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Jun 2016 DOI 10.14302/issn.2372-6601.jhor-16-1125
Kato Jun-yaCorresponding author
Graduate School of Biological Sciences, Nara Institute of Science and Technology, Nara, Japan
Senescence is a powerful mechanism that prevents the development of tumors in vivo; however, once tumors are formed, most are refractory to senescence in response to oncogenic stress. Therefore, a novel pathway leading to senescence is required. We herein demonstrated that the cell cycle regulator CDC6 translocated from the nucleus to the cytoplasm during senescence in a leptomycin B-resistant manner. In order to evaluate the translocation of CDC6, we utilized an estrogen receptor (ER) tag to retain CDC6 in the cytoplasm. ER-tagged CDC6 was exclusively cytoplasmic, inhibited cell proliferation, and induced senescence-associated (SA) b-galactosidase activity. Furthermore, ER-CDC6 inhibited the transformation of mouse fibroblasts by the active ras oncogene in vitro, and suppressed tumor formation in NOD-SCID mice. Thus, CDC6 may play a critical role in the regulation of senescence in the cytoplasm in order to counteract tumorigenesis.
Jul 2026 DOI 10.14302/issn.2470-0436.jos-26-6357
Awan MuhammadCorresponding author
Herpes zoster ophthalmicus (HZO) is a manifestation of varicella-zoster virus (VZV) reactivation involving the ophthalmic division of the trigeminal nerve, carrying significant risk of vision-threatening complications. Diplopia in HZO is often attributed to cranial nerve palsy, although orbital myositis remains a rare and underrecognized cause. We present a 79-year-old male who developed right-sided headache, binocular diplopia, and a V1 vesicular rash two weeks after receiving the recombinant zoster vaccine. Examination revealed restriction of extraocular movements without a localizing cranial nerve pattern, raising suspicion for orbital myositis. Neuroimaging was unremarkable, and VZV polymerase chain reaction confirmed the diagnosis of HZO. The patient received antiviral therapy and was discharged in stable condition after three days. This case highlights HZO presenting with suspected orbital myositis in temporal association with vaccination and underscores the need for vigilance for uncommon neuro-ophthalmic manifestations, as early recognition and treatment are essential to prevent vision-threatening complications. Given the patient's advanced age, this case also emphasizes the possibility that age-related immunosenescence may contribute to VZV reactivation and the development of HZO-related ocular complications. Potential therapeutic approaches targeting age-related immune dysfunction are also considered.
Jan 2015 DOI 10.14302/issn.2379-7835.ijn-14-606
Michael J. GladeCorresponding author
Telomeres are strings of DNA that are not themselves genes but that extend every chromosome beyond its last gene. Terminal telomeres are sacrificed during every mitotic event in human cells (“telomere attrition”), preserving the functional genome despite the “end replication problem.” However, the “telomeric theory of biological aging” suggests that when an individual cell has reproduced itself a sufficient number of times (the “Hayflick limit”), some the its telomeres have become critically shortened (“telomeric crisis”) and cannot completely “cap off” a chromosome, and any further attempts to replicate such a chromosome would produce damaged DNA and a dysfunctional cell (“cellular aging”). As cells enter telomeric crisis, they usually initiate intracellular signaling cascades that arrest DNA replication and mitotic activity, converting biologically active cells into inactive cells (“cellular senescence”). The progressive accumulation of senescent cells impairs the healthy functioning of tissues and produces “biological aging.” Oxidative stress damages telomeres and accelerates telomere attrition and biological aging. Premature biological aging is associated with degenerative diseases and diminished quality of life. Reducing the level of systemic oxidative stress can ease the oxidative drive toward cellular senescence and premature biological aging. Increased intakes of antioxidant-rich foods and specific antioxidant nutrients (such as fruits and vegetables, α -lipoic acid, astaxanthin, eicosapentaenoic acid, docosahexaenoic acid, trans-resveratrol, N-acetylcysteine, methylsulfonylmethane, lutein, vitamin C, vitamin D, vitamin E, and γ-tocotrienol) may decrease cellular and systemic oxidative stress and decelerate biological aging.