Objective To explore the relationship of leptin,leptin receptor and esophageal squamous cell carcinoma,and provide a scientific basis for prevention and treatment of esophageal cancer.Methods Samples were collected from 32 patients with esophageal squamous cell carcinoma,20 healthy control subjects in Shanxi Tumor Hospital.ELISA and immunohistochemistry were used to analyze leptin and leptin receptor,respectively.The correlation between their expression and clinicopathologieal parameters was also analysized.Results Patients with esophageal squamous cell carcinoma had significandy(t =4.64,P ＜ 0.001)higher leptin levels [(4.7 ±1.9)ng/ml] compared with normal [(2.54±1.01)ng/ml] oesophagus tissues.The expression rate of leptin receptor in esophageal carcinoma and normal esophagus was 81.25 ％ and 75.00 ％ respectively,not differ significantly.The expression levels of leptin was associated with position,(l)ymphatic metastasis.Conclusion Higher leptin levels seem to represent an additional,independent risk factor for esophageal squamous cell carcinoma,leptin receptor expression on oesophageal epithelial cells provides a pathway for leptin-mediated signal transduction.

Objective To explore the long-term outcome of postpartum glucose metabolism among patients with gestational hyperglycemia and its risk factors.Methods Patients with gestational hyperglycemia,diagnosed by 100 g oral glucose tolerance test (OGTT) during 24th to 28th gestation week between 2010 and 2012 and giving the childbirth in Peking Union Medical College Hospital,were included.The glucose metabolism outcomes were evaluated by 75 g OGTT.The risk factors influencing the glucose metabolism outcome and the glucose metabolism parameter changes between the pregnancy term and now were also analyzed.Results Forty patients with gestational hyperglycemia were included.The follow-up time was postpartum 5-8 years and (6.83±0.74) years on average.Among them,3 patients were diagnosed with type 2 diabetes and 9 patients were diagnosed with impaired glucose intolerance.The overall rate of abnormal glucose metabolism was 30 percent.The third-hour glucose of OGTT larger than 7.45 mmol/L and the area under the glucose curve (Glu AUC) during OGTT larger than 24.875 mmol×h/L were the risk factors for the abnormal glucose metabolism outcome,with the odds ratio of 5.769 (95％ confidence interval 1.064-31.270,P=0.042) and 12.5 (95％ confidence interval 2.226-70.187,P=0.004).Using the 2-hour glucose larger than 8.25 mmol/L and 3-hour glucose larger than 7.45 mmol/L in the OGTT of midtrimester to judge the glucose state in the follow-up visit can achieve the diagnostic efficacy with the sensitivity of 75％,specificity of 82％,positive prediction value of 64％ and negative prediction value of 88％.Comparing with now,the fasting glucose in the midtrimester was lower ([5.49±0.43] vs.[4.55±0.47] mmol/L,P＜0.001),the fasting insulin in the midtrimester was high-er (12.30 [6.35,16.55] vs.8.31 [6.79,12.00] μIU/ml,P=0.048),HOMA-β in the midtrimester was higher (202.67 [145.71,335.71] vs.85.41 [78.63,112.13],P＜0.001).Conclusion The third-hour glucose larger than 7.45 mmol/L and the glucose area under the curve larger than 24.88 mmol×h/L in the OGTT of midtrimester are the risk factors for the abnormal glucose state in the postpartum long-term follow-up.The combination of the second-hour and the third-hour glucoses in the 100 g OGTT of midtrimester can help to predict the postpartum long-term glucose state.

Objective To explore the relationship of MTNR1B DNA methylation with gestational diabetes and gestational glucose and lipid metabolism features.Methods 50 patients with gestational hyperglycemia,diagnosed by 100 g oral glucose tolerance test (OGTT) during mid-trimester were selected between 2009 and 2012.50 pregnant women with normal glucose tolkerance of matched age and body mass index were included in the control group.The blood samples during mid-trimester and the clinical parameters were collected.MTNR1B DNA methylation levels were measured.Results After adjusting age and body mass index,the CpG locus located at +64 bp away from the translation initiation site of MTNR1B was related with gestational diabetes (OR=0.859,95％ CI:0.772-0.955,P=0.005).DNA methylation level of several MTNR1B loci was also related with gestational glucose and lipid metabolism features.Conclusion MTNR1B DNA methylation is related with gestational diabetes and gestational glucose and lipid metabolism.

Objective:To retrospectively analyze the urodynamics quality in Southwest China, and find out the main issues of urodynamics quality in Southwest China and try to find out the improvement ways.Methods:In this study, a two-stage sampling method was used.In the first stage, 10 medical institutions in Southwest China were selected by cluster sampling from March to June, 2020.In the second stage, according to the development of UDS in Southwest China, the sample size estimation formula was adopted, and the loss of follow-up rate in reports extraction was considered, the initial sample size was 350. As the workload of UDS in the 10 medical institutions involved in the study was equivalent, 35 urodynamics traces from each medical institution were selected. The initial samples should also meet the inclusion criteria: ①patients with clear medical history and complete clinical data; ②UDS traces were clear; ③UDS system was water filled system; ④age>18, and 150 urodynamic traces were included in the final study. We evaluated the quality of enrolled urodynamics traces, and the quality evaluation standard according to the guidelines established by the International Continence Society (ICS). The evaluation conducted by two independent urologist with more than 10 years working experience. Artifacts were divided into non-technical artifacts: abnormal abdominal pressure changes, urine volume <150 ml when did the uroflow test, and technical artifacts: non-standard zero setting, fail to record all urodynamics parameters, baseline drift, catheter displacement, misjudgment of detrusor physiological contraction and detrusor overactive in voiding phase, misjudgment between detrusor overactive and bladder low compliance in filling phase.Results:non-technical artifacts: 32 cases were found abnormal abdominal pressure changes (21.3%), 21 cases (14.0%) were found when did the uroflow test the urine volume <150 ml, and technical artifacts: Non-standard zero setting in 28 cases (18.7%), fail to record all urodynamics parameters in 8 cases, baseline drift in 16 cases, catheter displacement in 9 cases and misjudgment of detrusor physiological contraction and detrusor overactive in voiding phase in 12 cases, misjudgment between detrusor overactive and bladder low compliance in filling phase in 24 cases (16.0%).Conclusions:At present, the urodynamics quality in Southwest China need to be improved. The main issues were that the operator didn’t obey the basic operation and quality control process, and the operator did not have enough basic knowledge of urodynamics. It can be improved by strictly carry out the operation standard of UDS, identifying and correcting artifacts in time, and promoting the standardized urodynamic training courses.

Mitochondrial dysfunctions play major roles in ageing. How mitochondrial stresses invoke downstream responses and how specificity of the signaling is achieved, however, remains unclear. We have previously discovered that the RNA component of Telomerase TERC is imported into mitochondria, processed to a shorter form TERC-53, and then exported back to the cytosol. Cytosolic TERC-53 levels respond to mitochondrial functions, but have no direct effect on these functions, suggesting that cytosolic TERC-53 functions downstream of mitochondria as a signal of mitochondrial functions. Here, we show that cytosolic TERC-53 plays a regulatory role on cellular senescence and is involved in cognition decline in 10 months old mice, independent of its telomerase function. Manipulation of cytosolic TERC-53 levels affects cellular senescence and cognition decline in 10 months old mouse hippocampi without affecting telomerase activity, and most importantly, affects cellular senescence in terc cells. These findings uncover a senescence-related regulatory pathway with a non-coding RNA as the signal in mammals.