The most severe sequelae after rehabilitation from SARS are femoral head necrosis and pulmonary fibrosis. We performed a 15-year follow-up on the lung and bone conditions of SARS patients. We evaluated the recovery from lung damage and femoral head necrosis in an observational cohort study of SARS patients using pulmonary CT scans, hip joint MRI examinations, pulmonary function tests and hip joint function questionnaires. Eighty medical staff contracted SARS in 2003. Two patients died of SARS, and 78 were enrolled in this study from August 2003 to March 2018. Seventy-one patients completed the 15-year follow-up. The percentage of pulmonary lesions on CT scans diminished from 2003 (9.40 ± 7.83)% to 2004 (3.20 ± 4.78)% (P < 0.001) and remained stable thereafter until 2018 (4.60 ± 6.37)%. Between 2006 and 2018, the proportion of patients with interstitial changes who had improved pulmonary function was lower than that of patients without lesions, as demonstrated by the one-second ratio (FEV 1 /FVC %, t = 2.21, P = 0.04) and mid-flow of maximum expiration (FEF 25%-75% , t = 2.76, P = 0.01). The volume of femoral head necrosis decreased significantly from 2003 (38.83 ± 21.01)% to 2005 (30.38 ± 20.23)% (P = 0.000 2), then declined slowly from 2005 to 2013 (28.99 ± 20.59)% and plateaued until 2018 (25.52 ± 15.51)%. Pulmonary interstitial damage and functional decline caused by SARS mostly recovered, with a greater extent of recovery within 2 years after rehabilitation. Femoral head necrosis induced by large doses of steroid pulse therapy in SARS patients was not progressive and was partially reversible.Bone Research (2020) 8:8; https://doi.

Background Severe acute respiratory syndrome (SARS) broke out in China and spread to all over the world in 2003. Without comprehensive protection, during a severe hospital outbreak in the Peking University People's Hospital (PKUPH), there were 78 patients diagnosed with SARS and two deaths. During treatment, most patients received large doses of steroid shock therapy, which may result in complications of femoral head necrosis and pulmonary fibrosis. We aimed to follow up the condition of lung and bone in those patients. MethodsWe did an observational cohort study of patients with SARS from 2003 to 2018. We carried out pulmonary CT scans, hip joint MRI tests, pulmonary function tests, and hip joint functional assessment to evaluate the recovery condition of lung damage and femoral head necrosis according to patients' willingness. We used linear regression, and mixed-model repeated-measures analysis to measure the change of lung interstitial and femoral head necrosis volume. This study was authorised by the Ethics Committee of Peking University People's Hospital (2018PHB010-01). All recruited SARS patients signed informed consent for the study. This study is registered with ClinicalTrials.gov, number NCT03443102. FindingsThere were 80 medical staff patients with SARS altogether in Peking University People's Hospital. Two patients died of SARS in 2003 and 78 patients were enrolled in this study from August, 2003, to March, 2018. 71 patients completed the 15 years' follow-up and seven patients were missing. Pulmonary injury scope on lung CT improved from 2003 (9·40%, SD 7·83) to 2004 (3·20%, 4·78; p≤0·001), and thereafter remained steady to 2018 (4·60%, 6·37). Pulmonary function items in patients with SARS did not differ between 2006 and 2018. The recovery extent of pulmonary function items between 2006 and 2018 in patients with lung interstitial change (n=13), was less than that without lung interstitial changes (n=23), especially in one-second ratio (FEV1/FVC, t=2·21, p=0·04) and mid-flow of maximum expiration (FEF25-75%, t=2·76, p=0·01). The volume of femoral head necrosis decreased significantly from 2003 (38·83%, SD 21·01) to 2005 (30·38%, 20·23; p=0·0002), then decreased slowly from 2005 to 2013 (28·99%, 20·59) and thereafter remained steady to 2018 (25·52%, 15·51)%.Interpretation Damaged lung interstitial and functional decline induced by SARS mainly recovered in the next 1-2 years after rehabilitation. The natural process of femoral head necrosis caused by large doses of steroid shock therapy in SARS patients was not progressive, while partially reversible.

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For all 102 cases of ankle joint fracture involving the posterior malleolus, the treatment effect was satisfactory. Restoration of an even articular surface, especially when fragment size ≥ 25 %, should be attempted during treatment.

