Objective To compare and explore the impact of radical prostatectomy, external beam radiation therapy, and prostate brachytherapy on sexual function of patients with prostate cancer. Methods A total of 80 prostate cancer patients admitted to the Urology Department of Ji'an Central People's Hospital from January 2020 to December 2022 were retrospectively analyzed. According to the treatment plan, they were divided into a surgical resection group (n=26, underwent radical prostatectomy), an external beam irradiation group (n=28, treated with high-energy X-rays or particle beams directed at irradiate tumor cells from outside the body), and a brachytherapy group (n=26, radioactive material placed directly into the prostate to act on cancer cells). General data such as age, body mass index (BMI) and Gleason score were collected for all patients. Patients were assessed for erectile dysfunction using international index of erectile function (IIEF) scale, for sexual desire using sexual dysfunction index (SDI) scale, and for sexual function using male sexual health questionnaire (MSHQ) scale. Six months after the end of treatment, the patients' anxiety and depression were assessed using self-rating anxiety scale (SAS) and self-rating depression scale (SDS). Results There were no statistically significant differences in age, BMI and Gleason score among patients in each group (P>0.05). The brachytherapy group demonstrated a higher rate of no erectile dysfunction compared to surgical resection group and external beam radiation group (P<0.05), and lower rates of mild and moderate to severe erectile dysfunction compared to surgical resection group (P<0.05). The external beam irradiation group showed a higher rate of no erectile dysfunction and lower rates of moderate to severe erectile dysfunction compared to surgical resection group (P<0.05). The brachytherapy group showed higher scores in sexual fantasy, sexual desire, sexual frequency and total SDI score than those in surgical resection group and external beam radiation group (P<0.05). The external beam radiation group also had higher scores in these areas compared to surgical resection group (P<0.05). The total sexual function score was higher in brachytherapy group compared to the other two groups (P<0.05), and the external beam irradiation group had a higher sexual function score than surgical resection group (P<0.05). The SAS and SDS scores in brachytherapy group were lower than those in surgical resection group and external beam radiation group (P<0.05). Conclusion Among the treatment methods for prostate cancer, prostate brachytherapy is relatively more effective in maintaining sexual function, especially in terms of erectile function and sexual desire, outperforming radical prostatectomy and external beam therapy.

Traumatic Brain Injury (TBI) is a significant global cause of mortality and disability, severely compromising public health and quality of life. TBI can be divided into primary and secondary brain injuries according to pathological mechanism, with excessive infiltration of immune cells post-injury triggering neuroinflammation being one of the crucial mechanisms in the cascade of secondary brain injury. Currently, There is a lack of targeted therapeutic agents for TBI, and treatment mainly relies on symptomatic care. Mesenchymal stem cells (MSCs) have shown promising potential in the treatment of brain injury through their immune-modulatory properties, which can mediate immune responses to reduce neuroinflammation and repair nerve damage. The review summarizes the recent research progress on immune responses following TBI and the immune regulatory effects of MSCs, aiming to provide references for subsequent research and clinical applications.

Objective To develop a matrix metalloproteinase (MMP)-responsive hyaluronic acid (HA)-based controlled-release material for brain-derived neurotrophic factor (BDNF) to provide a novel therapeutic strategy for intervention and repair of traumatic brain injury (TBI). Methods HA was modified with amination, followed by condensation with Suflo-SMCC carboxyl group to form amide, and then linked with glutathione (GSH) to synthesize HA-GSH. The recombinant glutathione S-transferase(GST)-tissue inhibitor of metalloproteinase(TIMP)-BDNF (GST-TIMP-BDNF) expression plasmid was constructed using molecular cloning technique with double enzyme digestion by BamH Ⅰ and EcoR Ⅰ. The recombinant GST-TIMP-BDNF protein was expressed in the Escherichia coli prokaryotic expression system, and purified by ion exchange chromatography, confirmed by Western blotting. MMP diluents were supplemented with PBS, MMP inhibitor marimastat, and varing concentrations (0.4, 0.6, 0.8 mg/ml) of GST-TIMP-BDNF or GST-BDNF. MMP-2 activity was analyzed using an MMP activity detection kit to evaluate the inhibitory effect of the recombinant protein on MMP. Primary rat neurons were extracted and cultured to establish an iron death model induced by RSL3. The effect of recombinant protein GST-TIMP-BDNF on neuronal injury was detected by immunofluorescence staining. Results MRI hydrogen spectrum identification confirmed the successful synthesis of HA-GSH. Western blotting results showed the successful expression of the recombinant protein GST-TIMP-BDNF containing the GST tag using the E. coli prokaryotic expression system. MMP activity detection results indicated that the recombinant protein GST-TIMP-BDNF had a superior inhibitory effect on MMP-2 activity compared to GST-BDNF (P<0.05). Immunofluorescence staining results showed a significant increase in fluorescence intensity in rat neurons treated with GST-TIMP-BDNF after RSL3 induction (P<0.05). Conclusion A MMP-responsive HA-based BDNF controlled-release material has been successfully developed, exhibiting a protective effect on neuron damage.

