Glioma is diagnosed as the most common intracranial malignant tumor. cancer stem cells determine stemness and radioresistance, and may facilitate glioma recurrence. The present study aimed to investigate whether the long non-coding rna (lncrna) transmembrane phosphatase with tensin homology pseudogene 1 (TPTeP1) regulated cell stemness and radioresistance of glioma, and determine the underlying molecular mechanism of TPTeP1 in the modulation of glioma progression. cell and molecular biology techniques were applied for investigating the role of TPTeP1 in glioma cell lines, animal model, and clinical samples. The results demonstrated that TPTeP1 attenuated stemness and radioresistance of glioma both in vitro and in vivo. in addition, TPTeP1 augmented MaPK14 expression by competitively interacting with microrna (mir)-106a-5p, thus activating the P38 MaPK signaling pathway, and suppressing glioma stemness and radioresistance. TPTeP1 functionally bound to mir-106a-5p, which formed a reciprocal regulatory loop to stimulate the P38 MaPK signaling pathway. low TPTeP1 expression levels were detected in high-grade glioma tissues compared with low-grade glioma tissues, and were positively associated with poor prognosis of patients with glioma. Furthermore, analysis using data from The cancer Genome atlas database confirmed the molecular mechanism and biological significance of dysregulation of TPTEP1 in glioma progression. Taken together, the results of the present study suggest that TPTeP1 may be applied as a diagnostic and prognostic indicator for glioma, and may be an alternative target for the treatment of glioma.

Mobile phone use has rapidly increased worldwide, and pregnant women are passively or actively exposed to the associated electromagnetic radiation. Maternal cell phone exposure is related to behavioral difficulties in young offspring. However, whether prenatal mobile phone exposure can predispose the elderly offspring to cognitive impairment is unclear. The enriched environment (EE) has shown positive effects on cognition in an immature brain, but its impact on aging offspring after prenatal cell phone exposure is unknown. This study aimed to investigate whether prenatal exposure to mobile phone exerts long-term effects on cognition in elderly rat offspring and whether EE during adulthood can rescue cognitive impairment by altering the synaptic plasticity. Pregnant rats were subjected to prenatal short-term or long-term cell phone exposure and offspring rats were randomly assigned to standard or EE. Spatial learning and memory were investigated using Morris water maze (MWM) in elderly rat offspring. Hippocampal cellular morphology was assessed by hematoxylineosin staining and synaptic ultrastructure was evaluated with transmission electron microscopy. Expression of synaptophysin (SYN), postsynaptic density-95 (PSD-95), and brain-derived neurotrophic factor (BDNF) were detected by western blot. The results demonstrated that prenatal long-term but not short-term exposure to mobile phone lead to cognitive impairment, morphological changes in the hippocampal cells, reduced synaptic number, decreased SYN, PSD-95, and BDNF expression in elderly offspring, which were alleviated by postnatal EE housing. These findings suggest that prenatal long-term mobile phone exposure may pose life-long adverse effects on elderly offspring and impair cognition by disrupting the synaptic plasticity, which may be reversed by postnatal EE housing.

Fucosidosis is a rare lysosomal storage disease, resulting from a deficiency in an alpha-L-fucosidase enzyme. There are fewer than 120 cases of this disease worldwide and very few reported in Chinese children. Here, we report a Chinese boy presenting with psychomotor regression, dermatological abnormality, dysostosis multiplex, and classic changes observed with head magnetic resonance imaging. He was diagnosed with fucosidosis, with a previously reported homozygous mutation of c.393(exon2)T >A, p.Tyr131Stop, in the FUCA1 gene. Increasing awareness of fucosidosis will help in the early diagnosis of this disease and could shed light on the therapeutic role of hematopoietic stem cell transplantation, which may be effective in early stages of the disease.

Rationale:Rhabdomyolysis owing to status epilepticus (SE) can be life-threating, with acute kidney injury (AKI) the most serious complication; therefore, early recognition of the risk factors is important. Hyperuricemia after epileptic seizures has been reported, and severe hyperuricemia can lead to acute renal function damage.Patient concerns:We present the case of a 21-year-old man hospitalized for SE, who had especially high level of blood uric acid (UA) at initial presentation.Diagnosis:The patient was diagnosed with rhabdomyolysis due to SE.Interventions:The patient was treated with hydration and bicarbonate therapy. But he developed acute kidney failure (AKF) and hemodialysis was performed.Outcomes:After hemodialysis, his symptoms disappeared and laboratory data returned to normal.Lessons:Hyperuricemia after SE might indicate severe muscle damage or reduced clearance of metabolites, and could be a risk factor for kidney dysfunction, especially with rhabdomyolysis. To our knowledge, this is the first report of rhabdomyolysis following SE with hyperuricemia.