Objective:To analysis the difficulties and complications emerged during transurethral ureteroscopy and offer their management strategies. Methods: A total of 900 patients accepting rigid transurethral ureteroscopy from May 1998 to October 2008, were evaluated retropspeetively. Results: Among 900 cases, 83 cases were found difficulties during transurethral ureteroscopy, of which 45 cases were early cases. 2.6% cases (24 cases) were converted to open surgery, of which 14 cases were early cases. The causes of conversion to open include: ureteral orifice of 3 patients could not be found (12.5%), ureteroscopy failed to enter ureteral orific in 5 patients (20.9%), ureteroscopy failed to get to the ill place in 5 patients (20.9%), ureter perforation occurred in 7 pa-tients (29.1%) , ureter avulsion occurred in 2 patients (8.3%), stones shifted to renal pelvis in 2 patients (8.3%). Conclusions: There are more difficulties and complications during ureteroscopy at early stage. Strictly mastering surgical indications, strengthening preoperative training, mastering the surgical technique is the key to reduce the failure rate and complications of ureteroscopy.

Background::Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s dementia. Mitochondrial dysfunction is involved in the pathology of PD. Coiled-coil-helix-coiled-coil-helix domain-containing 2 (CHCHD2) was identified as associated with autosomal dominant PD. However, the mechanism of CHCHD2 in PD remains unclear.Methods::Short hairpin RNA (ShRNA)-mediated CHCHD2 knockdown or lentivirus-mediated CHCHD2 overexpression was performed to investigate the impact of CHCHD2 on mitochondrial morphology and function in neuronal tumor cell lines represented with human neuroblastoma (SHSY5Y) and HeLa cells. Blue-native polyacrylamide gel electrophoresis (PAGE) and two-dimensional sodium dodecyl sulfate-PAGE analysis were used to illustrate the role of CHCHD2 in mitochondrial contact site and cristae organizing system (MICOS). Co-immunoprecipitation and immunoblotting were used to address the interaction between CHCHD2 and Mic10. Serotype injection of adeno-associated vector-mediated CHCHD2 and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration were used to examine the influence of CHCHD2 in vivo.Results::We found that the overexpression of CHCHD2 can protect against methyl-4-phenylpyridinium (MPP+)-induced mitochondrial dysfunction and inhibit the loss of dopaminergic neurons in the MPTP-induced mouse model. Furthermore, we identified that CHCHD2 interacted with Mic10, and overexpression of CHCHD2 can protect against MPP +-induced MICOS impairment, while knockdown of CHCHD2 impaired the stability of MICOS. Conclusion::This study indicated that CHCHD2 could interact with Mic10 and maintain the stability of the MICOS complex, which contributes to protecting mitochondrial function in PD.

Objective:To investigate the characteristics of senile neurodegenerative diseases (NDDs) inpatients in south China, especially in Guangdong province, and explore the influencing factors for their medical expenses.Methods:The medical records of 7231 patients with NDDs≥65 years were collected in the electronic health database of our hospital from January 2010 to December 2019, including gender, age, admission ways, chief complaints, length of hospital stays and medical expenses. On the basis of median of the medical expenses (21 345 yuan) of these patients, they were divided into low cost (<21 345 yuan) group and high cost (≥21 345 yuan) group. Univariate Logistic analysis and multivariate Logistic regression analysis were conducted to screen the influencing factors for medical expenses and the independent influencing factors.Results:(1) The main age group of geriatric inpatients with NDDs were 70-79 years (40.96%); the admission source was mainly outpatient (56.70%), and length of hospital stays of a large percent of patients (44.50%) were 8-14 d. (2) From 2010 to 2019, the number of hospitalized geriatric patients with NDDs showed an increasing trend year by year, the overall trend of length of hospital stays was shortened, and the medical expenses showed gradual increase; the causes of hospitalization, percentages of patients caused by infection, abnormal blood pressure and water-electrolyte metabolism disturbances showed decreased trend, percentages of patients caused by heart diseases, cerebrovascular accidents and mental-psychological diseases showed increased trend, and the proportions of patients caused by fracture/trauma/wound injuries were generally stable. The proportion of patients returning home and mortality rate after hospital discharge were declined, and the proportion of patients returning to other medical or community institutions was increased. (3) Living in ICU, length of hospital stays, diabetes, nosocomial infection, chronic kidney disease, urinary tract infection, tumble, body mass index, and anticholinergic drugs were independent risk factors influencing the medical expenses ( P<0.05). Conclusions:An aging trend is noted in patients with NDDs; the number of hospitalized patients and medical expenses increase year by year, and the length of hospital stays gradually decreases. In view of the many factors that influence the medical expenses of this disease, it is suggested to develop the corresponding standardized treatment plan for the main influencing factors in clinical practice.

Previous studies suggest that the reduction of SMAD3 (mothers against decapentaplegic homolog 3) has a great impact on tumor development, but its exact pathological function remains unclear. In this study, we found that the protein level of SMAD3 was greatly reduced in human-grade IV glioblastoma tissues, in which LAMP2A (lysosome-associated membrane protein type 2A) was significantly up-regulated. LAMP2A is a key rate-limiting protein of chaperone-mediated autophagy (CMA), a lysosome pathway of protein degradation that is activated in glioma. We carefully analyzed the amino-acid sequence of SMAD3 and found that it contained a pentapeptide motif biochemically related to KFERQ, which has been proposed to be a targeting sequence for CMA. In vitro, we confirmed that SMAD3 was degraded in either serum-free or KFERQ motif deleted condition, which was regulated by LAMP2A and interacted with HSC70 (heat shock cognate 71 kDa protein). Using isolated lysosomes, amino-acid residues 75 and 128 of SMAD3 were found to be of importance for this process, which affected the CMA pathway in which SMAD3 was involved. Similarly, down-regulating SMAD3 or up-regulating LAMP2A in cultured glioma cells enhanced their proliferation and invasion. Taken together, these results suggest that excessive activation of CMA regulates glioma cell growth by promoting the degradation of SMAD3. Therefore, targeting the SMAD3-LAMP2A-mediated CMA-lysosome pathway may be a promising approach in anti-cancer therapy.