Objective To investigate the clinical characteristics, management and prognosis of gestational trophoblastic disease in women aged 50 years or more. Methods Thirty-eight cases of gestational trophoblastic disease in women aged 50 years or more, who were treated in Peking Union Medical College Hospital between 1992 and 2002, were reviewed retrospectively. Results The median age was 52 years (range from 50 to 58 years ). The lesions included 5 hydatidiform moles (13%), 19 invasive moles (50%), 12 choriocarcinomas (32%) and 2 placenta site trophoblastic tumors (5%). All of 38 cases presented with abnormal vaginal bleeding. Twenty-three cases of hydatidiform moles were diagnosed at their first visit to the hospital, and 15 of them received prophylactic chemotherapy, of whom 10 progressed to invasive mole, 3 developed lung metastasis. All of the other 8 cases without prophylactic chemotherapy progressed to malignant changes with metastasis of lung. The use of prophylactic chemotherapy reduced the incidence of subsequent metastasis. All of 38 cases received chemotherapy. Thirty-two cases underwent hysterectomy, complete remission was achieved in 91% of patients; complete remission was achieved in 2 of 6 patients without hysterectomy. Conclusions The diagnosis of pregnancy and pregnancy-related disease should be considered in the elderly women presenting with abnormal vaginal bleeding. Once gestational trophoblastic disease in women aged 50 years or more is diagnosed, chemotherapy should be given as soon as possible. Hysterectomy is frequently required to improve the prognosis of gestational trophoblastic disease in the elderly women.

Objective To explore a new modified stable genioplasty with modified MortiseTenon joints technique and to analyze the surgicaI results in clinic as well as to discuss the advantages in theory.Methods Eleven patients were performed by the genioplasty with Mortise-Tenon joints technique intraoral approach from June 2012 to March 2014,who were suffered from retrusion of chin with different degree accompanying with long chin.The two segments of the chin by osteotomy were made into the Mortise-Tenon joints and fixed by titanium plates.The results were evaluated by clinical appearances and image analyses.Results All 11 patients were satisfied with the procedure and the contour of the chin.The surgical effects were stable without any complications.The advancement in average Mortise-Tenon joints technique was 7.38 mm.Conclusions Much better in stablility and less relapse are achieved by using modified Mortise-Tenon joints technique;furthermore,the genioglossal muscle and geniohyoid muscle are reserved as much as possible,and therefore the normal function of them could be maintained.This method is a good alternative technique for chin retrusion coexisted withlong chin.

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38MAPK) signaling pathways in reduction of ischemia-reperfusion (I/R) injury by morphine preconditioning in the rats with heart failure.Methods Adult male Sprague-Dawley rats,weighing 200-230 g,in which doxorubicin 2 mg/kg was injected via the tail vein once a week for 6 consecutive weeks to induce chronic heart failure,were studied.At the end of 8th week,45 rats with chronic heart failure were randomly divided into 5 groups (n =9 each) using a random number table:sham operation group (group S),group I/R,morphine preconditioning group (group MPC),SP600125 (JNK inhibitor) + morphine preconditioning group (group MSP) and SB203580 (p38MAPK inhibitor) + morphine preconditioning group (group MSB).Myocardial I/R was induced by 30 min occlusion of the anterior descending branch of the coronary artery followed by 120 min reperfusion in each group except group S.In group MPC,the rats were subjected to 3 cycles of 5-min infusion of 0.1 mg/kg morphine via the femoral vein at 5 min interval before ischemia.In MSP and MSB groups,SP600125 0.5 mg/kg and SB203580 0.2 mg/kg were injected via the femoral vein,respectively,at 10 min before morphine preconditioning.The animals were sacrificed at 120 min of reperfusion,and the myocardial specimens were obtained for determination of the total areas of right and left ventricles (LV+RV),area at risk (AAR),infarct size (IS),and expression of PKC δ in myocardial tissues (by immunohistochemistry),and IS/AAR ratio was calculated.Results There was no significant difference in LV+RV and AAR between the five groups (P＞0.05).Compared with group S,IS and IS/AAR were significantly increased,and the expression of PKC δ was upregulated in I/R and MSB groups (P＜0.05).Compared with group I/R,IS and IS/AAR were significantly decreased,and the expression of PKC δ was down-regulated in MPC and MSP groups (P＜0.05).Compared with group MPC,IS and IS/AAR were significantly increased,and the expression of PKC δ was upregulated in group MSB (P＜0.05),and no significant change was found in the parameters mentioned above in group MSP (P＞0.05).Conclusion Activation of p38MAPK signaling pathway is involved in reduction of myocardial I/R injury by morphine preconditioning,and the mechanism is related to down-regulation of PKC δ expression in rats with heart failure;JNK signaling pathway is not involved in this process.

