1.Slow-growing venous malformation in a 92-year-old man, mimicking axillary lymphadenopathy
Hideo TSUZUKI ; Hiroe OISHI ; Atsushi MORISHITA ; Chizuko UEMURA ; Mitsuko IGUCHI ; Tsutomu SHINOHARA
Journal of Rural Medicine 2025;20(4):311-313
Objective: Venous malformations (VMs) are low-flow blood reservoir mass lesions with spongy or cystic venous lumens caused by dilation of the venous system vasculature. A VM is a congenital lesion that presents at birth and enlarges during childhood as the host grows. Subcutaneous lesions due to VMs are rarely diagnosed at an advanced age. We report a case of axillary VM in an older patient.Patient: A 92-year-old man was suspected of having left axillary lymphadenopathy (single nodule, 23 mm long) on chest computed tomography (CT) scan. Seven years earlier, a chest CT scan showed a small, 13 mm nodule in the same area.Results: On ultrasound elastography, the lesion did not appear hard, however, color Doppler imaging revealed abundant blood flow, suggesting a malignant lesion. Histologically, the lesions were consistent with VM.Conclusion: VMs should be considered a differential diagnosis for superficial lymphadenopathy, even in older patients.
2.Studies on The Interactions Between NIRF and P53
Changzhu DUAN ; Shuping PU ; Mori TSUTOMU ; Kochi HIDEO ; Zongyin QIU
Progress in Biochemistry and Biophysics 2006;0(02):-
HEK293 or HeLa cells were transfected by NIRF and, or P53, whole cell extracts andimmunoprecipitates were subjected to SDS-PAGE followed by Western blotting. GST pull-down was carried outto identify the interactions between NIRF and P53. In vitro ubiquitination reaction was carried out to identify P53ubquitinate by NIRF. The results suggested that NIRF could interact with P53 in vivo and in vitro. The results alsoshowed that NIRF could ubiquitinate P53 in vivo and in vitro. The results indicated that NIRF would be a newnegative regulator of P53.


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