Obstetrical outcomes of labor with and without analgesia in Robson classification groups 1 and 2a: a single-center retrospective study.

Purpose: This study aimed to elucidate the effects of neuraxial analgesia on labor in women classified based on the Robson classification system.

Methods: We retrospectively reviewed the clinical data of singleton cephalic nulliparous deliveries in labor at term between January 2018 and December 2021 and compared obstetrical outcomes between deliveries with and without neuraxial analgesia in women of Robson group 1 (spontaneous labor) and group 2a (induced labor). Statistical analyses were performed using the Wilcoxon ranked-sum test, Fisher's exact test, and logistic regression model.

Dietary intervention of mice using an improved Multiple Artificial-gravity Research System (MARS) under artificial 1 .

Japan Aerospace Exploration Agency (JAXA) has developed mouse habitat cage units equipped with an artificial gravity-producing centrifuge, called the Multiple Artificial-gravity Research System (MARS), that enables single housing of a mouse under artificial gravity (AG) in orbit. This is a report on a hardware evaluation. The MARS underwent improvement in water leakage under microgravity (MG), and was used in the second JAXA mouse mission to evaluate the effect of AG and diet on mouse biological system simultaneously.

Structural instability of lamin A tail domain modulates its assembly and higher order function in Emery-Dreifuss muscular dystrophy.

The C-terminal Ig-domain of lamin A plays critical roles in cell function via interaction with proteins, DNA, and chromatin. Mutations in this domain are known to cause various diseases including Emery-Dreifuss muscular dystrophy (EDMD) and familial partial lipodystrophy (FPLD). Here we examined the biophysical and biochemical properties of mutant Ig-domains identified in patients with EDMD and FPLD.

Successful pulmonary embolectomy for massive pulmonary embolism during pregnancy: a case report.

Background: Pulmonary embolism (PE) resulting from venous thromboembolism is a leading cause of maternal mortality in pregnancy. In patients with massive PE and hemodynamic instability, the treatment options often considered are thrombolytics, inferior vena caval filters, or embolectomy. We report here the case of a patient with massive PE at 28 weeks' gestation, who underwent emergency pulmonary embolectomy via cardiopulmonary bypass.

Dysferlinopathy Fibroblasts Are Defective in Plasma Membrane Repair.

Background: Dysferlin is a sarcolemmal protein that is defective in Miyoshi myopathy and limb-girdle muscular dystrophy type 2B, and is involved in sarcolemmal repair. Primary cultured myoblasts and myotubes established from patient muscle biopsies have been widely utilized to explore the molecular mechanism of dysferlinopathy.

Objectives: The purpose of this study was to explore the possible utility of dermal fibroblasts from dysferlin-deficient patients and SJL mice as a tool for studying dysferlinopathy.

Contribution of dysferlin deficiency to skeletal muscle pathology in asymptomatic and severe dystroglycanopathy models: generation of a new model for Fukuyama congenital muscular dystrophy.

Defects in dystroglycan glycosylation are associated with a group of muscular dystrophies, termed dystroglycanopathies, that include Fukuyama congenital muscular dystrophy (FCMD). It is widely believed that abnormal glycosylation of dystroglycan leads to disease-causing membrane fragility. We previously generated knock-in mice carrying a founder retrotransposal insertion in fukutin, the gene responsible for FCMD, but these mice did not develop muscular dystrophy, which hindered exploring therapeutic strategies.

Upregulated expression of FGF13/FHF2 mediates resistance to platinum drugs in cervical cancer cells.

Cancer cells often develop drug resistance. In cisplatin-resistant HeLa cisR cells, fibroblast growth factor 13 (FGF13/FHF2) gene and protein expression was strongly upregulated, and intracellular platinum concentrations were kept low. When the FGF13 expression was suppressed, both the cells' resistance to platinum drugs and their ability to keep intracellular platinum low were abolished.

[Ultrasound guided transversus abdominis plane block in early infancy].

We retrospectively examined the transversus abdominis plane (TAP) block performed in 8 infants (range, 1-115 days) from July 2010 to March 2011. Ultrasound images clearly visualized the fascial plane between the transversus abdominis and the internal oblique muscle and it was possible to confirm proper administration of local anesthetics into the plane in all patients. Complications resulting from opioid overdose were noted in two cases.

[Ultrasound guided nerve block in infants undergoing pyloromyotomy].

Background: Ultrasound guided nerve block has become popular in pediatric practice. We applied this technique to infants undergoing pyloromyotomy.

