Retroperitoneoscopic bladder neck closure for continuous urinary incontinence in Fournier's gangrene.

Introduction: A retroperitoneoscopic procedure for bladder neck closure has not yet been described.

Case Presentation: Case 1 was a 56-year-old man who underwent clean intermittent catheterization for spastic paraplegia due to a thoracic spinal cord injury 37 years prior. Case 2 was an 80-year-old bedridden woman who underwent urethral catheterization after a femoral fracture and brain infarction 3 years prior.

[Adenocarcinoma with Aplastic Anemia as an Immune-related Adverse Event Caused by Pembrolizumab: Report of a Case].

A 74-year-old man was found a left completely atelectasis on chest X-ray. He had undergone left lower lobe resection because of an adenocarcinoma at the age of 58. Bronchoscopy revealed a tumor near the left upper lobe branch entry that obstructed the lumen, and a biopsy confirmed the diagnosis of adenocarcinoma.

Novel insight into the correlation between hernia orifice of cystocele and lower urinary tract function: a pilot study.

Background: It has been hypothesized that women with significant pelvic organ prolapse (POP), particularly of the anterior vaginal wall, may have voiding dysfunction (VD). Although the VD mechanism due to cystocele is not fully understood, different vaginal compartments have rarely been closely examined. This study attempted to further elucidate the correlation between POP and VD through a new subgroup classification using cystoscopy.

Special AT-Rich Sequence-Binding Protein 1 Supports Survival and Maturation of Naive B Cells Stimulated by B Cell Receptors.

Epigenetic mechanisms underpin the elaborate activities of essential transcription factors in lymphocyte development. Special AT-rich sequence-binding protein 1 (SATB1) is a chromatin remodeler that orchestrates the spatial and temporal actions of transcription factors. Previous studies have revealed the significance of SATB1 in T cell lineage.

Autoimmune-mediated thrombocytopenia after allogeneic hematopoietic stem cell transplantation: significance of detecting reticulated platelets and glycoprotein-specific platelet autoantibodies.

Autoimmune hematological disorders are rare complications after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Diagnosis of immune thrombocytopenia (ITP) is challenging, especially after allo-HSCT, because various complications such as graft-versus-host disease, disease relapse, viral infection, thrombotic microangiopathy, and drug side effects can also cause thrombocytopenia. Assessment of reticulated platelets (RP) and plasma thrombopoietin (TPO) levels may be useful to distinguish between ITP and hypoplastic thrombocytopenia.

Autonomous TGFβ signaling induces phenotypic variation in human acute myeloid leukemia.

Heterogeneity of leukemia stem cells (LSCs) is involved in their collective chemoresistance. To eradicate LSCs, it is necessary to understand the mechanisms underlying their heterogeneity. Here, we aimed to identify signals responsible for heterogeneity and variation of LSCs in human acute myeloid leukemia (AML).

Endothelial Cell-Selective Adhesion Molecule Contributes to the Development of Definitive Hematopoiesis in the Fetal Liver.

Endothelial cell-selective adhesion molecule (ESAM) is a lifelong marker of hematopoietic stem cells (HSCs). Although we previously elucidated the functional importance of ESAM in HSCs in stress-induced hematopoiesis in adults, it is unclear how ESAM affects hematopoietic development during fetal life. To address this issue, we analyzed fetuses from conventional or conditional ESAM-knockout mice.

Granulocyte-colony stimulating factor attenuates oligomeric amyloid β neurotoxicity by activation of neprilysin.

Soluble oligomeric amyloid β (oAβ) causes synaptic dysfunction and neuronal cell death, which are involved in the pathogenesis of Alzheimer's disease (AD). The hematopoietic growth factor granulocyte-colony stimulating factor (G-CSF) is expressed in the central nervous system (CNS) and drives neurogenesis. Here we show that G-CSF attenuated oAβ neurotoxicity through the enhancement of the enzymatic activity of Aβ-degrading enzyme neprilysin (NEP) in neurons, while the NEP inhibitor thiorphan abolished the neuroprotection.

Fingolimod phosphate attenuates oligomeric amyloid β-induced neurotoxicity via increased brain-derived neurotrophic factor expression in neurons.

The neurodegenerative processes that underlie Alzheimer's disease are mediated, in part, by soluble oligomeric amyloid β, a neurotoxic protein that inhibits hippocampal long-term potentiation, disrupts synaptic plasticity, and induces the production of reactive oxygen species. Here we show that the sphingosine-1-phosphate (S1P) receptor (S1PR) agonist fingolimod phosphate (FTY720-P)-a new oral drug for multiple sclerosis-protects neurons against oligomeric amyloid β-induced neurotoxicity. We confirmed that primary mouse cortical neurons express all of the S1P receptor subtypes and FTY720-P directly affects the neurons.

GM-CSF increases LPS-induced production of proinflammatory mediators via upregulation of TLR4 and CD14 in murine microglia.

Background: Microglia are resident macrophage-like cells in the central nervous system (CNS) and cause innate immune responses via the LPS receptors, Toll-like receptor (TLR) 4 and CD14, in a variety of neuroinflammatory disorders including bacterial infection, Alzheimer's disease, and amyotrophic lateral sclerosis. Granulocyte macrophage-colony stimulating factor (GM-CSF) activates microglia and induces inflammatory responses via binding to GM-CSF receptor complex composed of two different subunit GM-CSF receptor α (GM-CSFRα) and common β chain (βc). GM-CSF has been shown to be associated with neuroinflammatory responses in multiple sclerosis and Alzheimer's disease.

TGF-β induced by interleukin-34-stimulated microglia regulates microglial proliferation and attenuates oligomeric amyloid β neurotoxicity.

Microglia play critical roles in the pathogenesis of Alzheimer's disease (AD). We have previously shown that interleukin-34 (IL-34) enhances microglial proliferation and induces microglial neuroprotective properties against oligomeric amyloid β (oAβ) toxicity by producing insulin degrading enzyme, an Aβ degrading enzyme, and anti-oxidant enzyme heme oxygenase-1. In this study, we found that IL-34 dose-dependently induces TGF-β in microglia, and that TGF-β attenuates oAβ neurotoxicity in neuron microglial co-cultures.

The neuroprotective effects of milk fat globule-EGF factor 8 against oligomeric amyloid β toxicity.

Background: Phosphatidylserine receptor is a key molecule that mediates the phagocytosis of apoptotic cells. Milk fat globule-EGF factor 8 (MFG-E8) is a phosphatidylserine receptor that is expressed on various macrophage lineage cells, including microglia in the central nervous system (CNS). Targeted clearance of degenerated neurons by microglia is essential to maintain healthy neural networks.

Immunoglobulin G(1) immune complex upregulates interferon-γ-induced nitric oxide production via ERK1/2 activation in murine microglia.

Intrathecal Immunoglobulin G (IgG) is elevated in some central nervous system (CNS) diseases and microglia upregulate Fcγ receptors in various neurological disorders. However, the interaction between IgG or IgG immune complexes and microglial Fcγ receptors is not fully understood. In this study, the effect of IgG(1) immune complexes on microglia was investigated.