Asymptomatic Complete Spiral Stent Fracture in Subclavian Artery with Progressive Restenosis in the Early Postoperative Period: A Case Report.

Objective: Stent fractures may be a risk factor for delayed restenosis, but it is difficult to diagnose asymptomatic stent fractures in the subclavian artery (SCA). We report a rare case of percutaneous transluminal angioplasty and stenting (PTAS) for SCA stenosis with asymptomatic severe stent fracture that showed progressive in-stent stenosis in the early postoperative period.

Case Presentation: A 70-year-old woman presented with left arm claudication.

Verification of optimal conditions for the scattering correction of I-FP-CIT SPECT on a single-photon emission tomography system with a two-detector whole-body cadmium-zinc-telluride semiconductor detector.

To identify the optimal scattering correction for 123I-FP-CIT SPECT (DAT-SPECT) using a two-detector whole-body cadmium-zinc-telluride semiconductor detector (C-SPECT) system with a medium-energy high-resolution sensitivity (MEHRS) collimator. The C-SPECT system with the MEHRS collimator assessed image quality and quantification using a striated phantom. Different reconstruction methods and scattering correction settings were compared, including filtered back projection (FBP) and ordered subset expectation maximization (OSEM).

Clinical results of 30 consecutive patients of carotid artery stenosis treated with CASPER stent placement: 1-year follow-up and in-stent findings on intravascular ultrasound examination immediately and 6 months after treatment.

Background: The CASPER stent is expected to reduce periprocedural ischemic complications, but there is concern about restenosis in the early period. One-year follow-up results of CASPER stenting and findings on intravascular ultrasound (IVUS) immediately and 6 months after treatment are evaluated.

Methods: Thirty consecutive patients were treated with CASPER stents for carotid artery stenosis.

Cerebral Aneurysm Coil Embolization with a Coil-Assisted Technique Using a Small-Diameter Helical Coil.

Objective: We introduce a coil-assisted technique using a small diameter helical coil to preserve a branch artery in the aneurysm neck or dome during coil embolization of a cerebral aneurysm.

Case Presentations: We report three cases that were treated with the coil-assisted technique. Using this method, the branch artery was preserved with a small diameter helical coil that was placed to support another frame coil.

Clinical Evaluations of the Ischemic Core in Acute Ischemic Stroke Using Modified Diffusion-Weighted Imaging-Alberta Stroke Program Early Computed Tomography Scores by Ischemic Reversibility Using the Signal Intensity.

Objective: Early recanalization of acute stroke caused by large vessel occlusion (LVO) may improve high signal intensity (HSI) on diffusion-weighted imaging (DWI). In this study, we investigated whether subtraction of reversible ischemic lesions (RIL) from the HSI lesions on DWI improves the diagnostic accuracy for the ischemic core.

Methods: A total of 35 patients from April 2013 and December 2019 were included in this study.

Simple and Reproducible Microcatheter Shaping Method for Coil Embolization of Medially-directed Paraclinoid Internal Carotid Artery Aneurysms.

Objective: It is important to guarantee intra-aneurysmal stability of microcatheters during coil embolization. We developed a simple and reproducible microcatheter shaping method for medially-directed paraclinoid internal carotid artery aneurysms.

Methods: An injection needle cap was used to make a smooth curve on the mandrel, which was first wound around the back end of the cap to create a primary curve.

The ABBA motif binds APC/C activators and is shared by APC/C substrates and regulators.

The anaphase-promoting complex or cyclosome (APC/C) is the ubiquitin ligase that regulates mitosis by targeting specific proteins for degradation at specific times under the control of the spindle assembly checkpoint (SAC). How the APC/C recognizes its different substrates is a key problem in the control of cell division. Here, we have identified the ABBA motif in cyclin A, BUBR1, BUB1, and Acm1, and we show that it binds to the APC/C coactivator CDC20.

The mitotic checkpoint complex binds a second CDC20 to inhibit active APC/C.