Objective To study the influence of CTP-OD1-HA and CTP-OD2-HA fusion peptides and combined with imatinib on proliferation of K562 cells.Methods K562 cells were treated with CTP-OD1-HA and CTP-OD2-HA peptides or together with imatinib.The proliferation of cells were detected and compared by MTT and clone formation methods.Results MTT examination demonstrated that CTP-OD1-HA and CTP-OD2-HA peptides could inhibit the proliferation of K562 cells,and the effect was more obvious when acted along with imatinib;Clone formation showed that CTP-OD1-HA and CTP-OD2-HA peptides suppressed the continuous colony forming ability of K562 cells.Conclusion CTP-OD1-HA and CTP-OD2-HA could specially inhibit the proliferation of K562 cells,and increase the sensitivity of imatinib.

Objective To evaluate the clinical efficacy of a stroke unit combined with community health services for treating stroke survivors. Methods A total of 120 stroke patients were randomly divided into a " stroke unit combined with community medicine" group ( combined group) , a stroke unit group and a general treatment group. Patients in the former 2 groups were treated in a hospital stroke unit during their hospitali-zation. The general treatment group was given conventional medical treatment. After discharge, the combined group continued to receive regular rehabilitation therapy and guidance in the form of community medical services, while the stroke unit group received follow-up only. Assessment was by means of Fugl-Meyer scores, the Barthel index and self-rating on a depression scale ( SDS). The patients were assessed at admission, on discharge and 3 months after discharge. Results There were no significant differences in average limb motor function, ability in the activities of daily living ( ADL) or depressive mood among the 3 groups on admission, but at discharge, limb motor function and ADL ability in the combined group and stroke unit groups were significantly superior to those in the general therapy group. Limb motor function and ADL ability in the combined and stroke unit groups had improved further 3 months after discharge, with more significant improvements in the combined group. No significant change in depression was observed in any group at discharge, but average depression scores in the combined and stroke unit groups improved significantly in the 3 months after discharge, and there was a statistically significant difference between the combined group and the general group. Conclusion Supplementing the work of a stroke unit with community health services significantly improves stroke patients' recovery of limb motor function and ADL ability.

