The BET PROTAC inhibitor dBET6 protects against retinal degeneration and inhibits the cGAS-STING in response to light damage.

BACKGROUND: Chronic inflammation significantly contributes to photoreceptor death in blinding retinal diseases such as age-related macular degeneration (AMD) and retinitis pigmentosa (RP). Bromodomain and extraterminal domain (BET) proteins are epigenetic readers that act as key proinflammatory factors. We recently found the first-generation BET inhibitor JQ1 alleviated sodium iodate-induced retinal degeneration by suppressing cGAS-STING innate immunity. Here, we investigated the effects and mechanism of dBET6, a proteolysis­targeting chimera (PROTAC) small molecule that selectively degrades BET by the ubiquitin‒proteasome system, in light-induced retinal degeneration. METHODS: Mice were exposed to bright light to induce retinal degeneration, and the activation of cGAS-STING was determined by RNA-sequencing and molecular biology. Retinal function, morphology, photoreceptor viability and retinal inflammation were examined in the presence and absence of dBET6 treatment. RESULTS: Intraperitoneal injection of dBET6 led to the rapid degradation of BET protein in the retina without detectable toxicity. dBET6 improved retinal responsiveness and visual acuity after light damage (LD). dBET6 also repressed LD-induced retinal macrophages/microglia activation, Müller cell gliosis, photoreceptor death and retinal degeneration. Analysis of single-cell RNA-sequencing results revealed cGAS-STING components were expressed in retinal microglia. LD led to dramatic activation of the cGAS-STING pathway, whereas dBET6 suppressed LD-induced STING expression in reactive macrophages/microglia and the related inflammatory response. CONCLUSIONS: This study indicates targeted degradation of BET by dBET6 exerts neuroprotective effects by inhibiting cGAS-STING in reactive retinal macrophages/microglia, and is expected to become a new strategy for treatment of retinal degeneration.

Treating open tibular fracture (Type gustillo IIIA) with medullary nail assisted by cortex screws: A case report.

BACKGROUND: Open fractures of the tibia are mostly caused by high-energy injuries, accompanied by severe soft tissue injuries. Staged operations are reported performing better prognosis in these cases. CASE SUMMARY: The author reports a case of open comminuted fracture of the left tibia (GustilloIIIA) and discusses its clinical features and treatment experience with the literature. The patient was admitted to our hospital by an ambulance for half an hour due to pain in her left leg caused by a car collision on an electric bike. During hospitalization, external fixation and an intramedullary nail were sequential used. CONCLUSION: The case report suggests that cortex screws are likely benefit the prognosis of severe open tibial fracture.

PSKH1 affects proliferation and invasion of osteosarcoma cells via the p38/MAPK signaling pathway.

Malignant osteosarcoma (OS) is a tumor of bone and soft tissue that metastasizes early and has a high mortality rate. Protein serine kinase H1 (PSKH1), an autophosphorylating human protein serine kinase, controls the trafficking of serine/arginine-rich domain, with downstream effects on mRNA processing. It is also associated with tumor progression. However, how this protein contributes to OS progression and metastasis is unknown. The present study evaluated the potential effect of PSKH1 on proliferation of human OS cells. OS cell lines were used in Cell Counting Kit-8, colony formation, wound-healing and Transwell assays, to investigate cellular processes such as proliferation, migration and invasion and underlying molecular mechanisms. Expression of PSKH1 in OS tissue was significantly greater than in adjacent non-malignant tissue. PSKH1 knockdown inhibited the proliferation, migration and invasion of OS cells. Conversely, PSKH1 overexpression promoted proliferation of OS cells. PSKH1 upregulated phosphorylated-p38 in OS cells. Moreover, the p38 MAPK inhibitor SB203580 effectively blocked the tumor-promoting action of PSKH1. Furthermore, PSKH1 knockdown inhibited tumor growth and metastasis in vivo. In conclusion, these findings suggested that PSKH1 promoted OS proliferation, migration and invasion. Thus, PSKH1 may serve an oncogenic role in the development of human OS.

Light damage induces inflammatory factors in mouse retina and vitreous humor.

