Journal: Turkish Journal of Urology

Article Title: Prostate MRI and transperineal TRUS/MRI fusion biopsy for prostate cancer detection: clinical practice updates

doi: 10.5152/tud.2019.19106

Figure Lengend Snippet: Biparametric MRI of the prostate at 1.5 T without endorectal coil in a 58 year-old patient with elevated PSA (7.3 ng/mL). Biparametric MRI shows in the mid of the gland in the right peripheral zone a hynomogeneous marked hypointense area on ADC (arrow in a), hyperintense on high b-value diffusion-weighted imaging (arrow in b), and hypointense on T2-weighted sequences (arrow in c) (S-PIRADS category 4 lesion); note on T2-weighted image (arrow-head in c) an hypointense area in right posterior transition zone. Transperineal US (d) and T2-weighted image (e) before fusion process for targeted biopsy. Histology of T0 target lesion: adenocarcinoma Gleason 7 (3+4) (f); Histology of T1 target lesion: chronic prostatitis (f)

Article Snippet: Histology of T0 target lesion: adenocarcinoma Gleason 7 (3+4) (f); Histology of T1 target lesion: chronic prostatitis (f) BiopSee ® system (MedCom GmbH, Germany): Transperineal Template assisted US-MRI fusion biopsy BiopSee ® was developed in Germany by MedCom GmbH, a company founded in 1997 that offers specialized telemedicine products and innovative imaging solutions in oncology, interventional radiology, and surgery.

Techniques: Diffusion-based Assay, Imaging

Journal: Cell Death and Differentiation

Article Title: A novel role for the apoptosis inhibitor ARC in suppressing TNF α -induced regulated necrosis

doi: 10.1038/cdd.2013.195

Figure Lengend Snippet: Endogenous levels of ARC suppresses TNFα-induced necrosis. (A) Immunoblot showing that TNFα-induced HMGB1 release is increased in L929 cells with stable ARC knockdown. Cells were treated with TNFα+Nec-1 for 10 h.Scr, scrambled control; KD, ARC shRNA knockdown; Nec-1, necrostatin-1. (B) TNFα-induced LDH release is increased by ARC knockdown in L929 cells. Data shown as mean±S.E. from n=3. ***P-value<0.001 versus scrambled control. (C) TNFα-induced LDH release is restored to baseline levels by reconstitution of ARC knockdown cells with wild-type (WT) ARC, but not the CARD mutant (DM). Mean±S.E. from n=7 are shown. ***P-value<0.001 KD:Empty versus Scr:Empty. #P-value<0.001 KD:ARC-HA compared with KD:Empty. Scr:Empty, scrambled shRNA+empty vector; KD:Empty, ARC shRNA+empty vector; KD:ARC-HA, ARC shRNA+WT ARC-HA; KD:DM-HA, ARC shRNA+ARC CARD double mutant (DM-HA). (D) Endogenous ARC suppresses necrosis in visceral fat resulting from vaccinia virus infection in vivo. Representative micrographs showing H&E staining of visceral fat from WT mice and mice lacking ARC (KO). Panels c and f are increased magnifications of the boxed areas in panels b and e, respectively. Bar=200 μm for panels a, b, d, and e; 50 μm for panels c and f. Arrowheads point to fatty tissue necrotic areas containing inflammatory cells. (E) Quantification of percentage of necrotic areas in fat tissue from WT and KO mice. Using ImageJ, percentage of necrotic area was determined in ≥90 fields per genotype (≥9 fields per mouse × 10 mice for each genotype.) **P-value<0.005 versus WT. (F) Representative micrographs showing H&E staining of liver tissue from WT and KO mice. Arrowheads point to focal clusters of inflammatory cells. Contrary to the adipose tissue, absence of ARC does not affect necrosis in the liver infected with vaccinia virus, as ARC is expressed at none to low levels in the livers of WT mice. Bar=100 μm. (G) Endogenous ARC suppresses TNFα-induced systemic inflammatory response syndrome. Rectal body temperature and survival of WT mice and mice lacking ARC (KO) injected intravenous with either recombinant mouse TNFα 500 μg/kg body weight or equivalent volume of phosphate-buffered saline (PBS). Time refers to after TNFα injection. Data shown as mean±S.E. WT-PBS (n=8), KO-PBS (n=8), WT-TNFα (n=11), KO-TNFα (n=11). Body temperatures were monitored, and mice with a temperature <22 °C were euthanized for ethical reasons and were considered dead. Statistics could only be performed up to 6 h post injection due to attrition (see Materials and Methods). Repeated measures two-way analysis of variance was used to compare body temperatures between ARC-deficient mice and WT mice injected with TNFα. ***P-value<0.0001 refers to differences between the entire curves, not at a single time point. A Kaplan–Meier curve was used to analyze KO injected with TNFα versus WT injected with TNFα survival curves. *P-value<0.05

