Closed reduction of hip dislocation associated with ipsilateral lower extremity fractures: A case report and review of the literature.

BACKGROUND: Traumatic hip dislocation usually occurs following high-velocity trauma. It is imperative that the dislocation be reduced in a timely manner, especially in a closed manner, as an orthopedic emergency. However, closed reduction can hardly be achieved in patients who also have ipsilateral lower extremity fractures. Herein, we focus on hip dislocation associated with ipsilateral lower extremity fractures, excluding intracapsular fractures (femoral head and neck fractures), present an early closed hip joint reduction method for this injury pattern, and review the literature to discuss the appropriate closed reduction technique for this rare injury pattern. CASE SUMMARY: We report a case of a 37-year-old male who sustained a left acetabular posterior wall fracture, an ipsilateral comminuted subtrochanteric fracture and dislocation of the hip. The hip dislocation was reduced urgently in a closed manner using the joy-stick technique with a T-shaped Schanz screw. The fractures were reduced and fixed as a 2nd-stage surgery procedure. At the 17-month postoperative follow-up, the patient had full range of motion of the affected hip. CONCLUSION: Closed reduction of a hip dislocation associated with ipsilateral lower extremity fractures is rarely achieved by regular maneuvers. Attempts at closed reduction, by means of indirectly controlling the proximal fracture fragment or reconstructing the femoral leverage rapidly with the aid of various external reduction apparatuses, were shown to be effective in some scenarios. Mandatory open reduction is indicated in cases of failed closed reduction, particularly in irreducible dislocations.

Delayed complications of intradural cement leakage after percutaneous vertebroplasty: A case report.

BACKGROUND: Intradural cement leakage following percutaneous vertebroplasty is a rare but acute and devastating complication that usually requires emergent treatment. Here, we report a delayed complication of intradural leakage after percutaneous vertebroplasty. CASE SUMMARY: A 71-year-old female patient with an L1 osteoporotic compression fracture underwent percutaneous vertebroplasty in 2014. She was referred to our hospital 5 years later due to complaints of progressive weakness and numbness in both legs combined with urinary incontinence and constipation. Initially, she was suspected to have a spinal meningioma at the level of L1 according to imaging examinations. Postoperative pathological tests confirmed that cement had leaked into the dura during the first percutaneous vertebroplasty. CONCLUSION: Guideline adherence is essential to prevent cement from leaking into the spinal canal or even the dura. Once leakage occurs, urgent evaluation and decompression surgery are necessary to prevent further neurological damage.

Maisonneuve injury with no fibula fracture: A case report.

BACKGROUND: Ankle syndesmosis injury is difficult to diagnose accurately at the initial visit. Missed diagnosis or improper treatment can lead to chronic complications. Complete syndesmosis injury with a concomitant rupture of the interosseous membrane (IOM) is more unstable and severe. The relationship between this type of injury and Maisonneuve injury, in which the syndesmosis is also injured, has not been discussed in the literature previously. CASE SUMMARY: A 16-year-old patient sustained left medial malleolar fracture, and the associated inferior tibiofibular syndesmotic instability was overlooked. After open reduction and internal fixation of the medial malleolar fracture, inferior tibiofibular syndesmosis diastasis with IOM rupture was detected by auxiliary imaging. Secondary surgical intervention was performed to reduce anatomically and fix with two trans-syndesmosis screws. Twelve weeks later, the screws were removed. At the 6-mo follow-up, the patient gained full range of motion of the ankle. CONCLUSION: Complete syndesmosis injury with IOM rupture should be considered Maisonneuve-type injury. Open reduction and internal fixation could obtain good outcomes.

LncRNA CamK-A Regulates Ca2+-Signaling-Mediated Tumor Microenvironment Remodeling.

