Potential biomarkers for immune monitoring after renal transplantation.

Renal transplantation represents the foremost efficacious approach for ameliorating end-stage renal disease. Despite the current state of advanced renal transplantation techniques and the established postoperative immunosuppression strategy, a subset of patients continues to experience immune rejection during both the early and late postoperative phases, ultimately leading to graft loss. Consequently, the identification of immunobiomarkers capable of predicting the onset of immune rejection becomes imperative in order to facilitate early intervention strategies and enhance long-term prognoses. Upon reviewing the pertinent literature, we identified several indicators that could potentially serve as immune biomarkers to varying extents. These include the T1/T2 ratio, Treg/Th17 ratio, IL-10/TNF-α ratio, IL-33, IL-34, IL-6, IL-4, other cytokines, and NOX2/4.

Fluorescence spectroscopic profiling of urine samples for predicting kidney transplant rejection.

Rejection is the primary factor affecting the functionality of a kidney post-transplant, where its prompt prediction of risk significantly influences therapeutic strategies and clinical outcomes. Current graft health assessment methods, including serum creatinine measurements and transplant kidney puncture biopsies, possess considerable limitations. In contrast, urine serves as a direct indicator of the graft's degenerative stage and provides a more accurate measure than peripheral blood analysis, given its non-invasive collection of kidney-specific metabolite. This research entailed collecting fluorescent fingerprint data from 120 urine samples of post-renal transplant patients using hyperspectral imaging, followed by the development of a learning model to detect various forms of immunological rejection. The model successfully identified multiple rejection types with an average diagnostic accuracy of 95.56 %.Beyond proposing an innovative approach for predicting the risk of complications post-kidney transplantation, this study heralds the potential introduction of a non-invasive, rapid, and accurate supplementary method for risk assessment in clinical practice.

Downregulation of miR-485-3p promotes proliferation, migration and invasion in prostate cancer through activation of TGF-ß signaling.

BACKGROUND: Prostate cancer (PC) is the second leading cause of cancer-related death among men worldwide. Downregulation of miR-485-3p has been revealed to participate in the tumorigenesis and progression of many types of cancer. However, the clinical and biological role of miR-485-3p in PC remains largely unknown. METHODS: The expression of miR-485-3p was analyzed in the published databases and detected in our clinical samples and cell lines by RT-qPCR assay. CCK8, transwell invasion and migration, and colony formation assays were performed to investigate the biological function of miR-485-3p. Bioinformatical analysis, RIP, western blotting and luciferase reporter assays were carried out to explore the downstream mechanism of miR-485-3p. RESULTS: The level of miR-485-3p was downregulated in PC tissues, particularly in primary PC tissues with metastasis relative to normal prostate tissues. miR-485-3p downregulation was positively correlated with poor disease-free and overall survival in patients with PC. Functionally, miR-485-3p overexpression dramatically suppressed the proliferation, migration and invasion ability of PC cells in vitro. Mechanistically, miR-485-3p overexpression suppressed the activity of TGF-ß signaling by targeting TGFBR2 to play tumor-suppressive roles in PC progression. CONCLUSION: Our study reports the miR-485-3p/TGFBR2/ TGF-ß signaling axis in tumor development of PC, suggesting miR-485-3p may be a potential target to develop therapeutic strategies against PC.

Thalidomide ameliorate graft chronic rejection in an allogenic kidney transplant model.

Chronic T cell mediated rejection (TCMR), which is characterized by infiltration of the interstitium by T cells and macrophages, still remains a major barrier to the long-term survival of kidney transplantation. Our recent report indicated that thalidomide can attenuate graft arteriosclerosis in an aortic transplant model. In this study, we investigated the effect of thalidomide on chronic TCMR in a rat model of kidney transplantation. Fischer or Lewis kidney allografts were transplanted into Lewis recipient rats. After kidney transplantation, recipient rats were divided into 3 groups: the isograft (Iso) group, allograft (Allo) group, and thalidomide (Tha) group. Rats were sacrificed at 8 weeks after kidney transplantation, and blood and kidney samples were collected. Serum concentrations of creatinine (SCr),interleukin (IL)-2, IL-6, IL-17, and TNF-α in recipients were determined, and flow cytometry was used to detect the percentages of CD4+CD25+, CD4+ Foxp3+and CD4+Th17+ cell subsets in the peripheral blood. Grafts were procured for histopathological examination, and the expressions of α-SMA, transforming growth-ß1 (TGF-ß1), and VEGF in kidney grafts were investigated using Western blot. Thalidomide treatment significantly ameliorated chronic rejection, reduced renal allograft tissue damage, and decreased serum creatinine levels. Attenuation of chronic TCMR was due to the prohibited production of inflammatory cytokines, altered distribution of the CD4+ CD25+ FoxP3+ regulatory T (Treg) and CD4+ Th17+ cells in the peripheral blood, and decreased expression of TGF-ß1, α-SMA, and VEGF in the kidney graft. These results demonstrated that thalidomide could effectively ameliorate chronic TCMR in a rat kidney transplant model.

