Paratesticular cellular angiofibroma: a case report

Introduction Paratesticular cellular angiofibroma is a rare benign mesenchymal tumor. The optimal management is surgical resection due to the difficulty of preoperative accurate diagnosis. Case presentation A 51-year-old Japanese male visited our hospital complaining of asymptomatic left scrotal swelling. Physical examination revealed a nontender elastic paratesticular mass (5.5 cm in diameter). Although testicular germ cell tumor was ruled out clinically, the possibility of malignant potential remained for the tumor. Since the patient consented to complete resection, a transinguinal radical orchiectomy was performed. The pathological diagnosis revealed cellular angiofibroma. The patient recovered without perioperative complications, and no apparent recurrence was observed at 5 years after surgery. Conclusion The pathological findings were compatible for cellular angiofibroma. The tumor was successfully resected, and no apparent recurrence was observed at 5 years after surgery.Citation: Murashima, T., Kida, K., Gi, T. et al. Paratesticular cellular angiofibroma: a case report. J Med Case Reports 18, 170 (2024). https://doi.org/10.1186/s13256-024-04499-

Production of Prompt Charmonia in e+e- Annihilation at sqrt[s] ≈ 10.6 GeV

journal articl

方法論としての町家--歴史都市・京都の「超再生」を促す原動力?

departmental bulletin pape

凍結期における自然地盤の熱流特性

journal articl

Polymorphisms in the promoter and downstream enhancer region between the HAB and LAB specific sequence with probable binding factors.

<p>Polymorphisms in the promoter and downstream enhancer region between the HAB and LAB specific sequence with probable binding factors.</p

Forward and reverse primers used for quantitative PCR and their specific annealing temperatures.

<p>Numbers for qPCR assay indicate the SYBR Green Kit used (1: Roche; 2: Qiagen).</p

Vasopressin (AVP) immunohistochemistry analysis.

<p>AVP fluorescence antibody-staining of the paraventricular nucleus (PVN) flanking the 3rd ventricle (3V) in HAB and LAB mice. For corresponding <i>in situ</i> hybridization, see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0005129#pone-0005129-g007" target="_blank">Fig. 7</a>.</p

Co-expression of hP2X7R-Gln460Arg with hP2X7R-WT diminishes normal receptor function.

<p>(A) Increase of intracellular calcium of stably transfected HEK293 cells was measured following BzATP application (50 μM) (repeated measures ANOVA, <i>P</i> < 0.01 hP2X7R-WT and hP2X7R-Gln460Arg versus HEK293; n = 4). For each cell line, nine individual clones were analyzed (B) Left: representative whole-cell measurements out of four independent experiments by whole-cell patch clamp analysis. Right: Quantification of inward currents elicited by BzATP (One-way ANOVA with Scheffé’s test, ns = non-significant versus hP2X7R-WT; n = 4) (C) Increase of intracellular calcium of HEK293 cells stably transfected with hP2X7R-WT (9 clones) and stably double transfected with hP2X7R-WT + hP2X7R-Gln460Arg (10 clones) was measured (repeated measures ANOVA, <i>P</i> < 0.01 hP2X7R-WT + Gln460Arg versus hP2X7R-WT; n = 4). (D) Left: representative whole-cell measurements by whole-cell patch clamp analysis. Right: Quantification of inward currents elicited by BzATP (One-way ANOVA with Scheffé’s test, *<i>P</i> < 0.05 versus hP2X7R-WT; n = 4) (E) BzATP (50 μM)-induced activation of p-ERK 1/2 in HEK293 cells expressing P2X7R variants. Each value of pERK1/2 was normalized to total ERK1/2. Results are expressed as the percentage of maximum pERK1/2 obtained at 2 minutes of stimulation in hP2X7R-WT cells ± s.e.m. from 3 independent experiments. One-way ANOVA, * P < 0.05 versus hP2X7R-WT and versus hP2X7R-Gln460Arg at the same time points. Bottom panels show WBs of pERK1/2 and total ERK1/2 from a representative experiment. (+): Fetal calf serum 10% treatment for 10 min, positive control for p-ERK 1/2 activation. Inset: Quantification and representative example showing WB detection of hP2X7R variants in parental HEK293 cells and analyzed stable clones.</p

hP2X7R-Gln460Arg interacts with hP2X7R-WT at the cell membrane.