Purpose: Increased inflammatory factor levels have been reported in the vitreous humor (VH) of diabetic retinopathy and neovascular age-related macular degeneration, ocular diseases generally associated with the formation of new retinal blood vessels and leakage. However, the levels of inflammatory mediators are less known in retinal degeneration without neovascularization. Human retinitis pigmentosa (RP) and animal models of light-induced retinal degeneration (LIRD) share several features, such as photoreceptor death and retinal inflammation. Here, we aimed to determine the levels of inflammatory factors in the VH of the LIRD mouse model. Methods: LIRD was induced by exposing BALB/c mice to white light (15,000 lx, 2 h), and the mice were recovered for 2 days before analysis (n = 50 mice). We assessed retinal morphology using optical coherence tomography and hematoxylin and eosin staining; retinal cell viability was determined using terminal deoxynucleotidyl transferase dUTP nick-end labeling, and retinal responses were measured based on electroretinogram signals. Total retinal RNAs were extracted and subjected to RNA sequencing analysis. VH samples from control (n = 4) and LIRD mice (n = 9) were assayed in triplicate for a panel of four inflammatory mediators using the Simple Plex Cartridge on an Ella System. Results: Retinal degeneration, photoreceptor death, infiltration of microglia/macrophages into the photoreceptor layer, and loss of a- and b-waves were obviously detected after LIRD. RNA sequencing revealed that light damage (LD) led to the significant upregulation of inflammatory factors in mouse retinas. In the VH, LD increased the total protein concentration. Dramatic induction of CCL2 (~3000 fold) and IL6 (~10 fold) was detected in VH in response to LD. Increased but not significant levels of TNFα and IL1ß were also detected in light-exposed VH. Conclusions: Given that the LIRD model mimics RP pathogenesis in some aspects, these results suggest a causative link between retinal degeneration and VH inflammation in RP progression, and the increased CCL2 level in VH may reflect similar elevated CCL2 expression in the degenerative retina.

Multinucleated Retinal Pigment Epithelial Cells Adapt to Vision and Exhibit Increased DNA Damage Response.

Multinucleated retinal pigment epithelium (RPE) cells have been reported in humans and other mammals. Rodents have an extremely high percentage of multinucleated cells (more than 80%). Both mouse and human multinucleated RPE cells exhibit specific regional distributions that are potentially correlated with photoreceptor density. However, detailed investigations of multinucleated RPE in different species and their behavior after DNA damage are missing. Here, we compared the composition of multinucleated RPE cells in nocturnal and diurnal animals that possess distinct rod and cone proportions. We further investigated the reactive oxygen species (ROS) production and DNA damage response in mouse mononucleated and multinucleated RPE cells and determined the effect of p53 dosage on the DNA damage response in these cells. Our results revealed an unrealized association between multinucleated RPE cells and nocturnal vision. In addition, we found multinucleated RPE cells exhibited increased ROS production and DNA damage after X-ray irradiation. Furthermore, haploinsufficiency of p53 led to increased DNA damage frequency after irradiation, and mononucleated RPE cells were more sensitive to a change in p53 dosage. In conclusion, this study provides novel information on in vivo PRE topography and the DNA damage response, which may reflect specific requirements for vision adaption and macular function.

Temporal and spatial cellular and molecular pathological alterations with single-cell resolution in the adult spinal cord after injury.

Spinal cord injury (SCI) involves diverse injury responses in different cell types in a temporally and spatially specific manner. Here, using single-cell transcriptomic analyses combined with classic anatomical, behavioral, electrophysiological analyses, we report, with single-cell resolution, temporal molecular and cellular changes in crush-injured adult mouse spinal cord. Data revealed pathological changes of 12 different major cell types, three of which infiltrated into the spinal cord at distinct times post-injury. We discovered novel microglia and astrocyte subtypes in the uninjured spinal cord, and their dynamic conversions into additional stage-specific subtypes/states. Most dynamic changes occur at 3-days post-injury and by day-14 the second wave of microglial activation emerged, accompanied with changes in various cell types including neurons, indicative of the second round of attacks. By day-38, major cell types are still substantially deviated from uninjured states, demonstrating prolonged alterations. This study provides a comprehensive mapping of cellular/molecular pathological changes along the temporal axis after SCI, which may facilitate the development of novel therapeutic strategies, including those targeting microglia.

Inhibition of cGAS-STING by JQ1 alleviates oxidative stress-induced retina inflammation and degeneration.