OBJECTIVE: To explore the clinical characteristics and genetic variant in a child with neurodevelopmental disorders (NDDs). METHODS: Clinical data of a child who had presented at Xiaogan Hospital Affiliated to Wuhan University of Science and Technology in December 2020 due to intermittent convulsions for over a year were retrospectively analyzed. Peripheral blood samples of the child and his parents were collected and subjected to whole exome sequencing. Candidate variants were verified by Sanger sequencing and bioinformatic analysis. "HNRNPU gene", "epilepsy", "epileptic encephalopathy", "hereditary epilepsy", "neurodevelopmental disorder", "neurodevelopmental syndrome", "HNRNPU", and "NDDs" were used as the key words to search the CNKI, Wanfang and PubMed databases dated from January 1, 1994 to February 10, 2022. RESULTS: The patient was a 2-year-old boy who had developed seizure at the age of 5 months. His clinical features had included abnormal appearance, recurrent seizures, and low developmental quotients of each functional area as evaluated by the Gesell scale. The child was given sodium valproate for the antiepileptic treatment and rehabilitation training. He had become seizure-free within half a year of follow-up, but his intelligence and motor development did not improve significantly. Genetic testing revealed that he has harbored a heterozygous c.1720_1722delCTT (p.Lys574del) variant of the HNRNPU gene, which was not found in either of his parents. Based on the guidelines from the American College of Medical Genetics and Genomics (ACMG), the variant was rated as likely pathogenic (PS2+PM2_Supporting+PM4). A total of 13 articles were retrieved, and the types of HNRNPU gene mutations have included splice site mutation, nonsense mutation, missense mutation, in-frame deletion, gene duplication, frameshifting mutation, and multiple exon deletion. The main clinical manifestations have included mental retardation, language delay, global developmental delay, epilepsy, craniofacial deformity, mental and behavioral abnormalities. CONCLUSION The c.1720_1722delCTT variant of the HNRNPU gene probably underlay the NDDs in this child. Above finding has enriched the mutational spectrum of the HNRNPU gene.
Male ; Child ; Humans ; Infant ; Child, Preschool ; Retrospective Studies ; Neurodevelopmental Disorders/genetics* ; Intellectual Disability ; Mutation ; Seizures ; Epilepsy, Generalized

Spinal cord injury leads to extremely high mortality and disability rates and its treatment has always been a global challenge. The survival of patients with spinal cord injury is partially lengthened with the development of medical treatments, but the clinical outcome is still not satisfactory. Some important progress has been made in the basic researches over spinal cord injury, such as analysis of repair mechanism of spinal cord injury and development of cellular therapies and biological scaffolds of spinal cord injury in China. However, some basic researches show insufficient understanding of the microenvironment and animal model of spinal cord injury and lack support from clinical problems, leading to too simplistic or contradictory conclusions. There is an urgent need to reexamine the research methods and carry out basic and clinical translational researches. Therefore, the authors discuss the key problems and difficulties in basic researches over spinal cord injury and propose improvement suggestions, aiming to provide a reference for conducting basic researches correctly and accelerating clinical innovational transformation.

Spinal cord injury is a common clinical disease secondary to spinal cord fractures that causes patients with motor and sensory dysfunction or even paralysis. In recent years, exosomes have participated in the occurrence and development of various diseases as nanometer-sized cell particles, and have received extensive attention. Exosomes derived from spinal cord tissue cells during spinal cord injury affect the injury process and tissue repair. In addition, exosomes as a new treatment for spinal cord injury have been widely studied. The authors document the mechanisms of various exosomes from spinal cord tissue and the repair effects of various cell-derived exosomes in spinal cord injury, in order to deepen the understanding of the role of exosomes in spinal cord injury and provide new ideas for studying the course and treatment of spinal cord injury.

Osteoporotic thoracolumbar fracture in the elderly will seriously reduce their quality of life and life expectancy. For osteoporotic thoracolumbar fracture in the elderly, spinal reconstruction is necessary, which should comprehensively consider factors such as the physical condition, fracture type, clinical characteristics and osteoporosis degree. While there lacks relevant clinical norms or guidelines on selection of spinal reconstruction strategies. In order to standardize the concept of spinal reconstruction for osteoporotic thoracolumbar fracture in the elderly, based on the principles of scientificity, practicality and progressiveness, the authors formulated the Clinical guideline for spinal reconstruction of osteoporotic thoracolumbar fracture in elderly patients ( version 2022), in which suggestions based on evidence of evidence-based medicine were put forward upon 10 important issues related to the fracture classification, non-operative treatment strategies and surgical treatment strategies in spinal reconstruction after osteoporosis thoracolumbar fracture in the elderly, hoping to provide a reference for clinical treatment.