The spindle assembly checkpoint (SAC) maintains genomic stability by delaying chromosome segregation until the last chromosome has attached to the mitotic spindle. The SAC prevents the anaphase promoting complex/cyclosome (APC/C) ubiquitin ligase from recognizing cyclin B and securin by catalysing the incorporation of the APC/C co-activator, CDC20, into a complex called the mitotic checkpoint complex (MCC). The SAC works through unattached kinetochores generating a diffusible 'wait anaphase' signal that inhibits the APC/C in the cytoplasm, but the nature of this signal remains a key unsolved problem.

Mad2 and the APC/C compete for the same site on Cdc20 to ensure proper chromosome segregation.

The spindle assembly checkpoint (SAC) is essential to ensure proper chromosome segregation and thereby maintain genomic stability. The SAC monitors chromosome attachment, and any unattached chromosomes generate a "wait anaphase" signal that blocks chromosome segregation. The target of the SAC is Cdc20, which activates the anaphase-promoting complex/cyclosome (APC/C) that triggers anaphase and mitotic exit by ubiquitylating securin and cyclin B1.

[Two cases of Nocardia farcinica brain abscess].

Brain abscess caused by Nocardia is a relatively rare disease, but its prognosis is poor, with the fatality being 3 times as high as that of other types of brain abscess. Nocardiosis caused by N. farcinica has higher fatality rates than nocardiosis caused by the other bacteria of the genus Nocardia.

How APC/C-Cdc20 changes its substrate specificity in mitosis.

Progress through mitosis requires that the right protein be degraded at the right time. One ubiquitin ligase, the anaphase-promoting complex or cyclosome (APC/C) targets most of the crucial mitotic regulators by changing its substrate specificity throughout mitosis. The spindle assembly checkpoint (SAC) acts on the APC/C co-activator, Cdc20 (cell division cycle 20), to block the degradation of metaphase substrates (for example, cyclin B1 and securin), but not others (for example, cyclin A).

A mutual inhibition between APC/C and its substrate Mes1 required for meiotic progression in fission yeast.

The anaphase-promoting complex/cyclosome (APC/C) is a cell-cycle-regulated essential E3 ubiquitin ligase; however, very little is known about its meiotic regulation. Here we show that fission yeast Mes1 is a substrate of the APC/C as well as an inhibitor, allowing autoregulation of the APC/C in meiosis. Both traits require a functional destruction box (D box) and KEN box.

Fission yeast Mes1p ensures the onset of meiosis II by blocking degradation of cyclin Cdc13p.

Meiosis is a special form of nuclear division to generate eggs, sperm and spores in eukaryotes. Meiosis consists of the first (MI) and the second (MII) meiotic divisions, which occur consecutively. MI is reductional, in which homologous chromosomes derived from parents segregate.

Corneal epithelial cells and stromal keratocytes efficently produce CC chemokine-ligand 20 (CCL20) and attract cells expressing its receptor CCR6 in mouse herpetic stromal keratitis.

Purpose: CC chemokine-ligand 20 (CCL20) is known to be selectively expressed by surface-lining mucosal epithelial cells and skin epidermal keratinocytes and to attract cells such as immature dendritic cells and effector T cells via CCR6. This study evaluated the ability of corneal epithelial cells and stromal keratocytes to produce CCL20 in vitro and in vivo.

Methods: Human corneal epithelial cells (HCE) and corneal keratocytes (HCK) were treated without or with various cytokines and expression of CCL20 mRNA and secreion of its protein were evaluated by RT-PCR and ELISA.

A high endothelial venule-expressing promiscuous chemokine receptor DARC can bind inflammatory, but not lymphoid, chemokines and is dispensable for lymphocyte homing under physiological conditions.

Chemokines displayed on the luminal surface of blood vessels play pivotal roles in inflammatory and homeostatic leukocyte trafficking in vivo. However, the mechanisms underlying the functional regulation of chemokines on the endothelial cell surface remain ill-defined. A promiscuous chemokine receptor, the Duffy antigen receptor for chemokines (DARC), has been implicated in the regulation of chemokine functions.

