Chronic kidney disease with malignant peripheral nerve sheath tumor of the ureter: a case report.

Malignant peripheral nerve sheath tumors (MPNSTs) are a complex group of malignant tumors originating from nerve cells or benign peripheral nerve sheath tumors and are commonly found in major plexus/nerve root sites such as the limbs, head, and neck. Malignant peripheral nerve sheath tumors originating in the ureter are extremely rare. Herein, we report the case of a 63-year-old patient with a malignant peripheral nerve sheath tumor of the right ureter who underwent laparoscopic radical resection of the right kidney and ureter. The patient also had stage 5 chronic kidney disease (CKD). Therefore, chemotherapy and radiotherapy were not considered. No tumor recurrence was observed during the follow-up period.

MIF-mediated NF-κB signaling pathway regulates the pathogenesis of polycystic ovary syndrome in rats.

Polycystic ovary syndrome (PCOS) resulting from abnormal glucose metabolism is a relatively common and complex endocrine disorder among women in their reproductive years, However, the pathogenesis of PCOS is still unclear. The purpose of this study is to investigate the macrophage migration inhibitory factor (MIF) involvement of the nuclear factor (NF)-κB in rats with PCOS. Results indicated that testosterone promoted the increase in the levels of MIF and luteinizing hormone (LH) but inhibited the increase in the level of follicular stimulating hormone (FSH). The MIF antibody could alleviate the process of PCOS to a certain extent. Testosterone promoted the expression of interleukin 1-beta (IL-1ß), interleukin 6 (IL-6), Inducible nitric oxide synthase (iNOS), and tumor necrosis factor alpha (TNF-α); the MIF antibody could reverse this effect. Testosterone could inhibit the expression of NF-κB protein whereas MIF antibody could promote the expression in the ovarian cytoplasm. Testosterone promoted the expression of NF-κB protein in the nucleus, this effect also could be reversed by the MIF antibody. Hyperandrogenism activated the NF-κB pathway. After using the MIF antibody, this effect was reversed. This finding suggested that hyperandrogenism activated the NF-κB pathway through MIF. In short, increased MIF levels activated the NF-κB pathway in ovaries, leading to inflammation and the increase in the levels of relevant inflammatory indicators, which might be one of the important factors in the pathogenesis of PCOS.

A phosphoryl radical-initiated Atherton-Todd-type reaction under open air.

A phosphoryl radical-initiated Atherton-Todd-type reaction using air as the radical initiator and CHCl3 as the halogenating reagent for the phosphorylation of alcohols, phenols, and amines has been developed. This novel transformation provides a highly efficient route to important phosphinates, phosphinic amides, and phosphoramidates in up to 99% yield with a broad substrate scope under very mild conditions (48 examples).

Simvastatin accelerates hematoma resolution after intracerebral hemorrhage in a PPARγ-dependent manner.

To date, the neuroprotective effects of statins on intracerebral hemorrhage (ICH) are not well established. This study explored the effect and potential mechanism of simvastatin treatment on ICH. In the present study, the effects of simvastatin on hematoma absorption, neurological outcome, CD36 expression and microglia polarization were examined in rat model of ICH model. In the meantime, inhibitory effect of PPARγ inhibitor GW9662 was investigated following ICH. Additionally, the effect of simvastatin on PPARγ activation was also investigated in rat ICH model and primary microglia culture. Much more, the role of PPARγ and CD36 in simvastatin-mediated erythrocyte phagocytosis was also detected by using in vivo or in vitro phagocytosis models, respectively. After ICH, simvastatin promoted hematoma absorption and improved neurological outcome after ICH while upregulating CD36 expression and facilitating M2 phenotype polarization in perihematomal microglia. In addition, simvastatin increased PPARγ activation and reinforced microglia-induced erythrocyte phagocytosis in vivo and in vitro. All above effects of simvastatin were abolished by PPARγ inhibitor GW9662. In conclusion, our data suggested that simvastatin could enhance hematoma clearance and attenuate neurological deficits possibly by activating PPARγ.