Characterizing the need for tracheostomy placement and decannulation after cervical spinal cord injury

Purpose

There have been few reports on the risk factors for tracheostomy and the possibility of patients for decannulation. The purpose of this study was to identify factors necessitating tracheostomy after cervical spinal cord injury (SCI) and detect features predictive of successful decannulation in tracheostomy patients.

Methods

One hundred and sixty four patients with cervical fracture/dislocation were retrospectively reviewed. The patients comprised 142 men and 22 women with a mean age of 44.9 years. The clinical records were reviewed for patients’ demographic data, smoking history, level of cervical spine injury, injury patterns, neurological status, evidence of direct thoracic trauma and head injury, tracheostomy placement, and decannulation. Risk factors necessitating tracheostomy and factors predicting decannulation were statistically analysed.

Results

Twenty-five patients (15.2 %) required tracheostomy. Twenty-one patients were successfully decannulated. Smoking history (relative risk [RR], 3.05; p = 0.03) and complete SCI irrespective of injury level (C1–4 complete SCI: RR, 67.55; p < 0.001, C5–7 complete SCI: RR, 57.88; p < 0.001) were significant risk factors necessitating tracheostomy. C1–4 complete SCI was more frequent among those who could not be decannulated. However, even in patients with high cervical complete SCI at the time of injury, patients regaining sufficient movement to shrug their shoulders within 3 weeks after injury could later be decannulated.

Conclusions

The risk factors for tracheostomy after complete SCI were a history of smoking and complete paralysis irrespective of the level of injury. High cervical level complete SCI was found to be a risk factor for the failure of decannulation in patients without shoulder shrug within 3 weeks after injury.     

Increased expression and activation of cathepsin K in human osteoarthritic cartilage and synovial tissues

Few studies have analyzed Cathepsin K (CatK) expression in human osteoarthritic tissues. We investigated CatK expression and activation in human articular cartilage using clinical specimens. Human osteoarthritic cartilage was obtained during surgery of total hip arthroplasty (n = 10), and control cartilage was from that of femoral head replacement for femoral neck fracture (n = 10). CatB, CatK, CatL, CatS, and Cystatin C (CysC) expressions were evaluated immunohistochemically and by real‐time PCR. Intracellular CatK protein was quantified by ELISA. Intracellular CatK activity was also investigated. Osteoarthritis (OA) chondrocytes were strongly stained with CatK, particularly in the superficial layer and more damaged areas. CatB, CatL, CatS, and CysC were weakly stained. CatK mRNA expression was significantly higher in OA group compared to that in control group (p = 0.043), whereas those of CatB, CatL, CatS, and CysC did not differ significantly. Mean CatK concentration (4.83 pmol/g protein) in OA chondrocytes was higher than that (3.91 pmol/g protein) in control chondrocytes (p = 0.001). CatK was enzymatically more activated in OA chondrocytes as compared with control chondrocytes. This study, for the first time, revealed increased CatK expression and activation in human OA cartilage, suggesting possible crucial roles for it in the pathogenesis of osteoarthritic change in articular cartilage. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:127–134, 2016.     

Identification of physical and psychosocial problems associated with diabetic nephropathy using the International Classification of Functioning,Disability and Health Core Set for Diabetes Mellitus

Background

We previously demonstrated validation of the Comprehensive International Classification of Functioning, Disability and Health Core Set for Diabetes Mellitus (ICF-CS for DM) in patients with diabetic nephropathy (DMN). The objective of the present study was to identify differences in experience of physical and psychosocial problems between DMN patients with and without hemodialysis (HD), and diabetes patients without nephropathy using the ICF-CS for DM.

Methods

A total of 302 diabetes outpatients (men, 68 %; mean age, 62 years) were interviewed using four components of the ICF-CS for DM including “Body functions”, “Body structures”, “Activities and participation”, and “Environmental factors”.

Results

The mean number of categories in which difficulty was experienced in the four components was significantly greater in DMN patients with HD followed by DMN patients without HD, and diabetes patients without nephropathy (23.9 vs. 18.0 vs. 13.1, respectively). Multivariate logistic regression models revealed that, compared with diabetes patients without nephropathy, diabetes patients with nephropathy were more likely to have difficulty with physical problems and social activities and participation. Among DMN patients, dialysis patients were found to have larger numbers of problems, and face difficulty with employment status after adjusting for sex, age, type, and duration of diabetes.

Conclusion

The results of this study using the ICF-CS for DM identified the areas for improvement among physical and psychosocial problems in DMN patients with and without HD in contrast to diabetes patients without nephropathy.

     

Bcl10 is phosphorylated on Ser138 by Ca2+/calmodulin-dependent protein kinase II

Ordered assembly of scaffold proteins Carma1-Bcl10-Malt1 determines NF-kappaB activation following T cell receptor (TCR) engagement. Carma1-Bcl10 interaction and the signaling pathway are controlled by Carma1 phosphorylation, which are induced by PKCtheta and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). In addition to Carma1 phosphorylation, previous studies have demonstrated that Bcl10 is phosphorylated in the C-terminal Ser/Thr rich region following TCR engagement. However the kinases that phosphorylate Bcl10 are incompletely understood. Here we show that CaMKII phosphorylates Bcl10 on Ser138. Furthermore, a CaMKII inhibitor, KN93, and CaMKII siRNA substantially reduce Bcl10 phosphorylation induced by phorbol myristate acetate/ionomycin. S138A mutation prolongs Bcl10-induced NF-kappaB activation, suggesting that Bcl10 phosphorylation is involved in attenuation of NF-kappaB activation. These findings suggest that CaMKII modulates NF-kappaB activation via phosphorylating Bcl10 as well as Carma1.