Atrophic ("dry") form of age-related macular degeneration (AMD) is a leading cause of vision loss characterized by macular retinal pigment epithelium (RPE) and the ensuing photoreceptor degeneration. cGAS-STING signaling is a key cytosolic DNA sensor system in innate immunity and have recently been shown promotes RPE degeneration. However, expression regulation and therapeutic potential of cGAS and STING are not explored in retina under dry AMD pathogenic conditions. Our analysis shows upregulated STING RNA and increased chromatin accessibility around cGAS and STING promoters in macular retinas from dry AMD patients. cGAS-STING activation was detected in oxidative stress-induced mouse retina degeneration, accompanied with cytosolic leakage of damaged DNA in photoreceptors. Pharmaceutical or genetic approaches indicates STING promotes retina inflammation and degeneration upon oxidative damage. Drug screening reveals that BRD4 inhibitor JQ1 reduces cGAS-STING activation, inflammation and photoreceptor degeneration in the injured retina. BRD4 inhibition epigenetically suppresses STING transcription, and promotes autophagy-dependent cytosolic DNA clearance. Together, our results show that activation of cGAS-STING in retina may present pivotal innate immunity response in GA pathogenesis, whereas inhibition of cGAS-STING signaling by JQ1 could serve as a potential therapeutic strategy.

MYPT1/PP1-Mediated EZH2 Dephosphorylation at S21 Promotes Epithelial-Mesenchymal Transition in Fibrosis through Control of Multiple Families of Genes.

The methyltransferase EZH2 plays an important role in regulating chromatin conformation and gene transcription. Phosphorylation of EZH2 at S21 by AKT kinase suppresses its function. However, protein phosphatases responsible for the dephosphorylation of EZH2-S21 remain elusive. Here, it is demonstrated that EZH2 is highly expressed in the ocular lens, and AKT-EZH2 axis is important in TGFß-induced epithelial-mesenchymal transition (EMT). More importantly, it is identified that MYPT1/PP1 dephosphorylates EZH2-S21 and thus modulates its functions. MYPT1 knockout accelerates EMT, but expression of the EZH2-S21A mutant suppresses EMT through control of multiple families of genes. Furthermore, the phosphorylation status and gene expression modulation of EZH2 are implicated in control of anterior subcapsular cataracts (ASC) in human and mouse eyes. Together, the results identify the specific phosphatase for EZH2-S21 and reveal EZH2 dephosphorylation control of several families of genes implicated in lens EMT and ASC pathogenesis. These results provide important novel information in EZH2 function and regulation.

Locking compression plate + T-type steel plate for postoperative weight bearing and functional recovery in complex tibial plateau fractures.

BACKGROUND: Complex tibial plateau fractures can seriously affect quality of life and physical and mental health of patients. The anatomical relationship between the proximal tibial bone and soft tissue is complex, resulting in different types of tibial plateau fractures. Violent trauma can lead to displaced fracture, serious soft tissue injury, and potentially, dislocation of the knee joint. Therefore, tibial plateau fractures are extremely unstable. AIM: To assess the use of locking compression plate (LCP) + T-type steel plate for postoperative weight bearing and functional recovery of complex tibial plateau fractures. METHODS: Ninety-seven patients with complex tibial plateau fractures who underwent surgery at our hospital were selected for retrospective study. Forty-nine patients had been treated with LCP + T-type steel plate limited internal fixation (study group), and 48 patients with bilateral ordinary steel plate support (control group). The operation process index, postoperative rehabilitation related index, Rasmussen score of the knee joint, tibial plateau varus angle (TPA), tibial plateau retroversion angle (PA), and surgical complications of the two groups were compared. RESULTS: The operation time and intraoperative bone graft volume in the study group were lower than those in the control group (P < 0.05). There were no significant differences in surgical bleeding, anterior external incision length, postoperative drainage, hospital stay duration, and fracture healing time between the groups (P > 0.05). There was no significant difference in the TPA and PA angle between the groups immediately and 18 mo after surgery (P > 0.05). At 12 mo after surgery, the Rasmussen scale score was higher in the study group than in the control group (P < 0.05). There was no significant difference in the Rasmussen scale score at 18 mo after surgery, and the radiology score at 12 and 18 mo after surgery, between the two groups (P > 0.05). The postoperative complication rate in the study group (3.77%) was lower than that in the control group (15.09%; P < 0.05). CONCLUSION: LCP + T-type steel plate internal fixation has advantages in terms of minimizing trauma and enabling early postoperative functional exercise, promoting functional recovery and lower limb weight-bearing, and reducing postoperative complications.

Heterochromatin inhibits cGAS and STING during oxidative stress-induced retinal pigment epithelium and retina degeneration.

