Objective:To explore the correlation between the semiquantitative score of bone ultrasound and the WOMAC OA index in knee osteoarthritis.Methods:From March 2017 to December 2018, 118 patients with knee osteoarthritis diagnosed and treated in Taizhou Hospital of Traditional Chinese Medicine were selected in the research.The patients' bone erosion, joint effusion, synovium hyperplasia and meniscus were evaluated by ultrasound semiquantitative scoring system.Osteoarthritis index of the patients was investigated at the same time.The correlation between the semiquantitative score of myoskeletal ultrasound and WOMAC OA index in knee osteoarthritis was analyzed.Results:In 118 patients with knee osteoarthritis, the semiquantitative scores of myoskeletal ultrasound of bone erosion was (2.33±0.37)points, joint effusion was (2.05±0.26)points, synovial hyperplasia was (2.24±0.15)points, abnormal meniscus position was (1.67±0.28)points, meniscus shape and signal was (1.15±0.14)points.The WOMAC OA index scores of patients' pain was (29.52±6.68)points, stiffness was (11.43±3.78)points, dysfunction was (93.85±18.73)points, and total score was (134.80±29.19)points.The scores of bone erosion, joint effusion, synovium hyperplasia and meniscus in semiquantitative score of muscle and bone ultrasound were positively correlated with the total score of WOMAC OA index( r=0.435, 0.317, 0.429, 0.294, 0.282, all P<0.05). Conclusion:Semiquantitative score of muscle and bone ultrasound can better reflect the degree of knee joint injury, which is positively correlated with WOMAC OA index.We can use the semiquantitative score of muscle and bone ultrasound and WOMAC OA index to predict the condition of patients with knee osteoarthritis.

OBJECTIVE To investigate the treatment plan for az treonam-resistant metallo- β-lactamase（MBL）-producing Enterobacteriaceae infection in pediatric solid organ transplant recipients. METHODS The clinical data of aztreonam-resistant MBL-producing Klebsiella pneumoniae caused intra-abdominal infection of an infant after liver transplantation were retrospectively analyzed. Abdominal infection occurred after operation. The pathogenic bacterium was MBL-producing K. pneumoniae . The drug sensitivity results showed that the infant was resistant to aztreonam. Based on the results of sensitivity test ，polymyxin B combined with tigecycline were selected as initial regimen. The treatment effect was poor ，with recurrent disease and shock spots. The clinical pharmacist assisted the clinician to formulate treatment regimen of ceftazidime avibactam 0.5 g，q8 h combined with aztreonam 0.18 g，q6 h. Relevant domestic and foreign literature were reviewed ，and the treatment plan of MBL-producing Enterobacteriaceae infection after solid organ transplantation was summarized. RESULTS & CONCLUSIONS The infant was finally cured and discharged with ceftazidime avibatan combined and aztreonam. Several foreign literature reported that ceftazidime avibactam combined with aztreonam could effectively treat the infection caused by aztreonam-resistant MBL-producing Enterobacteriaceae infection in patients with organ transplantation. It is expected to be an effective treatment for aztreonam-resistant MBL-producing Enterobacteriaceae infection in pediatric solid organ transplant recipients.

Many people affected by fragile X syndrome (FXS) and autism spectrum disorders have sensory processing deficits, such as hypersensitivity to auditory, tactile, and visual stimuli. Like FXS in humans, loss of Fmr1 in rodents also cause sensory, behavioral, and cognitive deficits. However, the neural mechanisms underlying sensory impairment, especially vision impairment, remain unclear. It remains elusive whether the visual processing deficits originate from corrupted inputs, impaired perception in the primary sensory cortex, or altered integration in the higher cortex, and there is no effective treatment. In this study, we used a genetic knockout mouse model (Fmr1^KO), in vivo imaging, and behavioral measurements to show that the loss of Fmr1 impaired signal processing in the primary visual cortex (V1). Specifically, Fmr1^KO mice showed enhanced responses to low-intensity stimuli but normal responses to high-intensity stimuli. This abnormality was accompanied by enhancements in local network connectivity in V1 microcircuits and increased dendritic complexity of V1 neurons. These effects were ameliorated by the acute application of GABA_A receptor activators, which enhanced the activity of inhibitory neurons, or by reintroducing Fmr1 gene expression in knockout V1 neurons in both juvenile and young-adult mice. Overall, V1 plays an important role in the visual abnormalities of Fmr1^KO mice and it could be possible to rescue the sensory disturbances in developed FXS and autism patients.
Animals ; Disease Models, Animal ; Fragile X Mental Retardation Protein/metabolism* ; Fragile X Syndrome/metabolism* ; Humans ; Mice ; Mice, Knockout ; Neurons/metabolism*