Arthroscopic physeal sparing all inside repair of the tibial avulsion fracture in the anterior cruciate ligament: technical note

We describe a new and effective arthroscopic physeal sparing repair of the tibial eminence avulsion fracture using all an inside repair technique. The treatment of ACL avulsion is controversial, especially in skeletally immature patients, with concerns about physeal damage, and a more reliable way of fixation is still being pursued for small or comminuted fragments. Screw fixation and suture cerclage has some limitations, especially in the small fragment or skeletally immature patients. We fixed avulsion fragment using all inside repair between the distal portion of the ACL and transverse ligament and periosteum. A crescent suture hook loaded with NO. 0 PDS is introduced and the suture hook pierces the transverse intermeniscal ligament and periosteum. The half length of the PDS is now advanced out through the hook and the end is brought out to the anterolateral portal. With the suture hook located intra-articularly and loaded with half the length of the original PDS, the suture hook repierces the transverse intermeniscal ligament at 5 mm on the side and the remaining half length of PDS is now advanced out through the hook and the end is brought out to the anterolateral portal. After that procedure, the suture hook loaded with NO. 0 absorbable Maxon is introduced through the anteromedial portal for the role of shuttle relay. The suture hook pierces the ACL just above the superior border of the avulsion fragment, the Maxon is now advanced out through the hook and the end is brought out to the anterolateral portal. Subsequently, the suture hook is removed and a suture retriever is introduced through the anterolateral portal. PDS and Maxon are held together and retrieved out of the anterolateral portal by the suture retriever at the same time. Our technique has advantages in small comminuted fractures and skeletally immature patients.     

Delayed presentation of arteriovenous fistula and pseudoaneurysms in a renal transplant patient 10 years after percutaneous allograft biopsy

A 51-year-old man was admitted with microscopic hematuria at 10 years after living donor renal transplantation. In order to distinguish between acute tubular necrosis and acute rejection, a graft biopsy was performed under ultrasound guidance at 1 month posttransplantation. Doppler sonography revealed 3 pulsatile cystic masses and an arteriovenous fistula (AVF) in the lower kidney pole. Selective transplant renal angiography revealed 3 pseudoaneurysms with an AVF supplied by a lobular artery in the lower pole. The diagnosis was AVF with pseudoaneurysm, which developed secondary to percutaneous renal allograft biopsy. Interventional treatment was performed because of the high risk for pseudoaneurysm rupture. The AVF and pseudoaneurysms were treated successfully by percutaneous transluminal embolization; renal function remained stable after embolization.     

Cyclosporine-induced renal injury induces toll-like receptor and maturation of dendritic cells

BACKGROUND: The toll-like receptor (TLR) is stimulated by not only pathogen-associated molecular patterns but also endogenous TLR ligands provided by injured cells. The influence of cyclosporine A (CsA)-induced renal injury on TLR expression and subsequent signaling pathway was evaluated. METHODS: Induction of chronic CsA nephropathy was made by administering CsA (15 mg/kg/day) for 28 days in rats. The TLR2 and TLR4 mRNA and protein expression, TLR-signaling pathway (MYD88, NF-kappaB and AP-1), putative TLR ligand (heat shock protein 70 [HSP70]), and maturation of dendritic cells were evaluated in CsA-treated rat kidneys. RESULTS: Long-term CsA treatment upregulated TLR2 and TLR4 mRNA and protein expression on renal tubular cells, and these were accompanied by increased MYD88, NF-kappaB and AP-1 expression. Putative TLR ligand (HSP70) was also significantly increased in CsA-treated rat kidney compared with vehicle-treated rat kidney. CsA-treatment increased expression of TNF-alpha mRNA, the number of dendritic cells, and expression of MHC class II antigen. Double-labeling of markers of dendritic cells and MHC class II antigen revealed that matured dendritic cells increased in CsA-treated rat kidney. CONCLUSIONS: CsA-induced renal injury stimulates components of innate immunity, and this finding suggests close association between CsA-induced renal injury and activation of innate immunity.     

