Low-dose irradiation (LDIR) has been proven to have differential biological effects on normal mammalian somatic cells and cancer cells. Our previous study showed that p53 gene status is a critical factor regulating the effect of LDIR on cancer cells. We investigated the effect of LDIR on the breast cancer cell line MDA-MB-231 that harbors a mutant p53 gene, and the normal breast fibroblast cell line Hs 578Bst. In the present study, we showed that 150 mGy LDIR pormoted growth of MDA-MB-231 cells but not Hs 578Bst cells. Through cell cycle analyses, we found that LDIR accelerated cell cycle into S phase in MDA-MB-231 cells, but did not affect the cell cycle of Hs 578Bst cells. Using western blotting, we demonstrated that the expression of CDK4, CDK6 and cyclin D1 was upregulated in MDA-MB-231 cells after LDIR. Although LDIR increased ataxia-telangiectasia mutated (ATM) level in both MDA-MB-231 cells and Hs 578Bst cells and activated ATM/p53/p21 pathway, only the mutant type of p53 (mtp53) protein in MDA-MB-231 cells was shown to be accumulated after LDIR. Using ATM inhibitor or lentivirus-mediated small interfering RNA (siRNA) to block the ATM/p53/p21 pathway in MDA-MB-231 cells, the LDIR-induced cell proliferation was abolished. When we introduced wild-type p53 (wtp53) protein into MDA-MB-231 cells, the LDIR-induced cell proliferation was also abolished. These findings suggest that normal p53 function is crucial in ATM/p53/p21 pathway activated by LDIR. The p53 status is the most probable reason leading to differential LDIR biological activities between breast tumor cells and normal breast cells.

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Kikuchi–Fujimoto disease (KFD), also known as histiocytic necrotizing lymphadenitis, is a rare, benign, self-limiting disease characterized by local lymphadenopathy. Central nervous system involvement in KFD is extremely rare and remains a diagnostic challenge. Only 41 cases of aseptic meningitis associated with KFD have been reported worldwide, with just four cases (including our case) of KFD with meningitis as the first symptom. We report a case of KFD accompanied by aseptic meningitis with severely high intracranial pressure (400 mmH2O), increased white blood cell count (56 × 106/L), and moderately elevated protein level (0.52 g/L). This case is unique in the delayed appearance of lymphadenopathy. After 1 month of treatment with steroids, fever, headache, and lymphadenopathy gradually disappeared, and the result of cerebrospinal fluid examination gradually became normal. In conclusion, based on our case findings and our literature review on KFD with aseptic meningitis, a diagnosis of KFD should be considered when delayed appearance of lymphadenopathy is observed in patients with aseptic meningitis.

As a novel reactive oxygen species (ROS) scavenger, deuterohemin His peptide-6 (DhHP-6) has been demonstrated to prolong the lifespan of Caenorhabditis elegans and has also exhibited protective effects in myocardial ischemia-reperfusion injury. Whether similar effects occur during cerebral ischemia-reperfusion (CIR) injury remains to be elucidated. The present study evaluated the function of DhHP-6 and its underlying mechanisms in a middle cerebral artery occlusion (MCAO) model in rats. The focal transient MCAO model was implemented using the Longa method of ischemia for 2 h followed by reperfusion for 22 h in male Wistar rats. DhHP-6 was administered at the onset of reperfusion via intraperitoneal injection. The infarct volume, brain edema, brain apoptosis and neurological function were evaluated 24 h following stroke. To further determine the role of DhHP-6 in CIR injury, the levels of ROS and malondialdehyde (MDA), the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the protein expression levels of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), cleaved caspase-3, cytochrome c, Bcl-2 and phosphorylated-Akt/Akt were measured in ischemic cortex tissues. The results demonstrated that DhHP-6 significantly improved infarct volume, brain edema and neurological deficits, and reduced the percentage of TUNEL-positive cells. The levels of ROS and MDA were decreased, whereas no significant changes in the activities of SOD, CAT and GSH-Px were observed. The levels of Bax, cleaved caspase-3, and cytochrome c were downregulated, whereas the levels of Bcl-2 and p-Akt/Akt were upregulated. The results of the present study indicated that DhHP-6 may offer therapeutic potential for cerebral ischemia. The neuroprotective effects of DhHP-6 maybe mediated by its anti-oxidative properties, anti-apoptotic activities, or activation of the phosphoinositide 3-kinase/Akt survival pathway.