Language：Japanese   Publisher：福岡産科婦人科学会  

臍帯furcate insertion(FI)は、臍帯が胎盤に付着する前に臍帯血管が分岐し、ワルトン膠質が欠損するまれな臍帯付着部異常である。症例は30歳、6妊4産。妊娠30週の妊婦健診で胎盤嚢胞を疑われ当科を紹介受診し、超音波カラードプラ法で胎盤胎児面に多房性嚢胞を認めた。臍帯血管は、動静脈が嚢胞壁に沿って別々に胎盤表面に向かって走行している所見を認め、Furcate insertion(FI)と診断した。FIは子宮内胎児死亡(IUFD)といった胎児合併症の原因になり得ることから、妊娠37週での分娩の方針としていたが、妊娠31週から胎児発育不全(FGR)、妊娠34週で妊娠高血圧腎症を発症した後に自然陣痛が発来し早産に至った。娩出された胎盤でFIであることを確認した。FIは正常妊娠経過をたどることが多いが、IUFDのリスクを考慮し、超音波検査を行う場合には、臍帯付着部の観察を十分に行うことが重要である。(著者抄録)

Language：Japanese   Publisher：福岡産科婦人科学会  

鉄欠乏性貧血は急性出血とともに妊産褥婦における貧血の主な原因である。貧血の治療に対して、カルボキシマルトース第二鉄の使用が開始された。今回、当施設における妊産褥婦における同薬剤を投与した患者背景を明らかにし、同薬剤の効果を検討した。対象は、2021年2月から2022年8月までの期間に、当院で妊娠・産褥期の貧血に対して、カルボキシマルトース第二鉄の静注を行った58症例とし、患者背景、カルボキシマルトース第二鉄投与前後のヘモグロビン値、初回投与から再評価時までの日数、EPDS値などの情報を診療録から抽出した。貧血の原因としては前置胎盤と双胎妊娠がともに11例で最も多かった。治療前のヘモグロビン値は7.7g/dlから10.9g/dlに上昇し有意差を認めた。また、初回投与から日数を経るに連れヘモグロビン値は上昇していた。退院時と一ヵ月健診時のEPDS値では差異を認めた。当院での検討の結果、分娩時異常出血や産褥期異常出血の対応に迫られる周産期センターにおいて、カルボキシマルトース第二鉄は貧血に対する治療薬として、十分な治療効果が期待できる薬剤であると考えた。(著者抄録)

Web of Science

Language：English   Publisher：Scientific Reports  

Chemotherapy is a standard therapy for muscle-invasive bladder cancer (MIBC). However, genomic alterations associated with chemotherapy sensitivity in MIBC have not been fully explored. This study aimed to investigate the genomic landscape of MIBC in association with the response to chemotherapy and to explore the biological role of genomic alterations. Genomic alterations in MIBC were sequenced by targeted exome sequencing of 409 genes. Gene expression in MIBC tissues was analyzed by western blotting, immunohistochemistry, and RNA microarray. Cellular sensitivity to gemcitabine and gemcitabine metabolite was examined in bladder cancer cells after modulation of candidate gene. Targeted exome sequencing in 20 cases with MIBC revealed various genomic alterations including pathogenic missense mutation of DPYD gene encoding dihydropyrimidine dehydrogenase (DPD). Conversely, high DPYD and DPD expression were associated with poor response to gemcitabine-containing chemotherapy among patients with MIBC, as well as gemcitabine resistance in bladder cancer cells. DPD suppression rendered cells sensitive to gemcitabine, while DPD overexpression made cells gemcitabine-resistant through reduced activity of the cytotoxic gemcitabine metabolite difluorodeoxycytidine diphosphate. This study revealed the novel role of DPD in gemcitabine metabolism. It has been suggested that DPYD genomic alterations and DPD expression are potential predictive biomarkers in gemcitabine treatment.

DOI： 10.1038/s41598-022-12528-3

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PubMed

Language：English   Publisher：Springer Nature  

Fetal growth restriction (FGR) and pre-eclampsia with fetal growth restriction (PE/FGR) are high-risk perinatal diseases that may involve high levels of human chorionic gonadotropin (hCG) and mitochondrial dysfunction. However, little is known about how these factors affect placental function. We investigated how mitochondrial dysfunction and high hCG expression affected placental function in unexplained FGR and PE/FGR. We observed elevated expression of hCGβ and growth differentiation factor 15 mRNA and protein levels in the placenta with both diseases. Likewise, antiangiogenic factors, such as Ang2, IP10, sFlt1, IL8, IL1B, and TNFα, were also upregulated at the mRNA level. In addition, the expression of COXI and COXII which encoded by mitochondrial DNA were significantly decreased in both diseases, suggesting that mitochondrial translation was impaired. Treatment with hCG increased Ang2, IP10, IL8, and TNFα mRNA levels in a dose-dependent manner via the p38 and JNK pathways. Mitochondrial translation inhibitors increased hCGβ expression through stabilization of HIF1α, and increased IL8 and TNFα mRNA expression. These results revealed that high expression of hCG due to mitochondrial translational dysfunction plays an important role in the pathogenesis of FGR and PE/FGR.

DOI： 10.1038/s41598-022-07893-y

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