Age-related macular degeneration (AMD) is a leading cause of blindness characterized by degeneration of retina pigment epithelium (RPE) and photoreceptors in the macular region. Activation of the innate immune cGAS-STING signaling has been detected in RPE of dry AMD patients, but the regulatory basis is largely unexplored. Heterochromatin is a highly compact, transcription inert chromatin status. We have recently shown that heterochromatin is required for RPE survival through epigenetically silencing p53-mediated apoptosis signaling. Here, we found that cGAS and STING were dose-dependently upregulated in mouse RPE and retina during oxidative injury, correlated with decreased chromatin compaction in their gene loci. Genetic or pharmaceutical disruption of heterochromatin leads to elevated cGAS and STING expression and enhanced inflammatory response in oxidative stress-induced RPE and retina degeneration. In contrast, application of methotrexate (MTX), a recently identified heterochromatin-promoting drug, inhibits cGAS and STING in both RPE and retina, attenuates RPE/retina degeneration and inflammation. Further, we show that intact heterochromatin is required for MTX to repress cGAS and STING. Together, we demonstrated an unrevealed regulatory function of heterochromatin on cGAS and STING expression and provide potential new therapeutic strategy for AMD treatment.

Immunomodulatory Layered Double Hydroxide Nanoparticles Enable Neurogenesis by Targeting Transforming Growth Factor-ß Receptor 2.

Immune microenvironment amelioration and reconstruction by functional biomaterials has become a promising strategy for spinal cord injury (SCI) recovery. In this study, we evaluated the neural regeneration and immunoregulation functions of Mg/Al layered double hydroxide (Mg/Al-LDH) nanoparticles in completely transected and excised mice and revealed the immune-related mechanisms. LDH achieved significant performance in accelerating neural stem cells (NSCs) migration, neural differentiation, L-Ca2+ channel activation, and inducible action potential generation. In vivo, the behavioral and electrophysiological performance of SCI mice was significantly improved by LDH implantation, with BrdU+ endogenous NSCs and neurons clearly observed in the lesion sites. According to RNA-seq and ingenuity pathway analysis, transforming growth factor-ß receptor 2 (TGFBR2) is the key gene through which LDH inhibits inflammatory responses and accelerates neural regeneration. Significant colocalization of TGFBR2 and LDH was found on the cell membranes of NSCs both in vitro and in vivo, and LDH increased the expression of TGF-ß2 in NSCs and activated the proliferation of precursor neural cells. LDH decreased the expression of M1 markers and increased the expression of M2 markers in both microglia and bone marrow-derived macrophages, and these effects were reversed by a TGFBR2 inhibitor. In addition, as a carrier, LDH loaded with NT3 exhibited better recovery effects with regard to the basso mouse scale score, motor evoked potential performance, and regenerated neural cell numbers than LDH itself. Thus, we have developed Mg/Al-LDH that can be used to construct a suitable immune microenvironment for SCI recovery and have revealed the targeted receptor.

A mouse model of complete-crush transection spinal cord injury made by two operations.

BACKGROUND: More and more studies have focused on the treatment of spinal cord injury (SCI) by tissue engineering, but there is still no ideal animal model that can genuinely and objectively simulate the real pathological process in clinical practice. Also, given the increasing availability and use of genetically modified animals in basic science research, it has become essential to develop clinically related models for SCI for use in mice. METHODS: Forty-eight C57BL/6 mice were divided into three groups (injured/sham/uninjured). We determined the scar range made by the first crush injury by specimen observation, hematoxylin and eosin (HE) staining, and immunofluorescence staining. Transection to completely remove a 2-mm spinal cord segment centered on the lesion core was completed 6 weeks after the first injury in injured groups, whereas the sham group only underwent re-exposure of the spinal cord without transection injury. The characteristics of this SCI model were fully ascertained by specimen observation, HE staining, immunofluorescence staining, and quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: No mice died after the first injury. Histopathological findings suggested a scar range of 2 mm. After the second operation, 2 mice of the injured group and 1 mouse of the sham group died. The Basso Mouse Scale (BMS) score and motor evoked potential (MEP) results showed that the neurological function of mice did not recover. Immunostaining showed that there were no neurons or neurofilament residues in the lesion core 4 weeks after the second injury. Astrocytes encapsulated immune cells to form dense glial scars. Most immune cells were confined to the core of the lesion and formed fibrous scars with the fibroblasts. At the same time, there was considerable angiogenesis in the lesion core and around the injury. The results of qRT-PCR showed that Ptprc was highly expressed in the lesion core, while Gfap, nestin, Cnp, and Sv2b were highly expressed in the adjacent region. This suggests that the lesion core is a highly inflammatory zone, but there may be spontaneous neurogenesis adjacent to the lesion core. CONCLUSIONS: The mouse crash-complete transection SCI model made by the two operations has good simulation, high feasibility, and high reproducibility; it will be a useful tool for pre-clinical testing of SCI treatment.

