Enhancing percutaneous kyphoplasty efficacy in elderly osteoporotic fractures through optimal cement filling ratio.

Objective: To explore the appropriate bone cement filling ratio in percutaneous kyphoplasty (PKP) for the treatment of osteoporotic vertebral compression fractures (OVCF). Methods: Clinical and radiological data from 150 OVCF patients treated with PKP were retrospectively analyzed. Patients were categorized into three groups based on bone cement filling ratio: low (<0.4), medium (0.4-0.6), and high (>0.6) filling ratio groups. The clinical characteristics (age, gender, BMI, etc.) and related study data (bone cement leakage and its location, pre/post-operative Visual Analogue Scale (VAS), pre/post-operative Oswestry Disability Index (ODI), vertebral height restoration, kyphotic Cobb angle, etc.) among the three groups were compared using statistical software to compare to identify the most appropriate cement filling ratio. Results: The 0.4-0.6 group presented a lower cement leakage rate compared to the >0.6 group, and there were no significant differences in pre-operative VAS, post-operative day 2 VAS, post-operative month 1 VAS, and pre-operative ODI (p>0.05). However, significant differences were observed in post-operative month 3 VAS (p=0.002), post-operative day 2 ODI (p=0.002), post-operative month 1 ODI (p<0.001), and post-operative month 3 ODI (p<0.001). The "0.4-0.6" group showed better pain improvement and functional recovery compared with the ">0.6" group at the 3-month follow-up. While presenting the best vertebral height restoration, the ">0.6" group also exhibited the greatest variability. Additionally, no significant difference in Cobb angle changes was observed among the groups. Conclusion: A bone cement filling ratio of 0.4-0.6 in PKP treatment for OVCF strikes a favorable balance between complication reduction and positive patient outcomes, warranting it as an optimal filling volume.

The potential value of the Purinergic pathway in the prognostic assessment and clinical application of kidney renal clear cell carcinoma.

The Purinergic pathway is involved in a variety of important physiological processes in living organisms, and previous studies have shown that aberrant expression of the Purinergic pathway may contribute to the development of a variety of cancers, including kidney renal clear cell carcinoma (KIRC). The aim of this study was to delve into the Purinergic pathway in KIRC and to investigate its potential significance in prognostic assessment and clinical treatment. 33 genes associated with the Purinergic pathway were selected for pan-cancer analysis. Cluster analysis, targeted drug sensitivity analysis and immune cell infiltration analysis were applied to explore the mechanism of Purinergic pathway in KIRC. Using the machine learning process, we found that combining the Lasso+survivalSVM algorithm worked well for predicting survival accuracy in KIRC. We used LASSO regression to pinpoint nine Purinergic genes closely linked to KIRC, using them to create a survival model for KIRC. ROC survival curve was analyzed, and this survival model could effectively predict the survival rate of KIRC patients in the next 5, 7 and 10 years. Further univariate and multivariate Cox regression analyses revealed that age, grading, staging, and risk scores of KIRC patients were significantly associated with their prognostic survival and were identified as independent risk factors for prognosis. The nomogram tool developed through this study can help physicians accurately assess patient prognosis and provide guidance for developing treatment plans. The results of this study may bring new ideas for optimizing the prognostic assessment and therapeutic approaches for KIRC patients.

The mechanism and clinical application of DNA damage repair inhibitors combined with immune checkpoint inhibitors in the treatment of urologic cancer.

Urologic cancers such as kidney, bladder, prostate, and uroepithelial cancers have recently become a considerable global health burden, and the response to immunotherapy is limited due to immune escape and immune resistance. Therefore, it is crucial to find appropriate and effective combination therapies to improve the sensitivity of patients to immunotherapy. DNA damage repair inhibitors can enhance the immunogenicity of tumor cells by increasing tumor mutational burden and neoantigen expression, activating immune-related signaling pathways, regulating PD-L1 expression, and reversing the immunosuppressive tumor microenvironment to activate the immune system and enhance the efficacy of immunotherapy. Based on promising experimental results from preclinical studies, many clinical trials combining DNA damage repair inhibitors (e.g., PARP inhibitors and ATR inhibitors) with immune checkpoint inhibitors (e.g., PD-1/PD-L1 inhibitors) are underway in patients with urologic cancers. Results from several clinical trials have shown that the combination of DNA damage repair inhibitors with immune checkpoint inhibitors can improve objective rates, progression-free survival, and overall survival (OS) in patients with urologic tumors, especially in patients with defective DNA damage repair genes or a high mutational load. In this review, we present the results of preclinical and clinical trials of different DNA damage repair inhibitors in combination with immune checkpoint inhibitors in urologic cancers and summarize the potential mechanism of action of the combination therapy. Finally, we also discuss the challenges of dose toxicity, biomarker selection, drug tolerance, drug interactions in the treatment of urologic tumors with this combination therapy and look into the future direction of this combination therapy.

