Objective To establish the regression equation for the maximum oxygen uptake(VO2max)of male young endurance athletes at altitudeby modeling relevant indicators.Methods A total of 81 young male endurance athletes(long-distance runner,marathoner,and race walker)aged 15～18 years old were selected as the research subjects.The VO2max,3000-meter timed run,400-meter timed run,body morphology,body composition,hematological indicators,and cardiac function of the ath-letes were tested in Kunming,Yunnan Province(1890 meters altitude high)in four consecutive days.The testing sequence of the exercise was randomly arranged.The data of the first 65 athletes were used for multiple linear regression modeling,while those of the rest 16 were employed for the verifica-tion of the established model.Results Based on the data of 65 athletes,the multiple linear regression equation of VO2max was:VO2max=2616.661+60.389×lean body mass(kg)-3.108×3000-meter run-ning time(s)-16.665×lower limb length A(cm)+6.356×maximum heart rate(bpm),R2=0.858,and that of the relative VO2max was:relative VO2max=119.685-0.058×3000-meter running time(s)-0.224×body weight(kg)-0.452×Achilles tendon length(cm),R2=0.681.Accord-ing to the data of the rest 16 athletes,there was no significant difference in the calculated values of VO2max and relative VO2max.Moreover,the calculated values and the direct test values of VO2max and rel-ative VO2max were positively correlated(r=0.735,P=0.001;r=0.509,P=0.044).Conclusion A regression model of VO2max and relative VO2max for young male endurance athletes at altitude(1890 meters altitude high)was established and verified through direct testing.The model established is worth popularization and application,and can provide references for indicators selection of young male endurance athletes at altitude(1890 meters altitude high).

Objective To establish the regression equation for the maximum oxygen uptake(VO2max)of male young endurance athletes at altitudeby modeling relevant indicators.Methods A total of 81 young male endurance athletes(long-distance runner,marathoner,and race walker)aged 15～18 years old were selected as the research subjects.The VO2max,3000-meter timed run,400-meter timed run,body morphology,body composition,hematological indicators,and cardiac function of the ath-letes were tested in Kunming,Yunnan Province(1890 meters altitude high)in four consecutive days.The testing sequence of the exercise was randomly arranged.The data of the first 65 athletes were used for multiple linear regression modeling,while those of the rest 16 were employed for the verifica-tion of the established model.Results Based on the data of 65 athletes,the multiple linear regression equation of VO2max was:VO2max=2616.661+60.389×lean body mass(kg)-3.108×3000-meter run-ning time(s)-16.665×lower limb length A(cm)+6.356×maximum heart rate(bpm),R2=0.858,and that of the relative VO2max was:relative VO2max=119.685-0.058×3000-meter running time(s)-0.224×body weight(kg)-0.452×Achilles tendon length(cm),R2=0.681.Accord-ing to the data of the rest 16 athletes,there was no significant difference in the calculated values of VO2max and relative VO2max.Moreover,the calculated values and the direct test values of VO2max and rel-ative VO2max were positively correlated(r=0.735,P=0.001;r=0.509,P=0.044).Conclusion A regression model of VO2max and relative VO2max for young male endurance athletes at altitude(1890 meters altitude high)was established and verified through direct testing.The model established is worth popularization and application,and can provide references for indicators selection of young male endurance athletes at altitude(1890 meters altitude high).