Fission yeast Rhp51 is required for the maintenance of telomere structure in the absence of the Ku heterodimer.

The Schizosaccharomyces pombe Ku70-Ku80 heterodimer is required for telomere length regulation. Lack of pku70+ results in telomere shortening and striking rearrangements of telomere-associated sequences. We found that the rearrangements of telomere-associated sequences in pku80+ mutants are Rhp51 dependent, but not Rad50 dependent.

CCL28 has dual roles in mucosal immunity as a chemokine with broad-spectrum antimicrobial activity.

CCL28 is a CC chemokine signaling via CCR10 and CCR3 that is selectively expressed in certain mucosal tissues such as exocrine glands, trachea, and colon. Notably, these tissues commonly secrete low-salt fluids. RT-PCR analysis demonstrated that salivary glands expressed CCL28 mRNA at the highest levels among various mouse tissues.

Cutting edge: profile of chemokine receptor expression on human plasma cells accounts for their efficient recruitment to target tissues.

We systematically examined the repertoire of chemokine receptors expressed by human plasma cells. Fresh bone marrow plasma cells and myeloma cells consistently expressed CXCR4, CXCR6, CCR10, and CCR3. Accordingly, plasma cells responded to their respective ligands in chemotaxis and very late Ag-4-dependent cell adhesion to fibronectin.

Human B cells immortalized with Epstein-Barr virus upregulate CCR6 and CCR10 and downregulate CXCR4 and CXCR5.

Compared to peripheral blood resting B cells, Epstein-Barr virus (EBV)-immortalized B cells consistently express CCR6 and CCR10 at high levels and CXCR4 and CXCR5 at low levels. Accordingly, these cells vigorously responded to the ligands of CCR6 and CCR10 but not to those of CXCR4 and CXCR5. In a human EBV-negative B-cell line, BJAB, stable expression of EBNA2 upregulated CCR6, while stable expression of EBNA2 as well as LMP1 downregulated CXCR4.

Frequent expression of CCR4 in adult T-cell leukemia and human T-cell leukemia virus type 1-transformed T cells.

Chemokines and chemokine receptors play important roles in migration and tissue localization of various lymphocyte subsets. Here, we report the highly frequent expression of CCR4 in adult T-cell leukemia (ATL) and human T-cell leukemia virus type 1 (HTLV-1)-immortalized T cells. Flow cytometric analysis revealed that ATL and HTLV-1-immortalized T-cell lines consistently expressed CCR4.

Gene expression profiling of mucosal addressin cell adhesion molecule-1+ high endothelial venule cells (HEV) and identification of a leucine-rich HEV glycoprotein as a HEV marker.

High endothelial venule (HEV) cells support lymphocyte migration from the peripheral blood into secondary lymphoid tissues. Using gene expression profiling of mucosal addressin cell adhesion molecule-1(+) mesenteric lymph node HEV cells by quantitative 3'-cDNA collection, we have identified a leucine-rich protein, named leucine-rich HEV glycoprotein (LRHG) that is selectively expressed in these cells. Northern blot analysis revealed that LRHG mRNA is approximately 1.

Proinflammatory cytokines induce liver and activation-regulated chemokine/macrophage inflammatory protein-3alpha/CCL20 in mucosal epithelial cells through NF-kappaB [correction of NK-kappaB].

Liver and activation-regulated chemokine (LARC)/CCL20 is expressed by surface-lining epithelial and epidermal cells, and is likely to link innate and acquired immunity by attracting immature dendritic cells, effector memory T cells and B cells via CCR6. Here we examined the mechanism of LARC expression in epithelial-type cells. Either IL-1beta or tumor necrosis factor (TNF)-alpha strongly induced LARC mRNA in intestinal cell lines Caco-2 and T84, while both were effective on HEK 293T cells.