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Delayed periprosthetic collection after cervical disc arthroplasty.

Cervical disc arthroplasty is a treatment option for symptomatic cervical disc disease. There is a paucity of literature on long-term safety outcomes, durability, and device-related failure rates. The M6-C artificial cervical disc is a device with titanium alloy endplates and a complex polymeric centerpiece. To date, trials have exhibited acceptable safety profiles.This case series describes the presentation, management, and pathological findings of a delayed prevertebral periprosthetic mass anterior to the M6-C disc. Four patients at 3 different institutions underwent cervical disc replacement with the M6-C disc. Two to seven years postoperatively, they presented with dysphagia secondary to a compressive mass anterior to the disc. Case notes were reviewed to collect data on symptoms, management, and outcomes. The patients were systemically well and presented with progressive dysphagia. They had imaging findings of a mass anterior to the disc. They underwent a decompressive procedure, with 2 patients undergoing device removal and fusion. In 2 cases, a soft-tissue mass was seen intraoperatively, with frank pus. In 3 cases, Propionibacterium acnes was identified and antibiotic treatment given. Histopathology demonstrated mixed inflammatory infiltrates with foreign body-type granulomas. Postoperatively, the dysphagia resolved.The development of delayed dysphagia in a patient with an M6-C disc should prompt investigation to identify a mass lesion. To the authors' knowledge, this is the first report of delayed infection, or suspected delayed-type hypersensitivity reaction, following M6-C disc implantation. It is important for this to be added to the device safety concerns. Further prospective studies are needed to establish the incidence and the long-term safety and failure rates of the M6-C disc.

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Multiple (uterine cervix) PAX6 Polyclonal Antibody1 Cat Tissue cDNA, Adult Ti Goat Anti-Human DISC1, (i rat FGF 225 ug[DISCONTINU recomb. Hu. Hsc 70[DISCON NucView 488 Caspase 3 Sub Anti Phosphorylated Histo Anti-Costal-2 (Cos2) Mono Geniposide[DISCONTINUED] Angiopoietin 2, human rec  ARID1A Monoclonal Antib

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QKI-V5 is downregulated in CNS inflammatory demyelinating diseases.

Neuromyelitis-optica (NMO) and multiple-sclerosis (MS) are inflammatory- demyelinating-diseases of the central-nervous-system (CNS). In a previous study, we identified 17 miRNAs that were significantly upregulated in the peripheral blood of patients with NMO, relative to healthy controls (HCs). Target gene analysis have demonstrated that QKI is targeted by 70% of the upregulated miRNAs. QKI gene encodes for a RNA-binding-protein that plays a central role in myelination. QKI variants 5, 6, 7 (QKI-V5, QKI-V6, QKI-V7) are generated via alternative splicing. Given the role played by QKI in myelination we aimed to study the expression levels of QKI variants in the circulation of patients with NMO and MS and in the circulation and brain tissue of mice-model to CNS-inflammatory-demyelinating-disease.

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Malaria pan antigen test, Rabbit Anti-IAA (Indole-3 Rabbit Anti-TNIP2 ABIN2 T Mouse Anti P. aeruginosa Rabbit Anti-Integrin alph Rat Macrophage Inflammato Rabbit Anti-IAA (Indole-3 Rabbit Anti-Insulin Recep Mouse Anti Shigella boydi Rabbit Anti-Cell death in Mouse Anti-Insulin(1D4:) Rabbit Anti-Phospho-INPPL

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Chemokines and their receptors promoting the recruitment of myeloid-derived suppressor cells into the tumor.

Myeloid-derived suppressor cells (MDSCs) expand in tumor-bearing host. They suppress anti-tumor immune response and promote tumor growth. Chemokines play a vital role in recruiting MDSCs into tumor tissue. They can also induce the generation of MDSCs in the bone marrow, maintain their suppressive activity, and promote their proliferation and differentiation. Here, we review CCL2/CCL12-CCR2, CCL3/4/5-CCR5, CCL15-CCR1, CX3CL1/CCL26-CX3CR1, CXCL5/2/1-CXCR2, CXCL8-CXCR1/2, CCL21-CCR7, CXCL13-CXCR5 signaling pathways, their role in MDSCs recruitment to tumor tissue, and their correlation with tumor development, metastasis and prognosis. Targeting chemokines and their receptors may serve as a promising strategy in immunotherapy, especially combined with other strategies such as chemotherapy, cyclin-dependent kinase or immune checkpoints inhibitors.

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Multiple organ cancer tis Tissue array of ovarian g Pfu DNA Polymerase protei Multiple organ tumor tiss FDA Standard Frozen Tissu Recombinant Human PKC the Normal rat multiple organ BACTERIOLOGY BACTEROIDES CSL Gradient Thermal Cycl Rat monoclonal anti mouse Single Strand DNA Ligase, Sheep Anti-Theophylline 3

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Size effect of curcumin nanocrystals on dissolution, airway mucosa penetration, lung tissue distribution and absorption by pulmonary delivery.

