胎児発育不全児胎盤におけるサイトメガロウイルス感染の免疫組織学的解析

藤田医科大

Similarities in rotavirus vaccine viral shedding and immune responses in pairs of twins

journal articl

The Acute-Phase Ambulation Program Improves Clinical Outcome for Acute Heart Failure

It remains unclear whether the acute-phase ambulation program (AAP) improves the prognosis of heart failure (HF) patients. We examined the association between the initiation of AAP and the prognosis of patients with worsening HF. We enrolled 560 consecutive patients admitted due to worsening HF from March 2019 to April 2021. Our hospital introduced AAP in May 2020, but we did not perform AAP until April 2020. We retrospectively compared cardiac events within 180 days after discharge between patients admitted before April 2020 (conventional group) and after May 2020 (AAP group). Primary endpoints were all-cause mortality and readmission for worsening HF. The Kaplan–Meier survival curves showed a significantly lower event rate in the AAP group in HF readmission or the primary endpoint (p = 0.020 and p = 0.014). The occurrence of the primary endpoint was associated with age, history of HF, systolic blood pressure, medications including renin–angiotensin system inhibitors or angiotensin receptor blocker, hemoglobin, NT-proBNP, and AAP participation. After adjusting for these parameters and sex, participation in AAP was an independent factor associated with a reduced risk of primary endpoint occurrence (hazard ratio of 0.62 (0.41–0.95), p = 0.028). The AAP for patients with acute HF might lead to improved short-term prognosis and should be considered for implementation

Retrospective immunohistochemical analysis of human cytomegalovirus infection in the placenta and its association with fetal growth restriction

Objectives: Fetal human cytomegalovirus (HCMV) infection might be involved in fetal growth restriction (FGR). Maternal serostatus and the prevalence of congenital HCMV infection are affected by various factors, such as socioeconomic status and ethnicity. Therefore, the prevalence of congenital HCMV-related FGR should be examined in each region. Methods: Seventy-eight cases of FGR with delivery between January 2012 and January 2017 at Fujita Health University Hospital were studied. Twenty-one non-FGR cases were also included as a control group. Placental sections obtained from the FGR and control cases were immunostained with two primary antibodies for detecting immediate early antigens. Results: Nineteen placental samples from FGR cases with another etiology were excluded. Finally, 59 placental samples from FGR cases of unknown etiology were included in the pathological analysis. Four of 59 (6.8%) placental samples were positive for HCMV antigen. All four positive cases were stained with the M0854 antibody, and there were no positive case with the MAB810R antibody. Neither maternal nor infantile clinical features were different between the HCMV-positive and -negative FGR cases. A pathological examination showed a hematoma in three of four cases and infarction in two of four cases. Conclusions: HCMV antigen was detected in 6.8% of placental samples obtained from FGR cases without an obvious etiology. No remarkable maternal or neonatal clinical features discriminated HCMV-related FGR from FGR due to other causes. Vasculitis and inflammation might play important roles in the pathogenesis of HCMV-related FGR

Mg²⁺ Extrusion from Intestinal Epithelia by CNNM Proteins Is Essential for Gonadogenesis via AMPK-TORC1 Signaling in <i>Caenorhabditis elegans</i>

<div><p>Mg²⁺ serves as an essential cofactor for numerous enzymes and its levels are tightly regulated by various Mg²⁺ transporters. Here, we analyzed <i>Caenorhabditis elegans</i> strains carrying mutations in genes encoding cyclin M (CNNM) Mg²⁺ transporters. We isolated inactivating mutants for each of the five <i>Caenorhabditis elegans cnnm</i> family genes, <i>cnnm-1</i> through <i>cnnm-5</i>. <i>cnnm-1</i>; <i>cnnm-3</i> double mutant worms showed various phenotypes, among which the sterile phenotype was rescued by supplementing the media with Mg²⁺. This sterility was caused by a gonadogenesis defect with severely attenuated proliferation of germ cells. Using this gonadogenesis defect as an indicator, we performed genome-wide RNAi screening, to search for genes associated with this phenotype. The results revealed that RNAi-mediated inactivation of several genes restores gonad elongation, including <i>aak-2</i>, which encodes the catalytic subunit of AMP-activated protein kinase (AMPK). We then generated triple mutant worms for <i>cnnm-1</i>; <i>cnnm-3</i>; <i>aak-2</i> and confirmed that the <i>aak-2</i> mutation also suppressed the defective gonadal elongation in <i>cnnm-1; cnnm-3</i> mutant worms. AMPK is activated under low-energy conditions and plays a central role in regulating cellular metabolism to adapt to the energy status of cells. Thus, we provide genetic evidence linking Mg²⁺ homeostasis to energy metabolism via AMPK.</p></div

Magnesium levels in wild-type and <i>cnnm-1; cnnm-3</i> mutant worms.

<p>Magnesium levels in wild-type and <i>cnnm-1; cnnm-3</i> mutant worms.</p