Primary Mucinous Adenocarcinoma of Appendix Invading Urinary Bladder with a Fistula: A Case Report.

An adenocarcinoma of the appendix invading the urinary bladder, which is difficult to be diagnosed before the operation, is an extremely rare disease. Only a few cases have been reported. Here we reported a case of patient diagnosed with the mucinous adenocarcinoma of the appendix invading the urinary bladder. The case reported in this study was a 54-years old man who was admitted due to a 6-month history of intermittent episodes of irritative voiding symptoms of the bladder, and weight loss. The patient did not have any gastrointestinal symptoms. The physical examination, laboratory examination, cytology of the urine, computed tomography and cystoscopy were inconclusive. The partial cystectomy, subsequent exploratory laparotomy and intraoperative frozen analysis revealed the appendiceal mucinous adenocarcinoma with a fistula to the urinary bladder. The appendectomy and the right hemicolectomy with a ileocolic anastomosis, the lymphadenectomy and the partial cystectomy limited to the anterior wall was performed. Six months after operation, the patient was in a good health with no obvious discomfort, no recurrence or distant metastases. The recommended treatment for the adenocarcinoma of the appendix invading the bladder with a fistula formation is as follows: appendectomy, right hemicolectomy with ileocolic anastomosis, lymphadenectomy, partial cystectomy and intraperitoneal hyperthermic chemoperfusion.

Genetic risk factors for post-transplantation diabetes mellitus in Chinese Han renal allograft recipients treated with tacrolimus.

BACKGROUND: Post-transplantation diabetes mellitus (PTDM) is a serious metabolic complication after kidney transplantation. The aim of this study was to explore the association of clinical variables and five selected single nucleotide polymorphisms (SNPs) with PTDM in Chinese Han renal allograft recipients taking tacrolimus (TAC). METHODS: A total of 129 non-diabetic, primary, Chinese Han renal allograft recipients treated with TAC were enrolled. Five SNPs (CYP3A5 rs776741, rs776746, rs15524, CYP24A1 rs2296241, and PPARG rs1801282) were genotyped and analyzed. RESULTS: Among 129 recipients, 17 (13.2%) developed PTDM. Both univariate and multivariate analysis demonstrated that age over 50 years old and CYP24A1 rs2296241 A allele were independently correlated with the development of PTDM, while no significant differences was observed in TAC pharmacokinetics and CYP3A5, PPARG polymorphisms between two groups. CONCLUSIONS: Patients with advanced age and CYP24A1 rs2296241 A allele had an increased risk of PTDM after kidney transplantation.

Comparison of clinical outcome of low-dose and high-dose rabbit antithymocyte globulin induction therapy in renal transplantation: a single-center experience.

BACKGROUND: To explore a better balance between efficacy and complications, we respectively compared the clinical outcome of low-dose and high-dose rATG induction therapy with a control group in renal transplantations from March 2009 to March 2012. MATERIAL AND METHODS: 281 kidney transplant recipients were included in 3 groups. The low-dose group (n=39) received rATG 1 mg/kg on the first day and 0.5 mg/kg on the next consecutive 3 days post-transplantation. The high-dose group (n=30) received rATG 1 mg/kg for 6 days. The control group (n=212) received no induction therapy. All patients were treated with Prednisolone, Mycophenolate mofetil, cyclosporine A, or tacrolimus capsules. Acute rejection rates, renal function, CMV infection, patient survival, and the adverse effects of rATG were reviewed. RESULTS: The acute rejection rate was significantly lower in the rATG group compared with the control group (low-dose 17.9% vs. control 35.4%, P=0.03, and high-dose 16.7% vs. control 35.4%, P=0.038). There was no statistically significant difference in 3-year survival and graft survival rates among the groups. Renal function early recovery was similar in the rATG and the control group. The CMV infection rate in the high-dose rATG group was higher than the low-dose rATG and the control group (p=0.037 and p=0.002, respectively). rATG induction therapy was associated with thrombocytopenia in our series, especially in the high-dose rATG group. CONCLUSIONS: Low-dose rATG induction may be superior to high-dose rATG induction therapy in renal transplantation.