Sirolimus inhibits platelet-derived growth factor-induced collagen synthesis in rat vascular smooth muscle cells

Vascular smooth muscle cell (VSMC) proliferation and extracellular matrix (ECM) accumulation play key roles in the development and the progression of vascular remodeling such as transplant arteriosclerosis and restenosis. The present study examined the effects of sirolimus (SRL) on platelet-derived growth factor (PDGF)-induced fibronectin secretion, collagen synthesis, and the related signaling pathways including reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPK) in rat VSMCs. Primary rat VSMCs were isolated from male Sprague-Dawley rats. Growth arrested, synchronized cells were treated with various concentrations of SRL before the addition of PDGF at 10 ng/mL. Proliferating cell nuclear antigen expression, fibronectin secretion, and the activation of extracellular signal-regulated protein kinase (ERK) and p38 MAPK were assessed by Western blot analysis, collagen synthesis by [(3)H]-proline incorporation, and cellular ROS by flow cytometry. PDGF (10 ng/mL) increased VSMC proliferation by 1.7-fold, fibronectin secretion by 1.5-fold, collagen synthesis by 2.1-fold, cellular ROS by 1.6-fold, and activation of ERK and p38 MAPK by 3.3- and 3.9-fold compared to controls. SRL above 1 nmol/L inhibited PDGF-induced VSMC proliferation and collagen synthesis but not PDGF-induced fibronectin secretion, cellular ROS, and activation of ERK and p38 MAPK. These data demonstrated that PDGF increased ECM synthesis as well as proliferation through cellular ROS and subsequent MAPK activation and that SRL inhibited PDGF-induced VSMC proliferation and collagen synthesis in a cellular ROS- and MAPK activation-independent way.     

The Surgical Treatment for Spinal Intradural Extramedullary Tumors

Background

We wanted to investigate the results of surgical treatment and analyze the factors that have an influence on the neurologic symptoms and prognosis of spinal intradural extramedullary (IDEM) tumors.

Methods

The spinal IDEM tumor patients (11 cases) who had been treated by surgical excision and who were followed up more than 1 year were retrospectively analyzed. Pain was evaluated by the visual analogue scale (VAS) and the neurologic function was assessed by Nurick''s grade. The pathological diagnosis, the preoperative symptom duration, the tumor location on the sagittal and axial planes and the percentage of tumor occupying the intradural space were investigated. In addition, all these factors were analyzed in relation to the degree of the preoperative symptoms and the prognosis. On the last follow-up, the MRI was checked to evaluate whether or not the tumor had recurred.

Results

The most common diagnosis was schwannomas (73%), followed by meningiomas (18%). The percentage of tumor occupying the intradural space was 82.9 ± 9.4%. The VAS score was reduced in all cases from 8.0 ± 1.2 to 1.2 ± 0.8 (p = 0.003) and the Nurick''s grade was improved in all cases from 3.0 ± 1.3 to 1.0 ± 0.0 (p = 0.005). The preoperative symptoms were correlated with only the percentage of tumor occupying the intradural space (VAS; r² = 0.75, p = 0.010, Nurick''s grade; r² = 0.69, p = 0.019). One case of schwannoma recurred.

Conclusions

The degree of neurologic symptoms was correlated with the percentage of tumor occupying the intradural space. All the tumors were able to be excised through the posterior approach. The postoperative neurologic recovery was excellent in all the cases regardless of any condition. Therefore, aggressive surgical excision is recommended even for cases with a long duration of symptoms or a severe neurologic deficit.     

