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Astrocytes have now been well accepted to play important roles in epileptogenesis by controlling gliotransmitter release and neuronal excitability, contributing to blood-brain barrier dysfunction and involving in brain inflammation. Recent studies indicate that abnormal expression of gap junction protein connexin (Cx) may also be a contributing factor for seizure generation. To further address this issue, we investigated the progressive changes of Cx 43 and Cx 40 in the mouse hippocampus at 4 h, 1 day, 1 week and 2 months during and after pilocarpine-induced status epilepticus (PISE). The co-localization of Cx 43 and Cx 40 with glial fibrillary acidic protein (GFAP) was also examined. We observed that Cx 43 and Cx 40 protein expression remained unaltered at 4 h during and at 1 day (acute stage) after PISE. However, their expression was significantly increased in CA1 and CA3 areas and in the dentate gyrus at 1 week (latent stage) and 2 months (chronic stage) after PISE. Double immunofluorescence labeling indicated the localization of Cx 43 and Cx 40 in astrocytes. Combined with progressive neuronal loss in the mouse hippocampus, our results suggest that the increase in gap junctions in the neuronoglial syncytium of reactive astrocytes may be implicated in synchronization of hippocampal hyperactivity leading to neuronal loss and epileptogenesis.

In the pituitary sella, the coexistence of pituitary adenoma and primary pituitary lymphoma is exceedingly rare. Thus far, only six cases have been reported. Here, we present the seventh case of coexisting pituitary adenoma and primary pituitary lymphoma, which was difficult to differentiate from other sellar tumors. To our knowledge, this is the first case of the prolactin subtype of the pituitary adenoma in literature. We have also systematically reviewed the literature and summarized the characteristics of coexisting pituitary adenoma and lymphoma. We believe this report provides a new clinical reference for the diagnosis and treatment of collision tumors of pituitary adenoma and lymphoma.

Organic cation transporter 2 (OCT2), encoded by the SLC22A2 gene, is the main cation transporter on the basolateral membrane of proximal tubular cells. OCT2 facilitates the entry step of the vectorial transport of most cations from the peritubular space into the urine. OCT2 downregulation in kidney disease models is apparent, yet not clear from a mechanistic vantage point. The aim of this study was to explore the role of inflammation, a common thread in kidney disease, and NF-kB in OCT2 modulation and tubular secretion. Among the OCTs, OCT2 was found consistently downregulated in the kidney of rats with chronic kidney disease (CKD) or acute kidney injury (AKI) and in patients diagnosed with CKD, and it was associated with the upregulation of TNFα renal expression. Exposure to TNFα reduced the expression and function of OCT2 in primary renal proximal tubule epithelial cells (RPTEC). Silencing or pharmacological inhibition of NF-kB rescued the expression of OCT2 in the presence of TNFα, indicating that OCT2 repression was NF-kB-dependent. In silico prediction coupled to gene reporter assay demonstrated the presence of at least one functional NF-kB cis-element upstream the transcription starting site of the SLC22A2 gene. Acute inflammation triggered by lipopolysaccharide injection induced TNFα expression and the downregulation of OCT2 in rat kidney. The inflammation did reduce the active secretion of the cation Rhodamine 123, with no impairment of the glomerular filtration. In conclusion, the NF-kB pathway plays a major role in the transcriptional regulation of OCT2 and, in turn, in the overall renal secretory capacity.