Autocrine Communication
Communication
Cell Communication
Animal Communication
Communication Disorders
Health Communication
Communication Aids for Disabled
Nonverbal Communication
Paracrine Communication
Communication Barriers
Computer Communication Networks
Connexin 43
Radiology Information Systems
Receptors, Autocrine Motility Factor
Signal Transduction
Interdisciplinary Communication
Cell Division
Cells, Cultured
RNA, Messenger
Communication Methods, Total
Connexins
Communications Media
Glucose-6-Phosphate Isomerase
Tumor Cells, Cultured
Transforming Growth Factor alpha
Growth Substances
Electronic Mail
Persuasive Communication
Patient Satisfaction
Culture Media, Conditioned
Attitude of Health Personnel
Internet
Transforming Growth Factor beta
Patient Simulation
Role Playing
Reverse Transcriptase Polymerase Chain Reaction
Teleradiology
Questionnaires
Models, Biological
Coexpression of transcripts encoding EPHB receptor protein tyrosine kinases and their ephrin-B ligands in human small cell lung carcinoma. (1/1262)
The EPH family is the largest subfamily of receptor protein tyrosine kinases, consisting of the EPHA and EPHB subgroups. Ephrin-B1, ephrin-B2, and ephrin-B3 are ligands of the EPHB subgroup and are encoded by the EFNB1, EFNB2, and EFNB3 genes, respectively. We have shown previously that EPHB2 transcripts are expressed in six small cell lung carcinoma (SCLC) cell lines. In this study, we examined the expression of EPHB1, EPHB2, EPHB3, EPHB4, and EPHB6 in 4 SCLC tumor specimens and 14 cell lines including 3 cell lines derived from these tumor specimens. To investigate whether potential autocrine loops of EPHB receptors and ephrin-B ligands exist in SCLC, the expression of EFNB1, EFNB2, and EFNB3 was also examined. Our data show that transcripts encoding multiple members of the EPHB subgroup and the ephrin-B subgroup are coexpressed in SCLC cell lines and tumors. These results suggest that the EPHB subgroup receptor kinases may modulate the biological behavior of SCLC through autocrine and/or juxtacrine activation by ephrin-B ligands that are expressed in the same or neighboring cells. (+info)Maturation, activation, and protection of dendritic cells induced by double-stranded RNA. (2/1262)
The initiation of an immune response is critically dependent on the activation of dendritic cells (DCs). This process is triggered by surface receptors specific for inflammatory cytokines or for conserved patterns characteristic of infectious agents. Here we show that human DCs are activated by influenza virus infection and by double-stranded (ds)RNA. This activation results not only in increased antigen presentation and T cell stimulatory capacity, but also in resistance to the cytopathic effect of the virus, mediated by the production of type I interferon, and upregulation of MxA. Because dsRNA stimulates both maturation and resistance, DCs can serve as altruistic antigen-presenting cells capable of sustaining viral antigen production while acquiring the capacity to trigger naive T cells and drive polarized T helper cell type 1 responses. (+info)Regulation of gelatinase B production in corneal cells is independent of autocrine IL-1alpha. (3/1262)
PURPOSE: The matrix metalloproteinase gelatinase B is synthesized by cells at the leading edge of the corneal epithelium migrating to heal a wound. Recent data from the authors' laboratory suggest that excessive synthesis contributes to repair defects. The goal of the study reported here was to investigate mechanisms controlling gelatinase B production by corneal epithelial cells. METHODS: Freshly isolated cultures of corneal epithelial cells and early passage stromal fibroblasts from rabbit were used for these studies. RESULTS: In a previous study, it was found that the cytokine interleukin (IL)-1alpha is released into the culture medium of corneal epithelial cells more efficiently when they are plated at low density with limited cell-cell contact than when plated at high density. In this study, we show that production of gelatinase B by these cells is similarly affected by cell plating density. However, it is further demonstrated that these two events are not dependent on one another but occur in parallel: IL-1alpha does not regulate gelatinase B production (synthesis), nor was there evidence that any other secreted autocrine