Risk factors for adjacent segment disease after lumbar fusion

The incidence of adjacent segment problems after lumbar fusion has been found to vary, and risk factors for these problems have not been precisely verified, especially based on structural changes determined by magnetic resonance imaging. The purpose of this retrospective clinical study was to describe the incidence and clinical features of adjacent segment disease (ASD) after lumbar fusion and to determine its risk factors. We assessed the incidence of ASD in patients who underwent lumbar or lumbosacral fusions for degenerative conditions between August 1995 and March 2006 with at least a 1-year follow-up. Patients less than 35 years of age at the index spinal fusion, patients with uninstrumented fusion, and patients who had not achieved successful union were excluded. Of the 1069 patients who underwent fusions, 28 (2.62%) needed secondary operations because of ASD and were included in this study. In order to identify the risk factors, we matched a disease group and a control group. The disease group consisted of 26 of the 28 patients with ASD, excluding the 2 patients for whom we did not have initial MRI data. Each patient in the disease group was matched by age, sex, fusion level and follow-up period with a control patient. The assumed risk factors included disc and facet degeneration, instability, listhesis, rotational deformity, and disc wedging. The mean age of the 28 patients with ASD requiring surgical treatment was 58.4 years, which did not differ significantly from that of the population in which ASD did not develop (58.2 years, p = 0.894). Of the 21 patients who underwent floating fusion, only 1 developed distal ASD. Facet degeneration was a significant risk factor (p < 0.01) on logistic regression analysis. The incidence of distal ASD was much lower than that of proximal ASD. Pre-existing facet degeneration may be associated with a high risk of adjacent segment problems following lumbar fusion procedures.     

PCGEM1 stimulates proliferation of osteoarthritic synoviocytes by acting as a sponge for miR‐770

Long non‐coding RNAs (lncRNAs) have been reported to play important roles in cellular metabolism and development. Various diseases have been associated with aberrant expression of lncRNAs and the related dysregulation of mRNAs. An lncRNA profiling assay was carried out to identify the key lncRNA in osteoarthritic human synoviocytes; the results revealed that prostate cancer gene expression marker 1 (PCGEM1) was significantly overexpressed in osteoarthritic synoviocytes. Exogenous overexpression of PCGEM1 inhibited apoptosis, induced autophagy, and stimulated the proliferation of human synoviocytes. The increased expression of PCGEM1 in human synoviocytes also suppressed the expression of miR‐770. Transfection of the miR‐770 precursor resulted in reduced proliferation, and induced apoptosis of human synoviocytes. This effect of miR‐770 expression was reversed by co‐introduction of PCGEM1. Target validation showed a direct binding between PCGEM1 and miR‐770. We demonstrate that PCGEM1 act as sponge lncRNA for miR‐770 that regulates proliferation/apoptosis and autophagy, and suggest PCGEM1 as possible target for OA therapy. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:412–418, 2016.     

Expression of cubilin in mouse testes and Leydig cells

Cubilin (cubn) is a receptor for vitamins and various protein ligands. Cubn lacks a transmembrane domain but anchors to apical membranes by forming complexes with Amnionless or Megalin. In an effort to better understand the uptake of nutrients in testis, we analysed cubn expression in the developing mice testes. In testes, cubn mRNA increased from birth to adulthood. In the inter‐stitium and isolated seminiferous tubules, neonatal increase in cubn mRNA until 14 days post‐partum (pp) was followed by a marked increase at puberty (28 days pp). Cubn was found in the gonocytes, spermatogonia, spermatocytes and spermatids in the developing testes. In adult testes, strong Cubn immunoreactivity was found in the elongating spermatids, suggesting the role of Cubn in endocytosis during early spermiogenesis. In Sertoli cells and peritubular cells, Cubn immunoreactivity was weak throughout the testis development. In the inter‐stitium, Cubn immunoreactivity was found in foetal Leydig cells, was weak to negligible in the stem cells and progenitor Leydig cells and was strong in immature and adult Leydig cells, demonstrating a positive association between Cubn and steroidogenic activity of Leydig cells. Collectively, these results suggest that Cubn may participate in the endocytotic uptake of nutrients in germ cells and somatic cells, supporting the spermatogenesis and steroidogenesis in mouse testes.     

Does obesity affect time to extubation in “fast track” cabg surgery?

Canadian Journal of Anesthesia/Journal canadien d'anesthésie -