Objective To summarize experience of nursing for thoracic breathing reconstruction in patients after cervical spinal cord in-jury (CSCI). Methods 6 cases accepting thoracic breathing reconstruction in our hospital from March 2013 to June 2014 were reviewed from 1 week before operation to 4 weeks after operation. Results All the patients, aged (41.7 ± 16.2) years, received tracheotomy (6.0 ± 5.8) days after injury because of weakened cough, retention of respiratory secretions and dyspnea;the ventilator was used for (45.3±25.9) days, and they received thoracic breathing reconstruction surgery (84±26.7) days after injury. Their vital capacity was (1085±92) ml before opera-tion and was (1680±283) ml 2 weeks after operation with 55%increment (P<0.01). Only 1 patient underwent a delayed wound healing. No pulmonary infection, urinary tract infections and pressure sore occurred until 4 weeks after operation. Conclusion Enhancement of airway care and prevention of pressure sore are the keys to reduce postoperative complications of thoracic breathing reconstruction.

Objective To explore the effects of health education based on survey findings of health needs in nursing among osteoporosis patients induced by endocrine dyscrasia. Methods From August 2015 to August 2017, we selected osteoporosis patients induced by endocrine dyscrasia as subjects by convenience sampling in Heping Hospital, Affiliated to Changzhi Medical College. All of the patients were divided into observation group and control group with the random number table, 51 cases in each group. Control group received routine nursing. Observation group carried out investigation on health needs before intervention and health education based on the findings of investigation. The Osteoporosis Knowledge Tests (OKT), Chinese Osteoporosis-Targeted Quality of Life Short Questionnaire (COQOL) were used to compare the level of disease knowledge and quality of life of patients before and after intervention. Results Before intervention, there was no statistical difference in the score of OKT and COQOL in two groups (P＞0.05). One month after intervention, the score of OKT and COQOL patients in observation group was (20.89±4.42) and (65.44±9.13) respectively higher than those in control group with significant differences (t=6.217, 4.639;P＜0.05). Conclusions Health education based on survey findings of health needs can increase osteoporosis patients' disease knowledge levels and improve their quality of life.

BACKGROUND:Many factors can cause disc degeneration,including aging,nutritional deficiency,and mechanical factors.The mechanical load is considered to be a very important factor,but its mechanism is still unclear. OBJECTIVE:To investigate the role of sclerostin(SOST)and Wnt/β-catenin signaling pathways in inducing degeneration of endplate cartilage. METHODS:Cartilage endplate cells were extracted from 4-week-old male Sprague-Dawley rats.Compressive stress was applied to endplate chondrocytes in vitro using a mechanical loading apparatus,and the cell viability was determined by the cell counting kit-8 assay at 1,3,5,and 7 days after compression.Western blot,reverse transcription quantitative PCR,and cellular immunofluorescence techniques were employed to examine intracellular cartilage markers(Aggrecan and type Ⅱ collagen)as well as calcification-related factors(Runx2 and osteocalcin).The expression of extracellular matrix degradation enzyme and genes related to the signaling pathway(SOST and β-catenin)was also analyzed. RESULTS AND CONCLUSION:Under compressive stress,the cell activity of endplate chondrocytes increased with both the duration and intensity of stress.Furthermore,the expression levels of Aggrecan and type Ⅱ collagen decreased in endplate cells under compressive stress,while those of calcification-related factors(Runx2 and osteocalcin)increased.Additionally,compressive stress promoted extracellular matrix degradation in endplate chondrocytes,leading to an increase in matrix metalloproteinase 3 and matrix metalloproteinase 13 expression.Abnormalities were observed in the Wnt/β-catenin signaling pathway within these cells under compressive stress,characterized by a decrease in specific inhibitory factor SOST expression accompanied by abnormal accumulation of β-catenin.To conclude,decreased SOST expression in endplate chondrocytes under compressive stress activates the Wnt/β-catenin signaling pathway,thereby promoting calcification,degeneration and extracellular matrix degradation in the cartilage endplate.