[Longitudinal study on catch-up growth in preterm infants with small for gestational age at corrected ages 0-24 months]. / æ—©äº§å°äºŽèƒŽé¾„å„¿æ ¡æ­£0~24æœˆé¾„è¿½èµ¶ç”Ÿé•¿çš„çºµå‘ç ”ç©¶.

OBJECTIVES: To understand the growth and development status and differences between small for gestational age (SGA) and appropriate for gestational age (AGA) preterm infants during corrected ages 0-24 months, and to provide a basis for early health interventions for preterm infants. METHODS: A retrospective study was conducted, selecting 824 preterm infants who received regular health care at the Guangzhou Women and Children's Medical Center from July 2019 to July 2022, including 144 SGA and 680 AGA infants. The growth data of SGA and AGA groups at birth and corrected ages 0-24 months were analyzed and compared. RESULTS: The SGA group had significantly lower weight and length than the AGA group at corrected ages 0-18 months (P<0.05), while there were no significant differences between the two groups at corrected age 24 months (P>0.05). At corrected age 24 months, 85% (34/40) of SGA and 79% (74/94) of AGA preterm infants achieved catch-up growth. Stratified analysis by gestational age showed that there were significant differences in weight and length at corrected ages 0-9 months between the SGA subgroup with gestational age <34 weeks and the AGA subgroups with gestational age <34 weeks and 34 weeks (P<0.05). In addition, the weight and length of the SGA subgroup with gestational age 34 weeks showed significant differences compared to the AGA subgroups with gestational age <34 weeks and 34 weeks at corrected ages 0-18 months and corrected ages 0-12 months, respectively (P<0.05). Catch-up growth for SGA infants with gestational age <34 weeks and 34 weeks mainly occurred at corrected ages 0-12 months and corrected ages 0-18 months, respectively. CONCLUSIONS: SGA infants exhibit delayed early-life physical growth compared to AGA infants, but can achieve a higher proportion of catch-up growth by corrected age 24 months than AGA infants. Catch-up growth can be achieved earlier in SGA infants with a gestational age of <34 weeks compared to those with 34 weeks.

Different ratios of DHA/EPA reverses insulin resistance by improving adipocyte dysfunction and lipid disorders in HFD-induced IR mice.

Objective: Insulin resistance (IR) is linked to the development of diabetes, non-alcoholic fatty liver disease (NAFLD), and cardiovascular disease (CVDs). Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) from fish oils (FOs) were used to investigate their potential in high-fat diet (HFD)-induced IR mice under different ratios. Methods: A total of 84 male C57BL/6J (6 weeks old) mice were fed with HFD containing 45% kcal from fat for 16 weeks to establish the IR model. The IR mice were then fed with HFD or HFD + 4% DHA/EPA with different ratios (3 : 1, 1.5 : 1, 1 : 1, 1 : 1.5, 1 : 3, respectively) for another 12 weeks. During the experiment, the CON group (n = 12) was set to feed with a basic diet containing 10% kcal from fat. Results: HFD feeding for 16 weeks reduced insulin sensitivity and accelerated hypertrophy of white adipose tissue (WAT). Different ratios of DHA/EPA except for 1 : 1 decreased the HOMA-IR index, average area of adipocytes, and serum MDA, but increased the protein expression of PI3K. All ratios of DHA/EPA increased the protein expression of IRS-1, GLUT4, and adiponectin. Moreover, dietary DHA/EPA changed serum fatty acid (FA) composition by increasing the serum concentration of n-3 PUFAs. DHA/EPA supplements also improved serum lipid profiles (TG/TC/LDL-c/HDL-c, FFA) and reduced the hepatic steatosis area. Conclusions: The results indicate that an appropriate higher ratio of DHA (1.5 : 1) in DHA/EPA supplementation is recommended for IR prevention.

[Impact of heparin on coagulation index during the therapy of molecular adsorbent recirculating system in patients with liver failure].