<p>(A) Immunoprecipitation (IP) assays on HEK293 clones constitutively co-expressing STREP-tagged hP2X7R-WT and HIS-tagged hP2X7R-Gln460Arg, using anti-HIS (αHIS) and anti-STREP (αSTREP) antibodies for the immunoblotting (IB). One representative experiment out of four with similar results is shown from two out of four clones analyzed. Mock: IP performed in parallel with normal mouse IgGs. Right: Control panel showing that neither HIS-tagged hP2X7R-Gln460Arg nor STREP-tagged hP2X7R-WT were detected in untransfected HEK293 cells. Duplicates are shown. (B) FRET-based confirmation of interaction between hP2X7R-Gln460Arg with hP2X7R-WT. Pixel-by-pixel quantification of sensitized emission FRET on living cells. First column: FRET image: Ex 458 nm/Em 530–630 nm. Second and third columns: Cerulean and cp49Venus fluorescence. The fourth column displays the NFRET image of the same cell. Brighter pixels show higher NFRET levels. Pixels with signal amplitude below threshold are shaded blue. Representative cell images for each condition are shown. Insets: representative magnifications of membrane areas where quantifications were performed. FRET Quantification: Measurement of FRET levels in the cell membrane. Each bar represents the mean ± s.e.m. of 5–10 cells, delimiting 4–6 ROIs per cell at the membrane level, in four independent experiments.</p

Silencing of either subunit in cells co-expressing hP2X7R-Gln460Arg and hP2X7R-WT restores normal P2X7R function.

<p>(A) Increase of intracellular calcium triggered by BzATP (50 μM) was evaluated in hP2X7R-WT and hP2X7R-Gln460Arg co-expressing HEK293 cells transfected with the corresponding scramble siRNA control, WT- or Gln460Arg-specific P2X7R siRNAs (100 nM) for 72 h (repeated measures ANOVA, <i>P</i> < 0.001 siRNA hP2X7R-WT and siRNA hP2X7R-Gln460Arg versus scramble siRNA; n = 4). (B) Silencing of mRNA coding for P2X7R-WT or P2X7R-Gln460Arg was confirmed by quantitative real-time RT-PCR (One-way ANOVA, *<i>P</i> < 0.01 versus scramble siRNA; n = 3). (C) BzATP (50 μM)-induced activation of p-ERK 1/2 in HEK293 cells expressing hP2X7R-WT (left), hP2X7R-Gln460Arg (middle) and co-expressing hP2X7R-WT and hP2X7R-Gln460Arg (right). Each value of pERK1/2 was normalized to total ERK1/2. Results are expressed as the percentage of pERK1/2 obtained at 6 minutes of stimulation in hP2X7R-WT cells ± s.e.m. from 3 independent experiments. One-way ANOVA, * P < 0.05 versus hP2X7R-WT and versus hP2X7R-Gln460Arg at the same time points. WBs from a representative experiment are shown. (D) HEK293 cells co-expressing hP2X7R-WT and hP2X7R-Gln460Arg P2X7R variants were silenced using siRNAs that specifically target hP2X7R-Gln460Arg (left), hP2X7R-WT (middle) and with the corresponding scramble siRNA as a control (right). Each value of pERK1/2 was normalized to total ERK1/2. Results are expressed as the percentage of pERK1/2 obtained at 6 minutes of stimulation in siRNA hP2X7R-Gln460Arg cells ± s.e.m. from 3 independent experiments. One-way ANOVA, * P < 0.05 versus siRNA hP2X7R-WT and versus siRNA hP2X7R-Gln460Arg at the same time points. WBs from a representative experiment are shown.</p