Nanocrystals (NCs) have been introduced for use in pulmonary delivery in recent decades. Although the deposition and bioavailability have been extensively studied, little is known about the biofate, which influences the drug release and absorption process of NCs. In this study, we fabricated three different sized curcumin NCs by adjusting the parameters of mill machine using a wet milling method and studied the size effect on pulmonary absorption. The small nanocrystals (NC-S, 246.16 ± 21.98 nm) exhibited a faster dissolution rate and higher diffusion percentage in vitro compared with middle (NC-M, 535.26 ± 50.33 nm) and large nanocrystals (NC-L, 1089.53 ± 194.34 nm). Multiple particle tracking experiments revealed that NC-S had larger mean squared displacement during diffusion in simulated mucus of 0.5% hydroxyethyl cellulose solution. Moreover, enhanced cellular uptake and transport efficiency were achieved by NC-S in Calu-3 cells and an air-liquid interface culturing model. NCs were mainly absorbed in the dissolved drug form, as assessed by using the Förster resonance energy transfer (FRET) technique. In vivo lung retention and distribution revealed that few smaller sized nanocrystals were retained in the lung after intratracheal administration. The pharmacokinetic study showed that the AUC values of small sized nanocrystals were 1.75- and 3.32-fold greater than NC-M and NC-L, respectively. In conclusion, this study demonstrated that smaller sized nanocrystals were more easily absorbed into the blood system by increasing the dissolution rate.

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Lung disease spectrum (pu Lung disease spectrum (pu Lung cancer with matched Lung non small cell cance Lung cancer tissue array Lung small cell carcinoma Incu Tissue(square vessel Lung cancer survey tissue Lung cancer test tissue a Tissue Culture Flask with Lung carcinoma tissue arr Lung cancer tissue array,

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Pre-conceptional folic acid supplementation: A possible cause for the increasing rates of ankyloglossia.

There is an increasing awareness to ankyloglossia (tongue-tie) in infants, with marked increase in its report in the medical literature. Some reports indicate increase in prevalence. Whether the increase ankyloglossia rate is a real phenomenon or merely reflects increased awareness and reports has to be determined. One explanation for the increasing ankyloglossia rates is the growing trend of breast feeding initiation, often impaired by ankyloglossia, which brings it to medical attention. We propose an alternative hypothetical explanation based on increasing utilization of periconceptional folic acid supplementation for the prevention of neural tube defects (NTDs). Inadequate folic acid supply during organogenesis impairs cell division, and the mid-line structures are at the highest risk. We postulated that higher folic acid supply during organogenesis might enhance tissue synthesis with tighter closure of mid-line structures including the lingual frenulum, resulting in ankyloglossia.

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4 (4 Formyl 3,5 dimethoxy (5Z)-7-[(5-Acetyloxy-2-fo Mouse Anti-Folic Acid 4 Formylphenylboronic aci 3-Formylindol-1-yl-acetic 5 Formyl 2 thiopheneboron N-Acetyl Folic Acid-d4 C2 Folic acid CAS Number [59 5 (4 Formyl 3,5 dimethoxy 4 Formylphenylboronic aci 2 Fluoro 5 formylphenylbo Formamidinesulfinic acid

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Quantitative analysis of ablation technique predicts arrhythmia recurrence following atrial fibrillation ablation.

Optimal ablation technique, including catheter-tissue contact during atrial fibrillation (AF) radiofrequency (RF) ablation, is associated with improved procedural outcomes. We used a custom developed software to analyze high-frequency catheter position data to study the interaction between catheter excursion during lesion placement, lesion-set sequentiality, and arrhythmia recurrence.

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Peroxide Block for Image EnzyChrom™ D-Lactate As Analysis Tool for AAM-ANG EIA for Quantitative Dete HBV Quantitative Real Tim Analysis Tool for AAM-CYT Chemokine (Human) Quantit MarkerGeneTM Hydrophobic Analysis Tool for AAM-CYT Inflammation (Human) Quan Human Mouse Rat Quantitat Analysis Tool for RayBio

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Emerging roles for the nucleus during neutrophil signal relay and NETosis.

The nucleus houses and protects genomic DNA, which is surrounded by the nuclear envelope. Owing to its size and stiffness, the nucleus is often a barrier to migration through confined spaces. Neutrophils are terminally differentiated, short-lived cells that migrate through tissues in response to injury and infections. The neutrophil nucleus is soft, multilobular, and exhibits altered levels of key nuclear envelope proteins. These alterations result in a multifunctional organelle that serves as a signaling hub during migration and NETosis, a process by which neutrophils release decondensed chromatin decorated with granular enzymes that entrap pathogens. In this review, we present emerging evidence suggesting that a unique, ambiguous cell-cycle state is critical for NETosis and migration. Finally, we discuss how the mechanisms underlying migration and NETosis are evolutionarily conserved.