OBJECTIVE: To investigate the impact of coagulative parameters on different anticoagulation systems in molecular adsorbent recirculating system (MARS) in subjects with liver failure, and to evaluate the safety of different anticoagulation methods . METHODS: A prospective experimental observation was designed. According to anticoagulation Methods , 174 MARS treatment sessions for 146 patients with liver failure and prothrombin time activity percentage (PTA) ≤ 40% were randomly divided into 2 groups: 92 MARS treatment sessions in the heparin-free group and 82 in the low-dose heparin group. Time points of 0, 0.5, 1, 2, 3, 4, 5 and 6 h were selected to observe the coagulation changes of prothrombin time (PT), PTA, thrombin time (TT), activated partial thromboplastin time (APTT) and international normalized ratio (INR) dynamically. Adverse events such as line / filter coagulation, rupture and bleeding were also investigated and compared due to frequency and severity between the 2 groups. RESULTS: There was no difference in PT, PTA, INR between the 2 groups, but significant differences were observed in APTT and TT and fibrinogen (Fbg). APTT and TT levels in the low-dose heparin group was increased rapidly after the first given dose of anticoagulant heparin and reached the peak within 30 min.The levels at each time point was statistically different between the 2 groups (P<0.05). A significant difference in the Fbg level was obtained between the 2 groups. In the low-dose heparin group it was stabilized and increased slightly at the end of the treatment. While in the heparin-free group it was decreased gradually and reached a ravine at the end of the treatment. A curve was observed after 2.5 h treatment between the 2 groups (P=0.001). There were 2 cases of severe bleeding after MARS was finished in the heparin group, and 1 was terminated because of degree III clotting in the heparin-free group. CONCLUSION: Fibrinogen should be adsorbed while the blood touches the MARS circuit path and anticoagulants can prevent it. Comprehensive analysis of blood platelet count (BPC), fibrin degradation products (FDP), D-dimer and clinical symptoms is critical and required to determine the coagulation status to select an anticoagulation system before MARS. The use of low dose heparin in MARS improves the disorder of hypercoagulable state during the high coaguation period, while heparin-free during low coagulation period can effectively prevent the occurrence of bleeding and improve the mechanism of blood coagulation by reducing heparin-like substance in the blood.

Soyasaponins A1 and A2 exert anti-atherosclerotic functionalities by decreasing hypercholesterolemia and inflammation in high fat diet (HFD)-fed ApoE-/- mice.

Atherosclerosis is a chronic inflammatory disease causing coronary heart attacks and strokes. Soyasaponins (SS), the phytochemicals naturally existing in soybeans and their products, have been shown to reduce hypercholesterolemia and inflammation, which are intimately related to the genesis and development of atherosclerosis. However, the anti-atherosclerotic functionality of soyasaponins remains unknown. The aim of this study was to investigate the effects of the supplementation of two types of soyasaponin monomers (A1 and A2) on atherosclerotic plaque formation, serum lipid profiles, and inflammation in ApoE gene knockout (ApoE-/-) mice. Sixty 5-week-old ApoE-/- male mice were fed with a high-fat diet (HFD) and intervened by SSA1 and SSA2 (10 and 20 µmol per kg BW, respectively) or simvastatin (10 µmol per kg BW) for 24 weeks. The atherosclerotic lesions in the aorta, aortic root, and innominate artery, lipid profile and inflammatory markers in serum, and TLR4/MyD88/NF-κB signaling in arterial tissues were determined. SSA1 and SSA2 decreased the plaque ratio in the aortic root and innominate artery but not in the entire aorta. In serum, SSA1 reduced TG, TC, and LDL-C but increased HDL-C; SSA2 decreased TC, TG, and LDL-C but did not affect HDL-C. Meanwhile, SSA1 increased TG, SSA2 increased TC, and both of them increased bile acids in the feces. SSA1 and SSA2 lowered TNF-α, MCP-1, and hs-crp in serum. Furthermore, SSA1 and SSA2 reduced the TLR4 and MyD88 expressions in the aorta and innominate artery and inhibited NF-κB p65 and IκBα phosphorylation in the aorta. These results suggest that SSA1 and SSA2 exert anti-atherosclerotic functionalities by decreasing hypercholesterolemia and inflammation in HFD-fed ApoE-/- mice.

