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BackgroundAccurate preoperative positioning is the key to the success of thoracoscopic surgery for small pulmonary nodules. There are many methods for locating pulmonary nodules in clinical practice, but there are currently few research reports on the value of medical adhesive localization.ObjectiveTo compare the clinical value of two positioning methods, medical adhesive and metal spring coil, in the preoperative application of VATS through retrospective analysis.MethodsA total of 288 patients who underwent thoracoscopic surgery in our hospital from January 2021 to June 2024 due to the discovery of solitary pulmonary nodules during chest CT examination were included in this study. Preoperative patients were randomly divided into two groups, with 205 patients undergoing preoperative medical adhesive positioning (Group A) and 83 patients undergoing metal spring coil positioning (Group B). After the positioning was completed, record the positioning time of each group of patients and the immediate pain score 15 min after the positioning was completed, the complications located in each group of patients, and whether there was positioning failure or not.ResultsThe localization success rate of the medicine adhesive positioning group [99.5% (204/205)] was higher than that of the metal spring coil positioning group [91.6% (76/83)] (P = 0.001). The positioning time of the medical adhesive positioning group was 12.00 (10.00, 14.00) min, which was shorter than the 13.00 (11.00, 16.00) min of the micro coil group (P = 0.001). The immediate pain score (2.32 ± 0.79) of the medical adhesive positioning group 15 min after positioning was significantly lower than that of the metal spring coil positioning group (3.97 ± 0.54) (P < 0.001). The incidence of complications such as pneumothorax [15.7% (13/83) vs 5.4% (11/205), P = 0.004], pulmonary hemorrhage/hemoptysis [20.5% (17/83) vs 4.9 (10/205), P < 0.001] was significantly higher in the metal coil positioning group than in the medical adhesive positioning group.ConclusionPreoperative medical adhesive positioning for pulmonary nodules is safe, reliable, and effective. Compared with metal spring coil positioning, it has shorter positioning time, milder pain after positioning, lower incidence of positioning related complications, and more flexible arrangement of surgical timing after positioning. It has high clinical application value.

BackgroundEpigenetic reprogramming through dysregulated histone lysine methylation (HLM) plays a crucial role in prostate cancer (PCa) progression. This study aimed to comprehensively evaluate HLM modification patterns in PCa microenvironment infiltration.Materials and methodsNinety-one HLM regulators in The Cancer Genome Atlas (TCGA) dataset were analyzed using bioinformatics. Differentially expressed genes (DEGs) and survival analyses were performed using TCGA-PRAD clinicopathologic and follow-up information. Consensus clustering analysis divided patients into subgroups. Gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the DEGs. Tumor mutation burden (TMB) and tumor microenvironment (TME) cell infiltration were evaluated in different HLM clusters. Quantitative real-time PCR (qPCR) analysis assessed HLM regulators in clinical PCa tissues.ResultsThe tumor vs. normal (TN), Gleason score (GS) > 7 vs. GS < 7, pathological T stage (pT) = 2 vs. pT = 3, and TP53 mutation vs. wild-type comparisons using TCGA-PRAD dataset revealed 3 intersecting HLM regulators (EZH2, NSD2, and KMT5C) that were consistently upregulated in advanced PCa (GS > 7, pT3, HR > 1, and TP53 mutation) (P < 0.05) and verified in clinical PCa tissues. Consensus clustering analysis revealed three distinct HLM modification patterns (HLMclusters). However, no significant differences in recurrence-free survival (RFS) rates were found among the groups (P > 0.05). We screened 189 HLM phenotype-related genes that overlapped in the pairwise comparisons of HLMclusters and P < 0.01 in the Cox regression analysis. Three distinct subgroups (geneClusters) were revealed based on the 189 genes, in which cluster A involved the most advanced PCa (PSA > 10, T3-4, GS8-10, and biochemical recurrence) and the poorest RFS. The HLM score (HLMscore) was calculated by principal component analysis (PCA) of HLM phenotype-related genes that have positive predictive value for RFS (P < 0.001) and immune therapy responses (in the CTLA4-positive and -negative responses accompanied by a PD1-negative response).ConclusionWe comprehensively evaluated HLM regulators in the PCa microenvironment using TCGA-PRAD, revealing a nonnegligible role of HLM patterns in PCa complexity and heterogeneity. Elucidating the effects of HLM regulators in PCa may enhance prognostics, aggressiveness assessments, and immunotherapy strategies.

Objective: Benign prostatic hyperplasia (BPH) is the most common urological disease in elderly men. The transforming growth factor beta 1 (TGFβ1) plays an important role in the proliferation and differentiation of BPH stroma. However, it is not clear yet which important pathways and key genes are the downstream of TGFβ1 acting on prostatic stromal cells.Methods: GSE132714 is currently the newer, available, and best high-throughput sequencing data set for BPH disease and includes the largest number of BPH cases. We examined the TGFβ1 expression level in BPH and normal prostate (NP) by analyzing the GSE132714 data set as well as carrying out immunohistochemistry of 15 BPH and 15 NP samples. Primary prostatic stromal cells (PrSCs) were isolated from five fresh BPH tissues. RNA sequencing and bioinformatics analysis were used to reveal important pathways and hub genes associated with TGFβ1 stimulation on PrSCs.Results: TGFβ1 was upregulated in BPH stroma compared to NP stroma. A total of 497 genes (244 upregulated and 253 downregulated) were differentially expressed in PrSCs with and without TGFβ1 stimulation. The Gene Ontology revealed that differentially expressed genes (DEGs) were mainly enriched in progesterone secretion, interleukin-7 receptor binding, and CSF1-CSF1R complex. The Wnt signaling pathway, PI3K−Akt signaling pathway, JAK−STAT signaling pathway, and Hippo signaling pathway were screened based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. FN1, SMAD3, CXCL12, VCAM1, and ICAM1 were selected as hub genes according to the degree of connection from the protein–protein interaction (PPI) network.Conclusion: This study sheds some new insights into the role of TGFβ1 in BPH stroma and provides some clues for the identification of potential downstream mechanisms and targets.