Currently, diabetic infectious wound treatments remain a significant challenge for regenerative medicine due to the unicity of clinical dressings, which lack systemic multifunctional wound dressings with high absorbability, customizable shape, rapid self-healing, guiding tissue regeneration, and restoring physiological functions. Here, a multi functional DNA hydrogel is conveniently obtained through grafting DNA units and polyethyleneimine dynamic cross-linking and doped heating function black phosphorus quantum dots. The obtained DNA hydrogel features excellent exudate absorption performance, adjustable heating ability, mechanical behavior, self-healing ability, writability, tissue adhesion, and antibacterial properties. The incorporation of procyanidin B2 (OPC B2) endows the DNA hydrogels with renowned scavenging free radicals and antioxidant properties. Furthermore, the DNA hydrogel dressing can promote the transformation of macrophages from pro-inflammatory M1 into repairing M2 phenotype, keeping the wound in a stable remodeled state. Astonishingly, the DNA hydrogel dressing can activate neurons to transform into a repair state, accelerating skin nerve regeneration and angiogenesis. Beyond that, it can recruit myeloid cells to activate the adaptive immune response, enhancing the ability of DNA hydrogel dressing to promote tissue regeneration, thereby promoting hair follicle and hair regeneration. Therefore, this advanced collaborative strategy provides an effective method for cascade management of clinical guided tissue regeneration.

Peripheral nerve injury (PNI) usually leads to progressive muscle atrophy and poor functional recovery. Previous studies have demonstrated that non-coding ribonucleic acid (ncRNA) is a key regulator of muscle atrophy and beneficial for the treatment of PNI. We aimed to analyze the whole transcriptome involved in denervated muscle atrophy after PNI. Animal models of sciatic nerve injury were assessed at 0 (control group), 1, 2, 4, and 8 weeks after injury. The expression patterns in the whole transcriptome in the gastrocnemius muscle were profiled using RNA sequencing at each time point and compared to that obtained in the control group. Six-hundred and sixty-four long non-coding RNAs, 671 microRNAs, 236 circular RNAs, and 12,768 messenger RNAs (mRNAs) were differentially expressed (DE) after injury. Changes in some of the DE ncRNAs and mRNAs were validated using quantitative polymerase chain reaction. Gene Ontology and Kyoko Encyclopedia of Genes and Genomes analysis revealed the potential functions of and relationships among the DE ncRNAs and mRNAs. To our knowledge, this is the first study to expound the whole transcriptome involved in denervated muscle atrophy, and provides a theoretical basis for further research targeting ncRNAs.

At present, repair methods for peripheral nerve injury often fail to get satisfactory result. Although various strategies have been adopted to investigate the microenvironment after peripheral nerve injury, the underlying molecular mechanisms of neurite outgrowth remain unclear. In this study, we evaluate the effects of exosomes from gingival mesenchymal stem cells (GMSCs) combined with biodegradable chitin conduits on peripheral nerve regeneration. GMSCs were isolated from human gingival tissue and characterized by surface antigen analysis and in vitro multipotent differentiation. The cell supernatant was collected to isolate the exosomes. The exosomes were characterized by transmission electron microscopy, Western blot, and size distribution analysis. The effects of exosomes on peripheral nerve regeneration in vitro were evaluated by coculture with Schwann cells and DRGs. The chitin conduit was prepared and combined with the exosomes to repair rat sciatic nerve defect. Histology, electrophysiology, and gait analysis were used to test the effects of exosomes on sciatic nerve function recovery in vivo. We have successfully cultured GMSCs and isolated exosomes. The exosomes from GMSCs could significantly promote Schwann cell proliferation and DRG axon growth. The in vivo studies showed that chitin conduit combined with exosomes from GMSCs could significantly increase the number and diameter of nerve fibers and promote myelin formation. In addition, muscle function, nerve conduction function, and motor function were also obviously recovered. In summary, this study suggests that GMSC-derived exosomes combined with biodegradable chitin conduits are a useful and novel therapeutic intervention in peripheral nerve repair.

In humeri with normal alignment, calcar screws can provide additional stability even when a medial deficiency exists. The use of calcar screws in humeri with varus deformity showed no biomechanical superiority.