Soyasaponins Reduce Inflammation and Improve Serum Lipid Profiles and Glucose Homeostasis in High Fat Diet-Induced Obese Mice.

SCOPE: Obesity is linked to a chronic low-grade inflammatory state that contributes to the development of obesity-associated metabolic disorders. The anti-inflammatory activities and mechanisms of soyasaponin monomers (A1 , A2 , and I) have been recently demonstrated in cell models. However, their potential in vivo abilities to reduce chronic inflammation and alleviate metabolic disorders in obese status remain unclear. METHODS AND RESULTS: High fat diet (HFD)-fed obese male C57BL/6J mice are intervened by aspirin (0.1 mg kg-1 body weight) or 20 mg kg-1 of soyasaponins A1 , A2 , or I for 8 weeks. Soyasaponins A1 , A2 , and I significantly reduce pro-inflammatory cytokines/mediators in serum, liver, and white adipose tissues (WATs), improve serum lipid profiles, decrease liver cholesterol, triglyceride and steatosis, and promote fecal excretion of cholesterol, triglycerides, and bile acids. Soyasaponins A1 , A2 , and I also decrease IKKα/ß phosphorylation in liver and WATs and reduce NF-κB p65 phosphorylation and CD68 mRNA and protein expression in WATs. Soyasaponins A1 and A2 but not I decrease NF-κB p65 phosphorylation in liver and adipocytes hypertrophy in WATs. In addition, Soyasaponin A2 but not A1 nor I decreases fasting blood glucose and improved insulin resistance. CONCLUSION: Soyasaponins reduce inflammation and improve serum lipid profiles and glucose homeostasis in HFD-induced obese mice.

Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.

Since 2002, WHO has strongly called scientists to investigate intensively the toxicity and potential carcinogenicity of acrylamide (AA), because humans are widely exposed to AA via various foodstuffs. In this study we measured the biomacromolecule adducts of [2,3-(14)C]AA (0, 7.5 x 10(-2), 7.5 x 10(-1), 7.5, 9.3 x 10(1), 2.4 x 10(2) and 1.0 x 10(3)microg/kg b.w.) in adult male mice by ultrasensitive accelerator mass spectrometry (AMS) technique. The aim is to evaluate the potential molecular toxicity of AA at human relevant dose levels, particularly towards the sperm cells. Hemoglobin (Hb), serum albumin (SA), protamine, sperm DNA, tails and heads were isolated 24h post dosing and the adduct levels were measured by AMS, respectively. Good log/log linear dose-response correlations were established. Moreover, the correlation of AA-protamine adducts, AA-sperm DNA adducts, as well as AA-sperm head/tail adducts with AA-Hb or AA-SA adducts presented a linear log/log mode. In sperm, the formation of AA-protamine adducts were predominating to AA-DNA adducts. The adducts on sperm heads/tails might both influence the fertility efficacy.

Inhibition of acrylamide toxicity in mice by three dietary constituents.

The inhibitory effects of three dietary constituents, tea polyphenols, resveratrol, and diallyl trisulfide, on acrylamide-biomacromolecule (liver DNA, protamine, and hemoglobin) adduct formation at human exposure level were studied by accelerator mass spectrometry. The results demonstrated that the three dietary constituents all significantly inhibited the formation of acrylamide adducts with liver DNA, whereas tea polyphenols and diallyl trisulfide reduced protamine and hemoglobin adducts, respectively. Further biochemical studies showed that acrylamide could significantly inactivate creatine kinase and glutathione S-transferase and deplete glutathione. When the inhibitors were cotreated with acrylamide, all of them could effectively recover the activities of creatine kinase. In addition, tea polyphenols and diallyl trisulfide could increase glutathione S-transferase activity remarkably. On the basis of these results, mechanisms of the effects are discussed. This study might provide a beneficial guide to people's diet for the purpose of reducing the harmful effect of acrylamide.