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Hh Signaling Pathway Anta succinate-CoA ligase, GDP Expression Media Products Rat PAI-1 (wild type acti Androgen Receptor (Phosph IGF-1R Signaling Phospho- Cellufine Formyl , 10 ml Cathepsin G, Human Neutro Rat Anti-Mouse Neutrophil Anti-BMP-1 (Bone Morphoge PathwayReady™ PI3 K Akt 6-Amino-1-benzyl-3-methyl

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Oral flavonoid fisetin treatment protects against prolonged high-fat-diet-induced cardiac dysfunction by regulation of multicombined signaling.

Excess high-fat diet (HFD) intake predisposes the occurrence of obesity-associated heart injury, but the mechanism is elusive. Fisetin (FIS), as a natural flavonoid, has potential activities to alleviate obesity-induced metabolic syndrome. However, the underlying molecular mechanisms of FIS against HFD-induced cardiac injury remain unclear. The present study was to explore the protective effects of FIS on cardiac dysfunction in HFD-fed mice. We found that FIS alleviated HFD-triggered metabolic disorder by reducing body weight, fasting blood glucose and insulin levels, and insulin resistance. Moreover, FIS supplements significantly alleviated dyslipidemia in both mouse hearts and cardiomyocytes stimulated by metabolic stress. FIS treatment abolished HFD-induced inflammatory response in heart tissues through suppressing TNF receptor-1/TNF receptor-associated factor-2 (Tnfr-1/Traf-2) signaling. Furthermore, FIS induced a strong reduction in the expression of fibrosis-related genes, contributing to the inhibition of fibrosis by inactivating transforming growth factor (Tgf)-β1/Smads/Erk1/2 signaling. Collectively, these results demonstrated that FIS could be a promising therapeutic strategy for the treatment of obesity-associated cardiac injury.

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Pig Cardiac Troponin-I, H Oral cavity squamous cell Rabbit Anti Mouse Plasmin Oral cavity (tongue and p Cytokeratin, High Molecu Histofine High Stain HRP Rabbit Anti-HDL high dens Tissue Pre Treatment Kit High density ovarian canc DAB Substrate (High Cont HIGH Density NICKEL Rabbit Anti-phospho-cardi

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A rare giant extraocular, anterior chest wall sebaceous carcinoma.

Sebaceous carcinoma (SC) is a rare aggressive cutaneous malignant tumour. It accounts for less than 1 % of all cutaneous malignant tumours. Sebaceous carcinomas are divided into ocular and extraocular constituting 75 % and 25 % respectively. The most common extraocular site is parotid gland. Chest wall is a rare site of this tumour.

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AccuPower Multiplex PCR P Hepatocellular carcinoma Prostate carcinoma (multi Colon carcinoma and norma AccuPower RT PCR PreMix t Metastatic carcinoma of e Breast cancer tissue arra Human Squamous Cell Carci AccuPower HotStart PCR Pr Prostatic carcinoma tissu High density breast invas Esophagus squamous cell c

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Epigenetic Inactivation of SOX30 Is Associated with Male Infertility and Offers a Therapy Target for Non-obstructive Azoospermia.

Non-obstructive azoospermia (NOA) is the most severe form of male infertility. However, the etiology of NOA is largely unknown, resulting in a lack of clinical treatments. Here, we performed a comparative genome-wide profiling of DNA methylation and identified SOX30 as the most notably hyper-methylated gene at promoter in testicular tissues from NOA patients. This hyper-methylation at promoter of SOX30 directly causes its silencing of expression in NOA. The reduced levels of SOX30 expression are correlated with severity of NOA disease. Deletion of Sox30 in mice uniquely impairs testis development and spermatogenesis with complete absence of spermatozoa in testes leading to male infertility, but does not influence ovary development and female fertility. The pathology and testicular size of Sox30 null mice highly simulate those of NOA patients. Re-expression of Sox30 in Sox30 null mice at adult age reverses the pathological damage of testis and restores the spermatogenesis. The re-presented spermatozoa after re-expression of Sox30 in Sox30 null mice have the ability to start a pregnancy. Moreover, the male offspring of Sox30 re-expression Sox30 null mice still can father children, and these male offspring and their children can live normally more than 1 year without significant difference of physical appearance compared with wild-type mice. In summary, methylated inactivation of SOX30 uniquely impairs spermatogenesis, probably causing NOA disease, and re-expression of SOX30 can successfully restore the spermatogenesis and actual fertility. This study advances our understanding of the pathogenesis of NOA, offering a promising therapy target for NOA disease.

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MOUSE ANTI HUMAN CD15, Pr 10x ELISA WASH BUFFER, Pr MOUSE ANTI HUMAN CD19 RPE PERMANENT AQUEOUS MOUNTIN RABBIT ANTI GSK3 BETA (pS MOUSE ANTI CANINE DISTEMP NATIVE HUMAN PROLACTIN, P 10X PHOSPHATE BUFFERED SA MOUSE ANTI HUMAN CD15, Pr NATIVE HUMAN PROLACTIN, P Mouse Anti-Ca19.9 Sialyl MOUSE ANTI BOVINE ROTAVIR

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