Objectives: To investigate clinical features and outcomes in patients with acute cholecystitis with gall bladder perforation receiving open cholecystectomy or percutaneous transhepatic gall bladder drainage in the emergency department. Methods: From 1996 through 2005, 33 patients with non-traumatic gall bladder perforation, among 585 patients with acute cholecystitis, were enrolled. Patients were divided into two groups: open cholecystectomy in 16 patients and percutaneous transhepatic gall bladder drainage in 17 patients. Medical records, including demographic data, past history of systemic diseases or gallbladder stones, initial clinical presentations, laboratory data, physical status, therapeutic interventions, and outcomes, were analysed. Results: Mean patient age was 72.6 years (range 54-92 years). 28 patients (84.8%) were male. Median time of symptom onset before emergency department diagnosis was 5 days (range 0.5-30 days). Estimated incidence of gall bladder perforation was 5.6% (33/585). 27 patients (81.8%) had gallstones operatively or in image studies. All patients had either right upper quadrant pain/tenderness or epigastric pain/tenderness. Only 9 (27.3%) patients had positive Murphy's sign. Six patients in the percutaneous transhepatic gall bladder drainage group received further open cholecystectomy. Overall mortality was 24.2% (8/33). The direct cause of death was disease related sepsis in all patients. Patients receiving percutaneous transhepatic gall bladder drainage had a higher survival rate than those receiving open cholecystectomy (100% vs 50%, p,0.001). No differences in complications and length of hospital stay of survivors were observed between groups. Conclusions: In this study, we delineated clinical features of patients with gall bladder perforation. Better clinical outcome is observed for percutaneous transhepatic gall bladder drainage, and this is suggested as an initial therapeutic choice, especially in high risk patients who are likely to need surgery.T he choice of therapeutic modalities for acute cholecystitis includes both open cholecystectomy and percutaneous transhepatic gallbladder drainage. If left untreated, acute cholecystitis can progress to gall bladder perforation. During the past decades, open cholecystectomy has been used to treat acute cholecystitis with gallbladder perforation contributing to the mortality rate ranging from 8.6% to 23% in respective studies.1 2 Risk factors, including older age, increased disease severity, and comorbidities with multiple systemic diseases, were considered to account for the high mortality rate.3 4 In recent years, percutaneous transhepatic gallbladder drainage has been successfully adopted as an alternative or a bridge before elective cholecystectomy for acute cholecystitis, 5 and even used in high risk patients for a greatly improved outcome.5-7 A favourable outcome was also demonstrated in patients with a localised gall bladder perforation under percutaneous transhepatic gallbladder drainage treatment.8 To the best of our knowled...
Objectives: To replicate the association of 7 single nucleotide polymorphisms (SNPs; which were identified as strong association with IgAN in a genome-wide association study) and investigate whether the 7 SNPs influence the clinical manifestation and prognostic for IgAN patients, a case-control genetic study from an independent western Han cohort was conducted. Methods: Genomic DNA was extracted from 521 patients with IgAN and 535 healthy controls, and TaqMan allelic discrimination assay was used to type SNP polymorphism. Traditional linear logistic regression analyses were used to detect 7 SNP associations in dominant, recessive and additive genetic models. Bonferroni correction was used to adjust the P-values for multiple testing. A total of 459 IgAN patients with integrated clinical data were investigated the relationship between the genotype and phenotype of IgAN. 315 IgAN patients were followed-up. Then, a retrospective cohort study of 315 IgAN patients was conducted to explore the relationship between genotype and the progression of renal disease over a mean period of 44.49 AE 19.94 months. Results: After Bonferroni correction, no significant SNP association was observed between IgAN patients and controls (Pc > 0.05). For genotypephenotype correlation studies, marginally significant association of rs 2856717 T/C recessive model for the T allele was significantly associated with eGFR (< 60 ml/min) of IgAN patients (P Z 0.008, Pc Z 0.056, OR Z 1.527). T allele at position of rs9275596 was significantly associated with macroscopic hematuria of IgAN patients under the dominant and additive models of inheritance (P < 0.001, Pc Z 0.007, OR Z 2.983) and (P < 0.001, Pc Z 0.007, OR Z 2.17), respectively. Results from Kaplan-Meier analysis showed that patients carrying the TT+TC genotype for rs2856717 had reduce renal survival rate than patients carrying the CC genotype (85.1% vs. 92.7%, P Z 0.046). Conclusion: Rs 2856717 may influence the clinical manifestations and poor outcome of IgAN. Further studies are required to definition of the mechanistic effects of genetic variants on clinical traits. http://dx. Objective:To investigate the effect of FK506 on IgAN rats with mesangial cell proliferation and its relationship with TRPC ion channels and calcineurin. Methods: IgAN model was established using "BSA + CCl 4 + LPS" method, in which rats were treated with 0.5, 1.0 mg/kg FK506 every day by intragastric administration for 2 weeks. We measured the hematuria, proteinuria and the renal function through the laboratory testing. HE staining were conducted to observe the pathological conditions. RT-PCR and Western Blotting were performed for detecting the rat renal cortical TRPC1, TRPC4/5, TRPC3/6/7 and calcineurin mRNA and protein expressions. Results: The levels of hematuria, proteinuria, serum BUN and sCr were elevated in IgAN group compared with normal group (P < 0.01), which could be ameliorated by treating with FK506 (P < 0.05), especially in high dose group (P < 0.01). HE staining showed that the degree of kidney pat...
was the only biomarker in the present study that had an association with dehydration levels. In the present study, the selected parameters of the RFA were not suitable to detect early changes in renal function induced by dehydration.