Unbiased transcriptomic analyses reveal distinct effects of immune deficiency in CNS function with and without injury.

The mammalian central nervous system (CNS) is considered an immune privileged system as it is separated from the periphery by the blood brain barrier (BBB). Yet, immune functions have been postulated to heavily influence the functional state of the CNS, especially after injury or during neurodegeneration. There is controversy regarding whether adaptive immune responses are beneficial or detrimental to CNS injury repair. In this study, we utilized immunocompromised SCID mice and subjected them to spinal cord injury (SCI). We analyzed motor function, electrophysiology, histochemistry, and performed unbiased RNA-sequencing. SCID mice displayed improved CNS functional recovery compared to WT mice after SCI. Weighted gene-coexpression network analysis (WGCNA) of spinal cord transcriptomes revealed that SCID mice had reduced expression of immune function-related genes and heightened expression of neural transmission-related genes after SCI, which was confirmed by immunohistochemical analysis and was consistent with better functional recovery. Transcriptomic analyses also indicated heightened expression of neurotransmission-related genes before injury in SCID mice, suggesting that a steady state of immune-deficiency potentially led to CNS hyper-connectivity. Consequently, SCID mice without injury demonstrated worse performance in Morris water maze test. Taken together, not only reduced inflammation after injury but also dampened steady-state immune function without injury heightened the neurotransmission program, resulting in better or worse behavioral outcomes respectively. This study revealed the intricate relationship between immune and nervous systems, raising the possibility for therapeutic manipulation of neural function via immune modulation.

The visible and hidden blood loss of Asia proximal femoral nail anti-rotation and dynamic hip screw in the treatment of intertrochanteric fractures of elderly high- risk patients: a retrospective comparative study with a minimum 3 years of follow-up.

BACKGROUND: The purpose of this study was to evaluate whether PFNA-II (Asia proximal femoral nail anti-rotation) and DHS (dynamic hip screw) carry substantial post-operative hidden blood loss and to compare PFNA-II with DHS in terms of post-operative hidden blood loss in elderly high-risk patients with intertrochanteric femur fractures(IFFs). METHODS: The clinical data from Jan 2005 to Apr 2015 of 186 patients with PFNA-II and 177 patients with DHS were analyzed retrospectively. Indexes including pre- and post-operative blood routine, intra- and post-operative blood loss and blood transfusion situation were analyzed. The situation of perioperative blood loss (visible and hidden) was assessed. RESULTS: The intra-operative blood loss in the PFNA-II group was 34.7 ± 2.5 ml, the post-operative visible blood loss was 54.7 ± 2.5 ml, and the hidden blood loss was 277.2 ± 7.6 ml. In the DHS group, the intra-operative blood loss was 102.0 ± 7.0 ml, the post-operative visible blood loss was 78.8 ± 4.7 ml, and the hidden blood loss was 139.3 ± 9.6 ml. The intra-operative blood loss and the post-operative visible blood loss in the PFNA-II group were significantly less than in the DHS group (p < 0.01). However, the post-operative hidden blood loss and the total blood loss in the PFNA-II group were larger than in the DHS group (p < 0.01). CONCLUSION: This study demonstrated that with PFNA-II and DHS, much post-operative hidden blood loss exists in the treatment of intertrochanteric fractures in elderly high-risk patients and DHS is more favourable than PFNA-II in terms of post-operative hidden blood loss.

Acute unstable complex radial head and neck fractures fixed with a mini T-shaped plate in a 20-year-old man: a case report.