Objective:To investigate the placenta tissue expression levels of monocyte chemotactic protein-1 (MCP-1), nuclear factor-κBp65 (NF-κBp65) and proliferating cell nuclear antigen (PCNA) in pregnant women with gestational diabetes mellitus (GDM), and to analyze their correlation with pregnancy outcomes.Methods:The clinical data of 124 pregnant women with GDM from May 2020 to December 2021 in PLA Northern Theater General Hospital were retrospectively analyzed. Among them, 62 pregnant women were willing to receive treatment (treatment group), while 62 pregnant women were unwilling to receive treatment (untreated group). In addition, 80 healthy pregnant women in the same period were selected as the healthy control group. The natural birth rate, neonatal Apgar score and the incidences of macrosomia, neonatal hypoglycemia, neonatal hyperbilirubinemia were record. The placenta tissue expression levels of MCP-1, NF-κBp65 and PCNA were detected by immunohistochemical.Results:The natural birth rate in untreated group was significantly lower than that in treatment group and healthy control group: 24.19% (15/62) vs. 75.81% (47/62) and 88.75% (71/80), the natural birth rate in treatment group was significantly lower than that in healthy control group, and there was statistical difference ( P<0.05). The Apgar score in untreated group was significantly lower than that in treatment group and healthy control group: (8.45 ± 2.02) scores vs. (9.46 ± 2.59) and (9.71 ± 3.21) scores, the incidences of macrosomia, neonatal hypoglycemia and neonatal hyperbilirubinemia were significantly higher than those in treatment group and healthy control group: 35.48% (22/62) vs. 11.29% (7/62) and 3.75% (3/80), 29.03% (18/62) vs. 8.06% (5/62) and 2.50% (2/80), 24.19% (15/62) vs. 9.68% (6/62) and 2.50% (2/80), and there were statistical differences ( P<0.05); there were no statistical difference in the indexes treatment group and healthy control group ( P>0.05). The positive expression rates of MCP-1, NF-κBp65 and PCNA in untreated group were significantly higher than those in treatment group and healthy control group: 72.58% (45/62) vs. 25.81% (16/62) and 12.50% (10/80), 69.35% (43/62) vs. 27.43% (17/62) and 13.75% (11/80), 69.35% (43/62) vs. 24.19% (15/62) and 11.25% (9/80), the indexes in treatment group were significantly higher than those in healthy control group, and there were statistical differences ( P<0.05). Conclusions:The placenta tissue expression levels of MCP-1, NF-κBp65 and PCNA in pregnant women with GDM are associated with adverse pregnancy outcomes. After active treatment, the positive rates of the three indexes in pregnant women with GDM significantly decrease, and the prognosis got improved.

Purpose: Drug resistance is one of the main causes of chemotherapy failure in patients with small cell lung cancer (SCLC), and extensive biological studies into chemotherapy drug resistance are required. Materials and Methods: In this study, we performed lncRNA microarray, in vitro functional assays, in vivo models and cDNA microarray to evaluate the impact of lncRNA in SCLC chemoresistance. Results: The results showed that KCNQ1OT1 expression was upregulated in SCLC tissues and was a poor prognostic factor for patients with SCLC. Knockdown of KCNQ1OT1 inhibited cell proliferation, migration, chemoresistance and promoted apoptosis of SCLC cells. Mechanistic investigation showed that KCNQ1OT1 can activate transforming growth factor-β1 mediated epithelial-to-mesenchymal transition in SCLC cells. Conclusion Taken together, our study revealed the role of KCNQ1OT1 in the progression and chemoresistance of SCLC, and suggested KCNQ1OT1 as a potential diagnostic and prognostic biomarker in SCLC clinical management.