Background: Breast cancer associated macrophages often promote tumor growth and metastasis by conditioning the tumor microenvironment and suppressing adaptive immune responses. Tartrate-resistant acid phosphatase (TRACP) is a novel serum biomarker associated with systemic macrophage burden in a variety of chronic inflammatory diseases and is strongly expressed by tumor-associated macrophages. We tested the hypothesis that TRACP is required for M2 macrophage polarization. Methods: Macrophage cell lines were polarized in vitro and tested for TRACP, iNOS and Arg-1 expression and their ability to promote or repress breast cancer cell growth and invasion in vitro and in vivo. A novel TRACP deficient, Acp5 mutant mouse was used as a macrophage source and as a breast cancer host to confirm a role for TRACP for macrophages to support cancer growth. Results: TRACP was up-regulated in concert with M2 polarization and down-regulated in M1 polarized cells. TRACP expression correlated with macrophage promotion of tumor growth and invasion in vitro. Although TRACP-deficient macrophages could be induced to express Arg-1 when stimulated with IL-4 plus IL-13 (M2 phenotype), the TRACP deficient macrophages behaved like M1 cells suppressing tumor growth and invasion compared to than WT cells. Tumor xenografts grew slower in primary subcutaneous grafts and metastasized less extensively in intravenous grafts in TRACP deficient mice compared to WT. Furthermore, the tumor metastatic patterns could be reversed in WT animals by co-grafting TRACP-deficient macrophages and in TRACP deficient hosts by co-grafting WT macrophages. Conclusions: TRACP expression is normally a phenotypic marker for alternatively activated macrophages, but not necessary for expression of Arg-1. In a host environment of TRACP deficiency, Arg-1 positive macrophages can be generated by cytokine stimulation in vitro and by tumor in vivo, however, TRACP deficiency still conveyed a tumor suppressive phenotype in cell based studies and in intact animals. TRACP plays a role in functional polarization of M2 macrophages and their ability to promote breast cancer growth and metastasis. Citation Format: Dai M-S, Janckila A, Lo H-C, Wu C-C, Chao T-Y, Yu J-C. Tartrate-resistant acid phosphatase (TRAcP) dependent polarization of breast cancer-promoting macrophages. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-03-08.
Tartrate-resistant acid phosphatase (TRAP) is a member of the purple acid phosphatase family and is also known as type 5 acid phosphatase. It is mainly expressed in cells of the monocyte lineage, including osteoclasts, macrophages, and dendritic cells (DCs). There are two isoforms of TRAP enzyme: TRAP-5a and TRAP5b, and TRAP-5b is produced by post-translational modification of TRAP-5a. TRAP-5b is the major isoform of TRAP secreted by osteoclasts and it has been shown that TRAP-5b activity correlates with the number of osteoclasts and serum activity in rat and human studies. In contrast, macrophages and DCs are thought to secrete TRAP-5a as the major subtype, whereas TRAP-5a is a non-specific marker of macrophage activation. The recent studies show that higher-grade proliferative tumors with much necrosis were associated with abundant macrophage expressing TRAP. Here we generate TRAP-/- knockout mice to study the function of TRAP in tumorigenesis. In vitro experiments have found that the expression of TRAP in macrophages is essential for the full promoting tumor function of M2-like tumor-associated macrophages (TAM) including tumor growth and metastasis. Marrow-derived macrophages (BMDM) extracted from the TRAP-/- mice lost promote tumor migration activity. The 4T1 tumor (murine breast cancer cell line) conditioned medium was used to induce TAM formation found M2-like TAM formation in wild type BMDM was promoted higher than that of TRAP-/- BMDM. In contrast, the TRAP-/- is much higher M1-like TAM formation than the wild type. Xenograft tumor formation assays were used to monitor tumor formation by combining 4T1 and different M2 polarized macrophages into BALB/c mice. M2-polarized macrophages with trap-defective BMDM showed reduced promoted neoplastic activity compared to wild type. In MMTV-PyMT transgenic mice, spontaneous tumor formation in knockout trap-/- significantly repressed tumor formation compared to TRAP+/+ wild type mice. Finally, we hypothesized that TRAP is essential for the full function of M2-like tumor-associated macrophages and promotes tumor metastasis. Citation Format: Dai M-S, Lo H-C, Chen L-C, Janckilla A, Tseng S-F. M2-like tumor-associated macrophages require Tartrate-resistant acid phosphatase as overall function to promote breast cancer metastasis [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P2-01-07.
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