Article Snippet: TNF α -induced systemic inflammatory response syndrome Recombinant mouse TNF α (R&D Systems) 500 μ g/kg body weight was injected intravenously through the tail vein in 10- to 14-week-old wild-type and nol3 −/− C57BL/6 mice.

Techniques: Western Blot, shRNA, Mutagenesis, Plasmid Preparation, Virus, Infection, In Vivo, Staining, Injection, Recombinant, Saline

Journal: Cell Death and Differentiation

Article Title: A novel role for the apoptosis inhibitor ARC in suppressing TNF α -induced regulated necrosis

doi: 10.1038/cdd.2013.195

Figure Lengend Snippet: ARC interacts with TNFR1 to inhibit TNFα-induced necrosis. (a) Immunoprecipitation (IP) of TNFR1 in lysates of TNFα-stimulated Jurkat cells stably transfected with empty vector (Φ) or ARC-HA. Immunoprecipitates were resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotted for ARC and TNFR1. Control IP performed with immunoglobulin G (IgG). Input lanes shown below IP. (b) Recombinant ARC-HA was mixed with recombinant His-TNFR1 intracellular domain (ICD). IP performed with the HA-conjugated agarose beads, immunoprecipitates were resolved by SDS-PAGE and immunoblotted for His and HA. TNFα-induced LDH release is inhibited by transient knockdown of TNFR1 with siRNA (c) or co-treatment with TNFR1 antagonist (d) to a similar extent as ARC overexpression (bar 8 versus bar 9, P-value=NS (not significant)). siScr, control siRNA; siTNFR1, siRNA targeting TNFR1. Data shown as mean±S.E. from n=3. #P-value<0.0001 as compared with cells transfected with empty vector and control siRNA (Emtpy; siScr) or transfected with empty vector and co-treated with vehicle (Emtpy; Vehicle). Transient knockdown of TNFR1 (e) or co-treatment with TNFR1 antagonist (f) rescues TNFα-induced LDH release in ARC knockdown L929 cells. Data shown as mean±S.E. from n=3. ****P-value<0.0001 as compared with cells transduced with scrambled shRNA (Scr) and transfected with control siRNA (Scr; siScr) or transduced with scrambled shRNA and co-treated with vehicle (Scr; Vehicle). #P-value<0.0001 versus cells transduced with shRNA targeting ARC and transfected with control siRNA (KD; siScr) or transduced with shRNA targeting ARC and co-treated with vehicle (KD; Vehicle). (g) ARC overexpression disrupts TNFα-induced association of RIP1 with TNFR1. IP of TNFR1 in TNFα-stimulated Jurkat cells stably transduced with empty vector (Φ) or ARC-HA, followed by immublotting for RIP1 and TNFR1. (h) Knockdown of ARC increases the association of RIP1 with TNFR1. IP of TNFR1 in TNFα-stimulated Jurkat cells stably transduced with scrambled shRNA (Scr) or ARC shRNA (KD), followed by immunoblotting for RIP1 and TNFR1

Article Snippet: TNF α -induced systemic inflammatory response syndrome Recombinant mouse TNF α (R&D Systems) 500 μ g/kg body weight was injected intravenously through the tail vein in 10- to 14-week-old wild-type and nol3 −/− C57BL/6 mice.

Techniques: Immunoprecipitation, Stable Transfection, Transfection, Plasmid Preparation, Polyacrylamide Gel Electrophoresis, SDS Page, Recombinant, Over Expression, Transduction, shRNA, Western Blot