Acute unstable complex radial head and neck fractures in adults are seldom reported in the literature. Early recognition and appropriate management are essential to prevent long-term consequences of the loss of elbow function, forearm rotation, and chronic pain. Here, we describe an unusual case of a 20-year-old man who exhibited acute unstable complex fractures of the head and neck of the right radius without other injuries or comorbidity. An open reduction and mini T-shaped plate fixation were performed within 3 hours after injury, and the results were satisfactory. A long plaster fixation was continued for 3 weeks. A gradual mobilization was started after the removal of the plaster under the supervision of a physiotherapist. At the 12-month follow-up, no complications associated with the use of the mini T-shaped plate were noted, and the Mayo Elbow Performance Score was 97 (excellent). To our knowledge, acute unstable complex radial head and neck fractures in adults can be successfully treated with a mini T-shaped plate reconstruction technique.

Proximal femoral nails anti-rotation versus dynamic hip screws for treatment of stable intertrochanteric femur fractures: an outcome analyses with a minimum 4 years of follow-up.

BACKGROUND: Dynamic hip screws (DHSs) and proximal femoral nails anti-rotation (PFNAs) are well-documented implants for stable intertrochanteric femur fractures(IFFs); however, there is no consensus regarding which type of implant is the better option for stable IFFs. This study aimed to compare DHSs with PFNAs in the management of stable intertrochanteric fractures. METHODS: A retrospective study was performed in our institution. Between June, 2005 and November, 2015, 267 patients (267 hips) with stable IFFs (AO/OTA Type 3.1A1) were treated with a DHS or a PFNA. Inclusion and exclusion criteria were designed to focus on isolated stable IFFs in ambulatory patients. Follow-up was undertaken at 1, 3, 12, 15, 18, 21, 24, 36, 48 postoperative months, and at final follow-up. Radiograph outcomes were obtained at all visits. The primary outcome measure was re-operation rate. The secondary outcome was patient function, evaluated using Harris hip score (HHS). Tertiary outcomes included: intra- and post-operative orthopaedic complications. RESULTS: Two hundred twenty two patients (110 in the PFNA group and 112 in the DHS group) were evaluated with a mean follow-up period of 53 months (range, 48-60 months). There was an increased risk of reoperation after DHS in one-year follow-up: 0 % and 5.4 % for PFNA and DHS, respectively (P = 0.029). The difference persisted with time: 6.4 % and 13.4 % at last follow-up (P < 0.05). There are statistical differences in postoperative HHS at 12, 15, 18, 21, 24, 36, 48 months postoperatively and at final follow-up. No statistical differences in medical complications was observed between the two groups. The orthopaedic complications were more in the DHS group (n = 42) compared with the PFNA group (n = 18) (P <0.05). CONCLUSION: Compared with PFNA device, DHS device might not be the preferred implant for stable intertrochanteric femur fractures.

Evaluation of artificial nerve conduit and autografts in peripheral nerve repair in the rat model of sciatic nerve injury.

OBJECTIVE: To investigate the therapeutic effect of artificial nerve conduit in the sciatic nerve injury and repair in the rat model. METHODS: A total of 60 adult male Sprague Dawley rats were evenly randomized into five groups to build the model of sciatic nerve injury and perform the injury repair experiment. The five groups were: group A which was treated with artificial nerve conduit, group B which was treated with common carotid artery (CCA) autograft, group C which was treated with sciatic nerve autograft, group D which was treated with sham operation, and group E as the normal control. The injury was repaired by direct coaptation of the nerve ends. Postoperatively, the rats' behavior, motor nerve conduction velocity (MNCV), incubation period, amplitude, remaining rate of wet weight of the gastrocnemius muscle, the diameter and section area of the gastrocnemius cell, and the histological changes were assessed. The results were analyzed by one-way ANOVA and two-way ANOVA. RESULTS: Twelve days postoperatively, 36 rats in groups A, B, and C presented with denervated adermotrophia on the injured ankle. The electrophysiological indicators in groups D and E were constant and similar. The values of MNCV and amplitude were group C > group A > group B, with an increasing tendency. The values of the incubation period were group C < group A < group B with statistical difference (p < 0.05) and showed a decreasing tendency. The wet gastrocnemius muscle in groups D and E showed plump morphology with luster and elasticity. Groups A and C had similar atrophic gastrocnemius muscles and reduced flexibility while the phenomena were more severe in group B. Progressive decrease of the cell diameter and sectional area was observed in groups A, B, and C. The adhesion between the sciatic nerve and the surrounding area in groups A, B, and C had statistical significance (P < 0.05), with group B the most serious. CONCLUSIONS: The results suggest that artificial nerve conduit facilitated functional and morphological regeneration of the nerve. It seemed more effective than CCA but inferior to sciatic nerve autograft in repairing sciatic nerve injury in the rat model.

