOFA score: 6.70±3.17 vs. 5.64±3.59, LYM (×10 9/L): 0.99±0.54 vs. 0.77±0.54, infection rate: 77.78% (42/54) vs. 59.33% (124/209), all P < 0.05], the NLR was significantly lower than that of the non-hypophosphatemia group [10.67 (7.08, 18.02) vs. 12.25 (7.25, 21.68), P < 0.05]. The length of hospital stay, ICU stay, and mechanical ventilation duration in the hypophosphatemia group were significantly longer than those in the non-hypophosphatemia group [length of hospital stay (days): 15 (11, 28) vs. 12 (6, 21), length of ICU stay (days): 10.35±7.80 vs 7.15±6.61, mechanical ventilation duration (days): 3 (0, 12) vs. 2 (0, 5), all P < 0.05]. There was no significant difference in the 28-day mortality between the hypophosphatemia group and the non-hypophosphatemia group [9.26% (5/54) vs. 11.00% (23/209), P > 0.05]. Multivariate Logistic regression analysis showed that APACHE Ⅱ score [odds ratio ( OR) = 1.188, 95% CI was 1.110-1.271], CRP ( OR = 1.016, 95% CI was 1.007-1.026), and NLR ( OR = 1.002, 95% CI was 0.996-1.008) were independent risk factors affecting the 28-day mortality of critically ill patients in ICU (all P < 0.05). ROC curve analysis showed that the AUC of serum phosphorus levels for predicting the length of hospital stay of critically ill patients in ICU > 10 days, ICU stay > 5 days, and mechanical ventilation duration > 5 days were 0.701 (95% CI was 0.632-0.770), 0.771 (95% CI was 0.691-0.852), 0.617 (95% CI was 0.541-0.692), respectively, all P < 0.01. Conclusion:Hypophosphatemia has some predictive value for the length of hospital and ICU stay and mechanical ventilation time in critically ill patients, but it cannot predict the 28-day mortality.