Advances in early detection methods for solid tumors.

During the last decade, non-invasive methods such as liquid biopsy have slowly replaced traditional imaging and invasive pathological methods used to diagnose and monitor cancer. Improvements in the available detection methods have enabled the early screening and diagnosis of solid tumors. In addition, advances in early detection methods have made the continuous monitoring of tumor progression using repeat sampling possible. Previously, the focus of liquid biopsy techniques included the following: 1) the isolation of circulating tumor cells, circulating tumor DNA, and extracellular tumor vesicles from solid tumor cells in the patient's blood; in addition to 2) analyzing genomic and proteomic data contained within the isolates. Recently, there has been a rapid devolvement in the techniques used to isolate and analyze molecular markers. This rapid evolvement in detection techniques improves their accuracy, especially when few samples are available. In addition, there is a tremendous expansion in the acquisition of samples and targets for testing; solid tumors can be detected from blood and other body fluids. Test objects have also expanded from samples taken directly from cancer to include indirect objects affected in cancer development. Liquid biopsy technology has limitations. Even so, this detection technique is the key to a new phase of oncogenetics. This review aims to provide an overview of the current advances in liquid biopsy marker selection, isolation, and detection methods for solid tumors. The advantages and disadvantages of liquid biopsy technology will also be explored.

Regulatory roles of ferroptosis-related non-coding RNAs and their research progress in urological malignancies.

Ferroptosis is a new type of cell death characterized by damage to the intracellular microenvironment, which causes the accumulation of lipid hydroperoxide and reactive oxygen species to cause cytotoxicity and regulated cell death. Non-coding RNAs (ncRNAs) play an important role in gene expression at the epigenetic, transcriptional, and post-transcriptional levels through interactions with different DNAs, RNAs, or proteins. Increasing evidence has shown that ferroptosis-related ncRNAs are closely related to the occurrence and progression of several diseases, including urological malignancies. Recently, the role of ferroptosis-associated ncRNAs (long non-coding RNAs, micro RNAs, and circular RNAs) in the occurrence, drug resistance, and prognosis of urological malignancies has attracted widespread attention. However, this has not yet been addressed systematically. In this review, we discuss this issue as much as possible to expand the knowledge and understanding of urological malignancies to provide new ideas for exploring the diagnosis and treatment of urological malignancies in the future. Furthermore, we propose some challenges in the clinical application of ferroptosis-associated ncRNAs.

Research progress in inducing immunogenic cell death of tumor cells.

Immunogenic cell death (ICD) is a regulated cell death (RCD) pathway. In response to physical and chemical signals, tumor cells activate specific signaling pathways that stimulate stress responses in the endoplasmic reticulum (ER) and expose damage-associated molecular patterns (DAMPs), which promote antitumor immune responses. As a result, the tumor microenvironment is altered, and many tumor cells are killed. The ICD response in tumor cells requires inducers. These inducers can be from different sources and contribute to the development of the ICD either indirectly or directly. The combination of ICD inducers with other tumor treatments further enhances the immune response in tumor cells, and more tumor cells are killed; however, it also produces side effects of varying severity. New induction methods based on nanotechnology improve the antitumor ability and significantly reduces side effects because they can target tumor cells precisely. In this review, we introduce the characteristics and mechanisms of ICD responses in tumor cells and the DAMPs associated with ICD responses, summarize the current methods of inducing ICD response in tumor cells in five distinct categories: chemical sources, physical sources, pathogenic sources, combination therapies, and innovative therapies. At the same time, we introduce the limitations of current ICD inducers and make a summary of the use of ICD responses in clinical trials. Finally, we provide an outlook on the future of ICD inducer development and provide some constructive suggestions.