Objective:To investigate the role of transforming growth factor β1 (TGF-β1) in multi-drug resistance in small cell lung cancer and its clinical significance.Methods:The mRNA and protein expressions of TGF-β 1 in H69 and H69AR cells were detected by real-time PCR and Western blot,respectively.After silence of TGF-[β1,the sensitivity of H69AR to drugs was detected by CCK8 assay.The expressions of TGF-β1 in lung cancer and paracarcinoma tissues were examined by QRT-PCR and immunohistochemistry.The relationship of TGF-β 1 expression with clinical pathological features and prognosis of patients was studied.Results:Compared to H69,the mRNA and protein expressions of TGF-β1 in H69AR cells were significantly increased by (5.93±0.47) and (8.49±1.92) folds,respectively (P＜0.01).Transfection ofTGF-β1 siRNA resulted in a decrease of TGF-β1 expression by 70.432％ in H69AR ceils (F=21.20,P＜0.01) and an increase insensitivity to chemotherapeutic agents of H69AR cells (t=4.576,P＜0.05).Compare with the paracarcinoma tissues,the expression of TGF-β1 was significantly increased in small cell lung cancer tissues (t=13.925,P＜0.01),which was closely related with clinical stage,chemosensitivity and overall survival (all P＜0.05),but not related with gender,age (both P＞0.05).Conclusion:TGF-β1 is involved in the regulation of small cell lung cancer multidrug resistance,which may be a potential marker to evaluate the chemosensitivity and dinical prognostic for small cell lung cancer.

OBJECTIVETo investigate the role of SALL4 in regulating multi-drug resistance in small cell lung cancer (SCLC), and to evaluate its clinical significance.

METHODSThe expression of SALL4 protein and gene was detected by Western blot and real-time PCR (RT-PCR) in both H69 and H69AR cell lines, respectively. SALL4 expression in H69AR was blocked by the siRNA, and then the drug-sensitivities of H69AR cell lines to chemotherapeutic drugs such as cisplatin, doxorubicin, and etoposide were evaluated by cell counting kit assay. SALL4 expression was also examined by immunohistochemistry, and correlated with patients' clinicopathological features and prognosis.

RESULTSThe expression of SALL4 was significantly increased in H69AR cells than in the H69 cells (P < 0.01). Down-regulation of SALL4 increased the drug-sensitivities of H69AR cells to chemotherapeutic drugs (P = 0.02). The expression of SALL4 was significantly increased in SCLC than in para-carcinoma tissues (P < 0.01). SALL4 expression correlated with clinical stage, chemosensitivity and overall survival (P < 0.05), but not with patients' age and gender.

CONCLUSIONSALL4 is involved in the regulation of multidrug resistance in SCLC; SALL4 may be a potential target gene to evaluate the chemosensitivity and clinical prognosis for SCLC.

Antineoplastic Agents ; pharmacology ; Cisplatin ; pharmacology ; Down-Regulation ; Doxorubicin ; pharmacology ; Drug Resistance, Multiple ; physiology ; Drug Resistance, Neoplasm ; physiology ; Etoposide ; pharmacology ; Humans ; Lung Neoplasms ; drug therapy ; metabolism ; RNA, Small Interfering ; Real-Time Polymerase Chain Reaction ; Small Cell Lung Carcinoma ; drug therapy ; metabolism ; Transcription Factors ; genetics ; physiology

Objective To investigate the role of SALL 4 in regulating multi-drug resistance in small cell lung cancer ( SCLC), and to evaluate its clinical significance .Methods The expression of SALL4 protein and gene was detected by Western blot and real-time PCR (RT-PCR) in both H69 and H69AR cell lines, respectively.SALL4 expression in H69AR was blocked by the siRNA, and then the drug-sensitivities of H69AR cell lines to chemotherapeutic drugs such as cisplatin , doxorubicin, and etoposide were evaluated by cell counting kit assay .SALL4 expression was also examined by immunohistochemistry , and correlated with patients′clinicopathological features and prognosis . Results The expression of SALL4 was significantly increased in H69AR cells than in the H69 cells ( P <0.01).Down-regulation of SALL4 increased the drug-sensitivities of H69AR cells to chemotherapeutic drugs (P=0.02).The expression of SALL4 was significantly increased in SCLC than in para-carcinoma tissues ( P<0.01 ) .SALL4 expression correlated with clinical stage , chemosensitivity and overall survival ( P<0.05 ) , but not with patients′age and gender .Conclusion SALL4 is involved in the regulation of multidrug resistance in SCLC;SALL4 may be a potential target gene to evaluate the chemosensitivity and clinical prognosis for SCLC .