Cancer cells entail metabolic adaptation and microenvironmental remodeling to survive and progress. Both calcium (Ca2+) flux and Ca2+-dependent signaling play a crucial role in this process, although the underlying mechanism has yet to be elucidated. Through RNA screening, we identified one long noncoding RNA (lncRNA) named CamK-A (lncRNA for calcium-dependent kinase activation) in tumorigenesis. CamK-A is highly expressed in multiple human cancers and involved in cancer microenvironment remodeling via activation of Ca2+-triggered signaling. Mechanistically, CamK-A activates Ca2+/calmodulin-dependent kinase PNCK, which in turn phosphorylates IκBα and triggers calcium-dependent nuclear factor κB (NF-κB) activation. This regulation results in the tumor microenvironment remodeling, including macrophage recruitment, angiogenesis, and tumor progression. Notably, our human-patient-derived xenograft (PDX) model studies demonstrate that targeting CamK-A robustly impaired cancer development. Clinically, CamK-A expression coordinates with the activation of CaMK-NF-κB axis, and its high expression indicates poor patient survival rate, suggesting its role as a potential biomarker and therapeutic target.

Stimulatory function of peroxiredoxin 1 in activating adaptive humoral immunity in a zebrafish model.

Peroxiredoxin 1 (Prdx1/Prx1), a ubiquitous antioxidant enzyme involved in preventing oxidative damage and maintaining redox homeostasis, is essential for various cellular activities. Extracellular Prdx1 also plays important roles in innate immune responses. However, little is known about the regulatory functions of Prdx1 in adaptive immunity. In the present study, we report the stimulatory role of Prdx1 in the initiation of adaptive humoral immunity in a zebrafish model. Administration of Prdx1 protein to zebrafish significantly induced the expression of TNF-α, IL-1ß, and IL-6 by the Toll-like-receptor-4a-mediated NF-κB signaling pathway and enhanced the activation of MHC-II+ antigen-presenting cells, CD4+ T cells, and mIgM+ B cells. Subsequently, increased production of antigen-specific IgM antibody was observed. Thus, Prdx1 can be used as a novel molecular adjuvant with great therapeutic value for the vaccination of fish diseases. Our study improved the understanding of the biology of Prdx1 family.

LncRNA wires up Hippo and Hedgehog signaling to reprogramme glucose metabolism.

The Hippo pathway plays essential roles in organ size control and cancer prevention via restricting its downstream effector, Yes-associated protein (YAP). Previous studies have revealed an oncogenic function of YAP in reprogramming glucose metabolism, while the underlying mechanism remains to be fully clarified. Accumulating evidence suggests long noncoding RNAs (lncRNAs) as attractive therapeutic targets, given their roles in modulating various cancer-related signaling pathways. In this study, we report that lncRNA breast cancer anti-estrogen resistance 4 (BCAR4) is required for YAP-dependent glycolysis. Mechanistically, YAP promotes the expression of BCAR4, which subsequently coordinates the Hedgehog signaling to enhance the transcription of glycolysis activators HK2 and PFKFB3. Therapeutic delivery of locked nucleic acids (LNAs) targeting BCAR4 attenuated YAP-dependent glycolysis and tumor growth. The expression levels of BCAR4 and YAP are positively correlated in tissue samples from breast cancer patients, where high expression of both BCAR4 and YAP is associated with poor patient survival outcome. Taken together, our study not only reveals the mechanism by which YAP reprograms glucose metabolism, but also highlights the therapeutic potential of targeting YAP-BCAR4-glycolysis axis for breast cancer treatment.

USP11 regulates p53 stability by deubiquitinating p53.

The p53 tumor suppressor protein coordinates the cellular responses to a broad range of cellular stresses, leading to DNA repair, cell cycle arrest or apoptosis. The stability of p53 is essential for its tumor suppressor function, which is tightly controlled by ubiquitin-dependent degradation primarily through its negative regulator murine double minute 2 (Mdm2). To better understand the regulation of p53, we tested the interaction between p53 and USP11 using co-immunoprecipitation. The results show that USP11, an ubiquitin-specific protease, forms specific complexes with p53 and stabilizes p53 by deubiquitinating it. Moreover, down-regulation of USP11 dramatically attenuated p53 induction in response to DNA damage stress. These findings reveal that USP11 is a novel regulator of p53, which is required for p53 activation in response to DNA damage.