PurposeThe purpose of this study was to summarize the existing evidence and develop a comprehensive systematic review of the impact of androgen suppression therapy (AST) on the incidence or clinical outcomes of bladder cancer.MethodsWe systematically searched the PubMed and Embase databases from inception to June 20, 2021 to identify all observational studies examining the incidence or clinical outcomes of bladder cancer in patients who received AST. AST is defined as the use of 5-alpha reductase inhibitors (5-ARIs) or androgen deprivation therapy (ADT).ResultsA total of 18 observational studies were included. Our results showed that AST was not significantly associated with a reduced risk of BCa incidence (OR: 0.92, 95% CI: 0.68–1.24) compared with the lack of AST. The subgroup analysis revealed that finasteride use was significantly associated with a reduction in the risk of BCa incidence (OR: 0.75, 95% CI: 0.64–0.88). Recurrence-free survival (RFS) was improved among AST users compared with nonusers (HR: 0.68, 95% CI: 0.48–0.95), while no significant difference between AST users versus nonusers was identified for cancer-specific survival (CSS), overall survival (OS) or progression-free survival (PFS).ConclusionCurrent evidence indicates that therapy with finasteride may represent a potential strategy aimed at reducing BCa incidence. Moreover, AST has a beneficial effect on the recurrence of bladder cancer. Further well-designed randomized trials or cohort studies with better characterized study populations are needed to validate our preliminary findings.Systematic Review RegistrationInternational Prospective Register of Systematic Reviews database [https://www.crd.york.ac.uk/PROSPERO/], identifier CRD42021261685.

BackgroundDiagnosing the well-known concomitant Rathke’s cleft cyst (RCC) and differentiating it from other sellar lesions are difficult because RCC is and other sellar lesions are closely related and represent a continuum from simple RCCs to more complex lesions. The purpose of this study is to better understand the adeno- and neurohypophysis adjacent to the par intermedia remnants and their role in the origin of the coexistence of these two distinct tumor neoplasias; to assess the incidence in different age groups; to categorize the pathohistological subtype, which can be incorporated in predictive/prognostic models; and finally, to evaluate the current evidence on collision tumors of the sellar embryonic remnant tract in terms of their biological behavior and pathology.MethodsUtilizing the PubMed database, data were collected from 1920 to 2019. Information about demographics, clinical characteristics, and age was summarized and analyzed by using univariable and multivariable models. The same cell type was observed regardless of whether the tumor was only one type or mixed types, and their histologic patterns were assessed.ResultsThe incidence rates were similar among patients stratified into three age subgroups: 40–49 years (24.57%), 50–59 years (19.54%), and older than 60 years (22.98%). We found that various types of sellar lesions, namely, squamous metaplasia (SM) + goblet cells (GC) (HR 46.326), foamy macrophages (FM) (HR 39.625), epithelial cells and multinucleated giant cells or cholesterin (EM) (HR 13.195), a cavernous portion of the right internal carotid artery (CP-ICA) (HR 9.427), epithelial cells with ciliated cuboidal (EC-CC) (HR 8.456), were independently associated with RCC pathological status. These divergent AUCs (0.848 for Hypo as RCC, 0.981 for RCC co PA, 0.926 for CD and CP co RCC) and subtypes of PA (HR 4.415, HR 2.286), Hypo (HR 3.310), CD and CP (HR 2.467), EC and DC and PG and SGR (HR 1.068), coexisting with the risk of a comorbid RCC lesion, may reflect the etiologic heterogeneity of coderivation and the different effects of some risk factors on tumor subtypes. Our analyses suggested that the greatest accuracy was observed for the pituitary adenoma subtype, with an AUC of 0.981 (95% confidence interval [CI]: 0.959–1.005), while the poorest accuracy was observed for aneurysms, with an AUC of 0.531 (95% CI: 0.104–0.958). We separately analyzed and confirmed the above results. Sensitivity analysis revealed no evidence of systematic bias due to missing data.ConclusionThis study showed that the histopathological changes in patients with sellar embryonic remnant-associated collision tumors showed highly consistent epithelial cell replacement (renewal) (ciliated columnar epithelium to ciliated squamous epithelium to squamous epithelium) or accumulation, and the RCC cyst wall was similar in structure to the tracheobronchial airway epithelium, with progenitor cell characteristics. The collision accuracy between RCC and other tumors (PAs, craniopharyngioma, chordoma, etc.) is different; these characteristics constitute the theoretical basis for the postmigration development of the pharyngeal bursa.