Methods: We retrospectively reviewed the hospital records of infants who underwent pyloromyotomy with the aid of the ultrasound guided nerve block from July 2010 to March 2011.

[The effect of nitroglycerin 200 microg on uterine relaxation during cesarean delivery].

Background: Rapid and transient uterine relaxation is sometimes required for fetal distress or difficult delivery due to uterine hyperactivity during cesarean section. For its rapid onset and short duration, intravenous nitroglycerin (NTG) is commonly used for this purpose. But its suitable dose is unclear.

The C2A domain in dysferlin is important for association with MG53 (TRIM72).

In skeletal muscle, Mitsugumin 53 (MG53), also known as muscle-specific tripartite motif 72, reportedly interacts with dysferlin to regulate membrane repair. To better understand the interactions between dysferlin and MG53, we conducted immunoprecipitation (IP) and pull-down assays. Based on IP assays, the C2A domain in dysferlin associated with MG53.

Augmented autocrine bone morphogenic protein (BMP) 7 signaling increases the metastatic potential of mouse breast cancer cells.

As malignant breast cancers progress, they acquire the ability to spread to other regions of the body, including bone and lung, but the molecular mechanism underlying the increase in metastatic potential is not fully understood. Here we studied murine 4T1E/M3 highly bone marrow metastatic breast cancer cells, which we established previously. These cells show upregulated expression of bone morphogenetic protein (BMP) 7 and BMP receptors, as well as augmented phosphorylation of Smad1/5/8.

Specific phosphorylation of Ser458 of A-type lamins in LMNA-associated myopathy patients.

Mutations in LMNA, which encodes A-type nuclear lamins, cause various human diseases, including myopathy, cardiomyopathy, lipodystrophy and progeria syndrome. To date, little is known about how mutations in a single gene cause a wide variety of diseases. Here, by characterizing an antibody that specifically recognizes the phosphorylation of Ser458 of A-type lamins, we uncover findings that might contribute to our understanding of laminopathies.

Human PTRF mutations cause secondary deficiency of caveolins resulting in muscular dystrophy with generalized lipodystrophy.

Caveolae are invaginations of the plasma membrane involved in many cellular processes, including clathrin-independent endocytosis, cholesterol transport, and signal transduction. They are characterized by the presence of caveolin proteins. Mutations that cause deficiency in caveolin-3, which is expressed exclusively in skeletal and cardiac muscle, have been linked to muscular dystrophy.

Defective myotilin homodimerization caused by a novel mutation in MYOT exon 9 in the first Japanese limb girdle muscular dystrophy 1A patient.

Myotilin is a muscle-specific Z disk protein. Several missense mutations in the myotilin gene (MYOT) have been identified in limb girdle muscular dystrophy (LGMD), myofibrillar myopathy, and distal myopathy patients. All previously reported pathogenic MYOT mutations have been identified only in Exon 2.

Targeted mutation of mouse skeletal muscle sodium channel produces myotonia and potassium-sensitive weakness.

Hyperkalemic periodic paralysis (HyperKPP) produces myotonia and attacks of muscle weakness triggered by rest after exercise or by K+ ingestion. We introduced a missense substitution corresponding to a human familial HyperKPP mutation (Met1592Val) into the mouse gene encoding the skeletal muscle voltage-gated Na+ channel NaV1.4.

Two endoplasmic reticulum-associated degradation (ERAD) systems for the novel variant of the mutant dysferlin: ubiquitin/proteasome ERAD(I) and autophagy/lysosome ERAD(II).

Dysferlin is a type-II transmembrane protein and the causative gene of limb girdle muscular dystrophy type 2B and Miyoshi myopathy (LGMD2B/MM), in which specific loss of dysferlin labeling has been frequently observed. Recently, a novel mutant (L1341P) dysferlin has been shown to aggregate in the muscle of the patient. Little is known about the relationship between degradation of dysferlin and pathogenesis of LGMD2B/MM.

The gamma-parvin-integrin-linked kinase complex is critically involved in leukocyte-substrate interaction.

Leukocyte extravasation is an important step of inflammation, in which integrins have been demonstrated to play an essential role by mediating the interaction of leukocytes with the vascular endothelium and the subendothelial extracellular matrix. Previously, we identified an integrin-linked kinase (ILK)-binding protein affixin (beta-parvin), which links initial integrin signals to rapid actin reorganization, and thus plays critical roles in fibroblast migration. In this study, we demonstrate that gamma-parvin, one of three mammalian parvin family members, is specifically expressed in several lymphoid and monocytic cell lines in a complementary manner to affixin.