The rs1050450 C > T polymorphism of GPX1 is associated with the risk of bladder but not prostate cancer: evidence from a meta-analysis.

Glutathione peroxidase (GPX) is an endogenous antioxidant enzyme counteracting oxidative stress. Accumulating evidence has demonstrated that the GPX1 rs1050450 C > T polymorphism may modulate cancer risk, but the association of GPX1 rs1050450 polymorphism with bladder cancer (BC) and prostate cancer (PCa) is still inconclusive. This meta-analysis was designed to determine the exact association of GPX1 rs1050450 C > T polymorphism with the risk of bladder cancer and prostate cancer. Odds ratios (ORs) and 95% confidence intervals (CI) were calculated to estimate the association strength. Databases of PubMed, EMBASE, and China National Knowledge Infrastructure were searched to retrieve eligible studies. In total, ten eligible studies with 6,194 participants were included. By pooling all eligible studies, we found that carriers of the variant T allele were associated with a significantly increased risk of urinary tract cancer (T vs. C: OR = 1.459 and 95% CI, 1.086-1.962; CT/TT vs. CC: OR = 1.411 and 95 % CI, 1.053-1.891). In stratified analysis, we observed that the rs1050450 C > T polymorphism was significantly associated with an increased risk of BC (T vs. C: OR = 2.111 and 95% CI, 1.020-4.368; CT/TT vs. CC: OR = 1.876 and 95% CI, 1.011-3.480), while the association was not significant for PCa. Egger's test and Begg's test revealed no publication bias. The present meta-analysis provides evidence that the GPX1 rs1050450 C > T polymorphism leads to an increased risk of BC but not the risk of PCa.

A new RNA-seq method to detect the transcription and non-coding RNA in prostate cancer.

Prostate cancer is a big killer in many regions especially American men, and this year, the diagnosed rate rises rapidly. We aimed to find the biomarker or any changing in prostate cancer patients. With the development of next generation sequencing, much genomic alteration has been found. Here, basing on the RNA-seq result of human prostate cancer tissue, we tried to find the transcription or non-coding RNA expressed differentially between normal tissue and prostate cancer tissue. 10 T sample data is the RNA-seq data for prostate cancer tissue in this study, we found the differential gene is TFF3-Trefoil factor 3, which was more than seven fold change from prostate cancer tissue to normal tissue, and the most outstanding transcript is C15orf21. Additionally, 9 lncRNAs were found according our method. Finally, we found the many important non-coding RNA related to prostate cancer, some of them were long non-coding RNA (lncRNA).

[Amniotic fluid: a novel source for tissue engineering].

OBJECTIVE: To investigate the possibility of using amniotic fluid cells as seed cells for tissue engineering. METHODS: Amniotic fluid was obtained by ultrasound-guided amniocentesis performed on pregnant women with a gestational age ranging from 16(th) approximately 23(rd) weeks. The cells isolated from the amniotic fluid were cultured in F10 culture fluid with 10% FBS. Immunocytochemistry was used to examine the standard intermediate filaments. After 3 passages of subculture, the cells were harvested and seeded onto PGA polymer scaffold. The cellular morphology, structure and adhesion with scaffold were evaluated by contrast microscope and scanning electronic microscope. RESULTS: The amniocytes expanded rapidly in culture media. Immunocytochemistry revealed positive signals for vimentin, smooth muscle action (SMA), and pan cytokeratin, and negative signals for desmin. Amniocytes-polymer complex analysis showed confluent cells firmly attached to the scaffold, with no evidence of cell death. CONCLUSION: The expansion potential of amniotic fluid cells is active. They express the characteristics of mesenchymal cells. The cells on PGA polymer scaffold can grow rapidly and maintain its morphological property. So the amniotic fluid may be a practical cell source for tissue engineering.