Non-functional pituitary adenomas (NFPAs) are relatively common intracranial sellar tumors. The diagnostic rate of NFPAs has significantly increased in recent years due to the widespread application of computed tomography (CT) and magnetic resonance imaging (MRI) in clinical practice. NFPAs do not exhibit increased biochemical hormone secretion, so they may not present with obvious clinical manifestations. However, as the tumor grows, it can cause mass effect symptoms, such as headache, visual impairment, and related pituitary target gland dysfunction, and even life-threatening pituitary stroke. The evaluation of pituitary function in patients with NFPAs and the selection of treatment plans require close collaboration and scientific management by a multidisciplinary team. The genetic and epigenetic mechanisms underlying the occurrence and development of NFPAs have not yet been fully elucidated. New treatment strategies may be developed through technologies such as whole-genome sequencing combined with chromatin structure analysis. This review systematically summarizes the research progress in epidemiology, histopathology, clinical diagnosis, treatment, and prognosis of NFPAs, aiming to provide reference and guidance for clinical management.

Aneurysmal subarachnoid hemorrhage (aSAH), primarily caused by the rupture of intracranial aneurysms with bleeding into the subarachnoid space, is an acute neurological disease associated with high disability and mortality. Brain injury after aSAH results from a combination of injury mechanisms, with early brain injury (EBI) occurring within 72 hours post-onset, laying the foundation for subsequent pathophysiological changes in the brain and poor prognosis of patients. Among them, the brain immunoinflammatory response, involving the interaction of various immune cells and active substances, plays a significant role in post-aSAH EBI, and is related to delayed brain injury and long-term prognosis. Systemic inflammatory response following aSAH can also affect the prognosis and outcome of patients. This review summarizes the role of local and systemic immune inflammatory responses in the occurrence and progression of aSAH, as well as the research progress on related inflammatory biomarkers and therapeutic prospects, aiming to provide a theoretical reference for new treatment for aSAH.

Objective To investigate the role and underlying mechanism of miR-15b-5p on hypoxia/reoxygenation (H/R) induced human renal tubular epithelial cell (HK-2) injury by targeting forkhead box O1 (FOXO1). Methods HK-2 cells in the log growth phase were set up as follows: (1) control group (normal culture) and H/R group (H/R induced culture). The expressions of miR-15b-5p and FOXO1 mRNA were detected using qRT-PCR, and the protein expression of FOXO1 was detected using Western blotting. (2) Control group (normal culture), H/R group (H/R induced culture), H/R+mimic control group (cells transfected with mimic control then induced by H/R), H/R+miR-15b-5p mimic group (cells transfected with miR-15b-5p mimic then induced by H/R), H/R+miR-15b-5p mimic+OE-NC group (cells co-transfected with miR-15b-5p mimic and OE-NC plasmid, then induced by H/R), and H/R+miR-15b-5p mimic+OE-FOXO1 group (cells co-transfected with miR-15b-5p mimic and FOXO1 overexpression plasmid, then induced by H/R). The expression of miR-15b-5p was detected using qRT-PCR, and the protein expressions of FOXO1, cleaved caspase-3, Bax, and Bcl-2 were detected using Western blotting. CCK-8 assay was used to detect cell viability. Cell apoptosis was measured by the TUNEL method. (3) Control group (normal culture), H/R group (H/R induced culture), H/R+miR-15b-5p mimic group (cells transfected with miR-15b-5p mimic then induced by H/R), and H/R+miR-15b-5p mimic+OE-FOXO1 group (cells co-transfected with miR-15b-5p mimic and FOXO1 overexpression plasmid, then induced by H/R). The protein expressions of LC3, p62 and Beclin1 were detected using Western blotting. LC3 immunofluorescence was used to detect the cell autophagy. The target reaction between miR-15b-5p and FOXO1 was assessed using dual luciferase reporting assay. Results Under an inverted microscope, it was observed that the control group had a higher number of cells, most of which were in a typical cobblestone shape and grew in a cobblestone-like manner; most of the cells in the H/R group contracted and became round, with a significant decrease in the number of adherent cells. In H/R-induced HK-2 cells, miR-15b-5p was significantly down-regulated, while miRNA and protein expression of FOXO1 was up-regulated (P<0.05). Luciferase assay results showed that miR-15b-5p directly targeted the 3'-UTR of FOXO1. Overexpression of miR-15b-5p increased cell viability, reduced cell apoptosis, and decreased autophagy in H/R-induced HK-2 cells (P<0.05). Compared with H/R+miR-15b-5p mimic group, the viability of HK-2 cells was decreased, the apoptosis and autophagy level were increased in H/R+miR-15b-5p mimic+OE-FOXO1 group (P<0.05). Conclusion miR-15b-5p inhibited autophagy and alleviated H/R-induced HK-2 cell injury by targeting FOXO1.

