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INTRODUCTION The incidence of periprosthetic fractures (PFFs) is estimated to range from 0.1% to 4.1%1, due to the increasing prevalence of joint arthroplasties, coupled with an aging population. Numerous risk factors, including advanced age (>80 years), female gender, implant type, prior diagnoses of osteonecrosis and rheumatoid arthritis, revision surgery, aseptic stem mobilization, and the use of non-cemented stems, have been identified. Survivors of periprosthetic fractures often experience functional deterioration, facing a fourfold higher risk of hospitalization for postoperative complications compared to patients undergoing primary implantation, especially in the first postoperative year. MATERIALS AND METHODS Between 2018 and 2022, at the Maggiore Hospitals in Bologna and the San Matteo Policlinic in Pavia, we performed osteosynthesis on 84 patients with periprosthetic fractures of Vancouver type B1 or C. In 38 patients, we employed angular stable plates with the Zimmer Biomet NCB-PP® system. In 46 patients, we utilized INTRAUMA plates: DF distal femur and PFF proximal. Relevant postoperative follow-up outcomes considered included reintervention, infectious complications, radiographic healing, and functional recovery, with reference to changes in the Glasgow Outcome Scale (GOS) and the Harris Hip Score (HHS). All patients underwent clinical and radiographic evaluations during the follow-up period, averaging 28 months (range: 12-48 months), with a minimum follow-up duration of 12 months. RESULTS At the 4-month postoperative assessment, 71% of patients maintained their preoperative functional level, 19% experienced a 1-point GOS scale drop, and 10% died (GOS 5). The average HHS at 4 months was 80.2 points (range: 65-90). At the 6-month follow-up, 98.2% of patients achieved complete healing on radiographic examination. Only 1 patient (1.2%) developed a pseudoarthrosis site with synthesis device rupture. Only 1 patient (1.2%) required additional surgical treatment 2 years later due to the development of un aseptic perisynthetic fluid collection, while the remaining 5 patients (6%) who developed complications benefited from conservative treatment: 4 patients (3.6%) with infectious complications were treated with intravenous antibiotics. In the 2 patients (2.3%) with mobilization or rupture of synthesis devices, clinical and radiographic monitoring was opted for. 8 patients (10.7%) died: one 48 hours after the surgery, and the other 7 more than one month after the surgery. CONCLUSION Our clinical findings align with to existing scientific literature on periprosthetic fractures (B1 and C according to Vancouver classification). Moreover, good stability has been guaranteed at the radiological follow up by Zimmer Biomet NCB-PP® and INTRAUMA DF distal femur and PFF proximal plates. The locking construct allows for improved stability especially in osteoporotic bone.

Introduction: Congenital dislocation of the patella (CDP) is a rare condition and its treatment is not well defined. In CDP, patella is dislocated on the lateral aspect of the distal femur, laterally from the trochlear groove, it cannot be reduced manually and it is almost always associated with genu valgum, lateral torsion of the proximal tibia, and flexion contracture of the knee. This condition is present at birth, but the clinical findings can be subtle at birth due to the size and character of the structures being examined; early diagnosis is essential, but it may be delayed to late childhood or adulthood. If CDP is not promptly treated, the disability increases during growth, so surgical correction should be planned as soon as the diagnosis is confirmed., Case Report: We report a case of bilateral CDP associated with bilateral proximal radioulnar joint stiffness; the patient at the age of diagnosis was 11 years old and underwent a bilateral delayed surgical procedure; the 4-year follow-up results are satisfactory. Surgical treatment rationale and literature are reviewed., Conclusion: Surgical correction for CDP is generally recommended, but there is no agreement in literature on the ideal treatment and in some cases, with mild impairment of the knee function, observation alone has been suggested. The decision about a surgical treatment can be difficult and depends on the degree of disability of the patient., Competing Interests: Conflict of Interest: Nil, (Copyright: © Indian Orthopaedic Research Group.)

