Reference intervals are very important for clinical laboratory diagnosis and physiological evaluation. 1 The accuracy and applicability of such reference intervals directly affect the efficient diagnosis and treatment of the disease. Hematology is commonly used to assess health and disease states associated with blood disorders, infectious diseases, and the immune system. 2 However, suitable age-and sexspecific reference intervals of hematologic analytes of children are often lacking or incomplete. Children are not small adults, and consensus guidelines for adults may not apply to children. 3 Hematological reference intervals are affected by many factors such as the location of the population, economic background, lifestyle habits, and dietary structure. While it is inappropriate to randomly use the reference intervals established in other countries, there are no standard pediatric reference intervals for China. Therefore, it is necessary to establish a hematological reference range for Chinese children. The purpose of this study was to establish the age-and Abstract Introduction: Reference intervals for pediatric laboratory tests need to be interpreted in the context of age-and sex-dependent dynamics. However, few reference intervals for healthy ethnic Han Chinese children have previously attempted to establish using large sample sizes. As such, there are no national hematological standards in China for pediatric reference intervals. Methods:We used a direct method to enroll a total of 2164 healthy 1-to 7-year-old children from Henan province. Hematological reference intervals were established by analyzing venous blood sample data on 17 hematologic analytes. The reference values for different ages and sexes were estimated using both parametric methods (mean ± 2 SD) and nonparametric methods (2.5-97.5th percentiles). Results:We provided reference intervals for 17 hematologic analytes including red blood count, hemoglobin concentration, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, and red cell distribution width, white blood count and differential count as well as platelet count and related parameters. Conclusion:We established age-and sex-specific reference intervals that can provide more evidence-based guidance for the diagnosis and treatment for pediatric diseases. Our findings provide the basis for the next step in establishing national blood testing standards. K E Y W O R D Schildren, hematologic analytes, reference interval, venous blood

Established reference intervals (RIs) of coagulation parameters generally based on the general population are not applicable to specific women. In order to accurately evaluate the coagulation status of non-pregnant women and pregnant women, specific RIs should be established. Our study recruited 465 non-pregnant women and 1972 pregnant women aged 20–45 years. Eight tests including antithrombin (AT), protein C (PC), free protein S (fPS), lupus anticoagulant (LA), D-dimer, fibrin/fibrinogen degradation products (FDP), coagulation factor VII (FVII), and factor VIII (FVIII) were performed on ACL TOP automated coagulation instrument. The RIs for these tests were established in non-pregnant and pregnant women at different gestational weeks. Compared to the non-pregnant group, the medians of AT and fPS were lower, while the medians of PC, LA normalized ratio, D-dimer, FDP, FVII, and FVIII were higher. During pregnancy, AT and fPS activity showed a decreasing trend, with the increase of gestational age. PC activity, LA normalized ratio, D-dimer concentrations, FDP concentrations, FVII, and FVIII activity presented an increasing trend, with the increase of gestational age. The non-pregnant women-specific RIs and the gestational age-specific RIs of AT, PC, fPS, LA normalized ratio, D-dimer, FDP, FVII, and FVIII needed to be established for accurate clinical diagnoses.

Background: Hypercholesterolemia is a risk factor for the development of cardiac hypertrophy. Astragaloside IV (AST-IV) possesses cardiovascular protective properties. We hypothesize that AST-IV prevents cardiac remodeling with hypercholesterolemia via modulating tissue homeostasis and alleviating oxidative stress. Methods: The ApoE^-/- mice were treated with AST-IV at 1 or 10 mg/kg for 8 weeks. The blood lipids tests, echocardiography, and TUNEL were performed. The mRNA expression profile was detected by real-time PCR. The myocytes size and number, and the expressions of proliferation (ki67), senescence (p16^INK4a), oxidant (NADPH oxidase 4, NOX4) and antioxidant (superoxide dismutase, SOD) were observed by immunofluorescence staining. Results: Neither 1 mg/kg nor 10 mg/kg AST-IV treatment could decrease blood lipids in ApoE^-/- mice. However, the decreased left ventricular ejection fraction (LVEF) and fractional shortening (FS) in ApoE^–/– mice were significantly improved after AST-IV treatment. The cardiac collagen volume fraction declined nearly in half after AST-IV treatment. The enlarged myocyte size was suppressed, and myocyte number was recovered, and the alterations of genes expressions linked to cell cycle, proliferation, senescence, p53-apoptosis pathway and oxidant-antioxidants in the hearts of ApoE^-/- mice were reversed after AST-IV treatment. The decreased ki67 and increased p16^INK4a in the hearts of ApoE^-/- mice were recovered after AST-IV treatment. The percentages of apoptotic myocytes and NOX4-positive cells in AST-IV treated mice were decreased, which were consistent with the gene expressions. Conclusion: AST-IV treatment could prevent cardiac remodeling and recover the impaired ventricular function induced by hypercholesterolemia. The beneficial effect of AST-IV might partly be through regulating cardiac homeostasis and anti-oxidative stress.

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Mitochondria are key regulators of cell fate, maintaining self‐stability by a fine‐tuned quality‐control network including mitophagy, biogenesis, fission and fusion processes. Myocardial mitochondria can be impaired by hypercholesterolemia. Statins, such as atorvastatin, are considered the cornerstone in the management of hypercholesterolaemia primarily due to their marked cholesterol‐lowering ability. The direct effect of atorvastatin on myocardial mitochondria remains unclear. We aimed to explore whether atorvastatin could attenuate myocardial mitochondrial defects induced by high cholesterol, and whether cycloastragenol, a potent telomerase activator, could be used as a potential complementary bioactive compound for obesity and hypercholesterolaemia treatment. We found that atorvastatin at a low dose (3 mg/kg) did not reduce elevated serum cholesterol, but reversed cardiac remodelling and dysfunction in C57BL/6J mice fed with high‐fat diet (HFD). Atorvastatin reversed the upregulated mitophagy, mitochondrial fission and fusion, accompanied by mitochondrial biogenesis activation in HFD‐fed mice hearts. Mitochondrial structural impairments were attenuated by atorvastatin in HFD‐fed mice and oxidized low‐density lipoprotein (ox‐LDL) exposed HL‐1 cardiomyocytes. The depolarized mitochondrial membrane potential and increased mitochondrial oxygen consumption rates in ox‐LDL exposed HL‐1 cells were recovered by atorvastatin. Furthermore, atorvastatin co‐treated with cycloastragenol had better effects on reducing body weight, improving cardiac remodelling and dysfunction, and protecting mitochondria in high cholesterol. Conclusively, low‐dose atorvastatin exhibited a cholesterol‐independent cardioprotective effect through improving the mitochondrial quality‐control network and repairing mitochondrial ultrastructure in high cholesterol. Atorvastatin plus cycloastragenol supplement therapy has a better effect on treating obesity and hypercholesterolaemia.

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