Cushing's disease is a severe endocrine disorder caused by excess secretion of adrenocorticotropic hormone from pituitary. Due to its subtle early clinical manifestations , the diagnosis of Cushing's disease is often delayed, and differentiating it from ectopic adrenocorticotropic hormone syndrome is a challenge. Combined functional tests can improve the diagnostic accuracy of Cushing's disease. The primary treatment for Cushing's disease is surgical removal of pituitary adenoma. However, about 1/3 of patients do not respond or experience recurrence after surgery, necessitating second-line treatments including medication. The development of novel drugs has enhanced the role of pharmacotherapy in the management of Cushing's disease. The review discusses the classic and emerging diagnostic methods and treatment strategies of Cushing's disease to deepen clinicians' understanding of its current treatment status and prospects.

Objective To investigate the effect of chemokine CXC ligand 9 (CXCL9) on cognitive function impairment in patients with breast cancer brain metastases undergoing whole-brain radiotherapy (WBRT) using bioinformatics methods. Methods The mRNA of breast cancer brain metastases datasets GSE43837 and GSE12276 and Alzheimer's disease (AD) dataset GSE161199 were screened and downloaded from GEO database. Limma method and Venn diagrams were used to identify common differentially expressed genes (DEGs), and protein-protein interaction and functional prediction through GeneMANIA website assays were performed. A total of 42 patients with breast cancer brain metastases who first visited the Department of Radiotherapy at the First Affiliated Hospital of Hebei North University from January 2021 to January 2023 were selected. Patients were divided into normal cognitive function group and cognitive function impairment group based on cognitive status. Enzyme-linked immunosorbent assay (ELISA) was employed to detect serum CXCL9 levels one week before and three months after radiotherapy. The mini-mental state examination (MMSE) was used to assess patients' cognitive function. Results The DEGs from datasets GSE43837 and GSE12276 included PKP1, POLDIP2, SPAG5, ALDOC, PTPRZ1, PKIA, TLCD1, CPE, PMP22 and CXCL9. The DEGs from GSE161199 included RPS16, CD79A, LYPD3, RPL28, HBG2, RPL23AP7, TRNR, CXCL9. Venn diagram showed that CXCL9 was a common DEG between breast cancer brain metastasis and AD. Functional enrichment analysis indicated that CXCL9 was involved in cellular responses to chemokines, negative regulation of immune system processes, negative regulation of vascular morphogenesis, Toll-like receptor signaling pathway, nucleotide oligomerization domain (NOD)‑like receptor signaling pathway, and JAK-STAT signaling pathway. Before radiotherapy, patients with cognitive function impairment and normal cognitive function accounted for 61.9% and 38.1%, respectively, with a statistically significant difference in MMSE scores [(24.53±2.19) vs. (28.89±1.36), P˂0.01]. Compared with normal cognitive function group, patients with cognitive function impairment had a significantly increased number of brain metastases and significantly lower Karnofsky performance status (KPS) scores and serum CXCL9 levels (P˂0.05). Three months after radiotherapy, patients with cognitive function impairment and normal cognitive function accounted for 47.6% and 52.4%, respectively, with a statistically significant difference in MMSE scores [(25.16±1.98) vs. (28.18±1.08), P˂0.01]. Compared with normal cognitive function group, patients with cognitive function impairment had significantly lower CXCL9 levels (P=0.003). In patients with normal cognitive function, CXCL9 levels were remarkably lower after radiotherapy compared to those before radiotherapy (P=0.009). Conclusions Patients with cognitive function impairment had significantly lower CXCL9 levels than those with normal cognitive function, and whole-brain radiotherapy may be related to a certain degree of reduction in CXCL9 levels.

Hemophilia, which includes different types such as hemophilia A and hemophilia B, is a hemorrhagic disorder with inherited blood clotting abnormalities. The main clinical manifestations are spontaneous bleeding of joints, muscles and deep tissues or repeated bleeding after trauma. It often starts at an early age and affects the whole life. The treatment of hemophilia patients is still dominated by alternative therapy, supplementing the corresponding clotting factors. In addition, non-factor drug therapy is adopted such as bispecific monoclonal antibodies and gene therapy. In recent years, the research on the pathogenesis of hemophilia A has made great progress, which is no longer limited to the mutation of the coding sequence of coagulation factor gene as the only cause of hemophilia. Many studies have found that abnormal expression of non-coding RNA (ncRNA) is involved in the regulation of coagulation factor Ⅷ (FⅧ) mRNA and protein, which not only explains why patients with normal FⅧ genotypes still present with hemophilia A, but also provides new directions for understanding the pathogenesis of other types of hemophilia. This paper reviews the research progress on the regulatory mechanism of ncRNA in hemophilia A.

Perioperative neurocognitive disorder (PND) significantly threatens brain health, leading to prolonged hospitalization, increased patient mortality risk, and poor long-term prognosis. Sleep disorder may substantially elevate the risk of neurocognitive dysfunction. However, the specific role of sleep in PND development remains to be elucidated. In addition, controversy exists over whether interventions for perioperative sleep disorder can effectively prevent PND. Therefore, this review aims to explore the basic function and regulatory principles of sleep, the clinical characteristics of perioperative sleep disorder, its role and potential mechanisms in PND development. Furthermore, we also provide new evidence on the potential therapeutic strategies to modulate sleep disorder for PND management, to improve patient's neurocognitive prognosis and long-term outcomes.