A retrospective analysis of the InterTan nail and proximal femoral nail anti-rotation-Asia in the treatment of unstable intertrochanteric femur fractures in the elderly.

BACKGROUND: The purpose of this study was to compare the clinical outcomes of elderly patients undergoing surgery for treatment of unstable trochanteric fractures receiving either proximal femoral nails anti-rotation-Asia (PFNA-IIs) or InterTan nails (ITs). METHODS: Between January 1, 2012, and June 31, 2015, 168 elderly patients with unstable intertrochanteric femur fractures enrolled in this study. The only intervention was ITs or PFNA-IIs of the unstable trochanteric femur fractures. Follow-up was at 1, 3, 6, and 12 months postoperatively and yearly thereafter. Intraoperative variables and postoperative complications were compared between the two groups. RESULTS: Eight patients died, six were too infirmed for follow-up, and seven were lost during follow-up, leaving 147 patients meeting the criteria were evaluated at a mean follow-up of 20 months (range 16-26 months). Significant differences were observed between the two groups regarding local complications (IT, n = 10 vs. PFNA-II, n = 20), varus collapse of the head/neck or femoral shaft fractures at the tip of the nail (IT, n = 1 vs. PFNA-II, n = 8), femoral neck shortening (IT, 4.4 ± 1.1 mm vs. PFNA-II, 7.4 ± 2.4 mm), fracture healing time (IT, 14.7 ± 2.1 weeks vs. PFNA-II, 15.7 ± 2.4 weeks), femoral shaft fractures (IT, n = 0 vs. PFNA-II, n = 4), rotational loss of reduction (IT, n = 0 vs. PFNA-II, n = 9), lateral cortex fractures of the proximal femur or lateral greater trochanter fractures (IT, n = 8 vs. PFNA-II, n = 1), operative time (IT, 71.9 ± 6.8 min vs. PFNA-II, 52.3 ± 4.0 min), intraoperative blood loss (IT, 190.6 ± 6.0 mL vs. PFNA-II, 180.9 ± 10.8 mL), fluoroscopy time (IT, 5.0 ± 0.48 min vs. PFNA-II, 2.8 ± 0.33 min), hospital stay (IT, 9.65 ± 0.95 days vs. PFNA-II, 8.58 ± 0.93 days), cut-out (IT, n = 0 vs. PFNA-II, n = 6), and tip-apex distance (IT, 26.7 ± 0.91 mm vs. PFNA-II, 23.2 ± 1.22 mm). No significant differences existed for the other observation indexes (p > 0.05). CONCLUSIONS: The IT nail may have more advantage for patients with unstable intertrochanteric fractures of the femur. However, for those complicated with lateral greater trochanter fractures, lateral cortex fractures of the proximal femurs, or unfit for surgery, the PFNA-II nail could be a good option. In addition, a large-sample, multicenter observational study is required for evaluation of its long-term efficacy, and optimal management strategies for specific unstable fracture patterns, different sorts of bone quality, and different levels of patient demand.

Clinical anatomy and mechanical tensile properties of the rectus femoris tendon.

PURPOSE: We aimed to provide anatomical data and mechanical tensile properties for the rectus femoris tendon to determine if it is a feasible substitute for the anterior cruciate ligament during knee joint reconstruction. METHODS: The length and width of the quadriceps femoris tendon were measured from ten adult cadavers (20 knees; age =48±2 years). The anatomic features of the patellar insertion on the quadriceps femoris tendon were also documented. The rectus femoris tendon and anterior cruciate ligament were harvested from an additional five fresh specimens (10 knees; age =41±3 years). To minimize dehydration, each specimen was wrapped in saline-moistened paper towels and stored at -10°C. We imposed tensile stresses on a total of twenty samples in a sample-driven machine at 10 mm/min until the specimens failed. RESULTS: The inserted and discrete widths of the rectus femoris tendon were 3.20±0.33 and 1.28±0.25 cm, respectively. The length of the tendon tissue was 6.96±0.80 cm and the length of mixing zone was 3.81±0.53 cm. The average thickness of the upper pole of the patella was 2.22±0.14 cm. In mechanical tensile properties, the unit modulus and unit maximum load of the rectus femoris tendon were both 63% of the anterior cruciate ligament. CONCLUSIONS: Based on its anatomical and mechanical tensile properties, the rectus femoris tendon is a feasible donor site to reconstitute the anterior cruciate ligament.