Mammalian genomes encode tens of thousands of noncoding RNAs. Most noncoding transcripts exhibit nuclear localization and several have been shown to play a role in the regulation of gene expression and chromatin remodeling. To investigate the function of such RNAs, methods to massively map the genomic interacting sites of multiple transcripts have been developed; however, these methods have some limitations. Here, we introduce RNA And DNA Interacting Complexes Ligated and sequenced (RADICL-seq), a technology that maps genome-wide RNA-chromatin interactions in intact nuclei. RADICL-seq is a proximity ligation-based methodology that reduces the bias for nascent transcription, while increasing genomic coverage and unique mapping rate efficiency compared with existing methods. RADICL-seq identifies distinct patterns of genome occupancy for different classes of transcripts as well as cell type-specific RNA-chromatin interactions, and highlights the role of transcription in the establishment of chromatin structure.

Human telomerase reverse transcriptase (TERT) is the catalytic subunit of telomerase, and it elongates telomere through RNA-dependent DNA polymerase activity. Although TERT is named as a reverse transcriptase, structural and phylogenetic analyses of TERT demonstrate that TERT is a member of right-handed polymerases, and relates to viral RNA-dependent RNA polymerases (RdRPs) as well as viral reverse transcriptase. We firstly identified RdRP activity of human TERT that generates complementary RNA stand to a template non-coding RNA and contributes to RNA silencing in cancer cells. To analyze this non-canonical enzymatic activity, we developed RdRP assay with recombinant TERT in 2009, thereafter established in vitro RdRP assay for endogenous TERT. In this manuscript, we describe the latter method. Briefly, TERT immune complexes are isolated from cells, and incubated with template RNA and rNTPs including radioactive rNTP for RdRP reaction. To eliminate single-stranded RNA, reaction products are treated with RNase I, and the final products are analyzed with polyacrylamide gel electrophoresis. Radiolabeled RdRP products can be detected by autoradiography after overnight exposure.

In this work we have investigated the ability of epinephrine to trigger the release of intracellular Ca2+ in thrombin-desensitized platelets. Addition of thrombin to platelets in the presence of extracellular EGTA caused a rapid and transient release of Ca2+ from intracellular stores and rendered platelets unresponsive to a second addition of the same agonist. Although epinephrine alone had no effect on intracellular Ca2+ mobilization, its addition to thrombin-desensitized platelets was associated to a rapid and evident secondary release of intracellular Ca2+. This effect of epinephrine was not observed when platelets were desensitized with other agonists able to induce phospholipase C activation, including convulxin, U46619, and ADP. Although the platelet receptor for epinephrine is coupled to the Gi family member Gz, no secondary Ca2+ release was seen in thrombin-desensitized platelets upon stimulation of other Gi-coupled receptors, including the P2Y12 receptor and the CXCR4. Addition of hirudin to thrombin-desensitized platelets prevented epinephrine-promoted secondary release of Ca2+, indicating that thrombin, rather than epinephrine itself, is actually responsible for this event as a consequence of thrombin receptors resensitization. Studies with platelets stimulated with specific PAR1- and PAR4- activating peptides proved that neither one of these thrombin receptors were involved in the secondary epinephrine-assisted Ca2+ release. Moreover, we found that thrombin was still able to induce a reduced, but evident release of Ca2+ from internal stores in PAR1- and PAR4-desensitized platelets, which could be followed by a secondary Ca2+ release upon subsequent addition of epinephrine. Importantly, both the primary and the secondary Ca2+ release induced by thrombin and epinephrine in PAR1- and PAR4-desensitized platelets were abrogated upon cleavage of GPIbalpha by the metalloproteinase mocarhagin. These results demonstrate a direct role of thrombin binding to GPIb-IX-V in the mobilization of Ca2+ from intracellular stores, and reveal that epinephrine can restore this process in desensitized platelets, thus prolonging the effect of thrombin stimulation.