cytokine acts as mediator. Instead, our data suggest that gelatinase B production is downregulated directly by high cell density and indicate a connection to the level of protein kinase C activity. Nevertheless, the anticancer agent suramin, which blocks collagenase synthesis by interfering with autocrine cytokine-receptor interactions, still inhibits synthesis of gelatinase B. CONCLUSIONS: Unlike collagenase synthesis by corneal stromal fibroblasts, production (synthesis) of gelatinase B does not appear to be controlled by secreted autocrine cytokines but can still be inhibited by suramin. Suramin may make an effective therapeutic agent for controlling pathologic overproduction of gelatinase B in corneal ulcers. (+info)Pituitary adenylate cyclase-activating polypeptide, interleukin-6 and glucocorticoids regulate the release of vascular endothelial growth factor in pituitary folliculostellate cells. (4/1262)
There is increasing evidence that hormones play an important role in the control of endothelial cell function and growth by regulating the production of vascular endothelial growth factor (VEGF). VEGF regulates vascular permeability and represents the most powerful growth factor for endothelial cells. In the normal anterior pituitary, VEGF has been detected only in folliculostellate (FS) cells. In the present study, the regulation of the release of VEGF from FS-like mouse TtT/GF cells, and from FS cells of rat pituitary monolayer cell cultures was investigated using a specific VEGF ELISA. Basal release of VEGF was demonstrated in cultures of both TtT/GF cells and rat pituitary cells. Interestingly, the VEGF secretion was stimulated by both forms of pituitary adenylate cyclase-activating polypeptide (PACAP-38 and PACAP-27), indicating that this hypothalamic peptide regulates endothelial cell function and growth within the pituitary. VEGF secretion was also stimulated by interleukin-6 (IL-6) whereas basal, IL-6- and PACAP-stimulated secretion was inhibited by the synthetic glucocorticoid dexamethasone. The inhibitory action of dexamethasone was reversed by the glucocorticoid receptor antagonist RU486, suggesting that in FS cells functional glucocorticoid receptors mediate the inhibitory action of glucocorticoids on the VEGF secretion. The endocrine and auto-/paracrine control of VEGF production in pituitary FS cells by PACAP, IL-6 and glucocorticoids may play an important role both in angiogenesis and vascular permeability regulation within the pituitary under physiological and pathophysiological conditions. (+info)Role of autocrine stimulation on the effects of cyclic AMP on protein and lipid phosphorylation in collagen-activated and thrombin-activated platelets. (5/1262)
We compared several responses in thrombin-stimulated and collagen (type I)-stimulated platelets with and without forskolin and inhibitors of autocrine stimulation (IAS: an ADP-removing system of creatine phosphate/creatine phosphokinase, Arg-Gly-Asp-Ser peptide to prevent fibrinogen/fibronectin binding to GPIIb/IIIa, SQ 29.548 as a thromboxane A2 receptor antagonist, cyproheptadine as a serotonin receptor antagonist, BN 52021 as a platelet-activating factor receptor antagonist). The pattern of tyrosine-phosphorylated proteins, the phosphorylation of lipids in the polyphosphoinositide cycle and phosphorylation of pleckstrin (P47) were studied as markers for signal-transducing responses, exposure of CD62 (P-selectin) and CD63 (Glycoprotein 53), as well as secretion of ADP + ATP and beta-N-acetyl-glycosaminidase were studied as final activation responses. Clear differences between thrombin-stimulated and collagen-stimulated platelets were observed. First, practically all protein-tyrosine phosphorylation induced by thrombin was inhibited by IAS, while a partial inhibition was observed for collagen; the phosphorylation due to collagen alone was apparently stimulated by elevation of cAMP. Secondly, the other responses to thrombin were inhibited by increased levels of cAMP, independent of autocrine stimulation. In contrast, only the autocrine part of the collagen-induced responses was inhibited by elevation of cAMP. Thus, the inhibition by elevated cAMP seen in collagen-stimulated platelets seems to be due to removal of the G-protein-mediated activation from secreted autocrine stimulators either by IAS or forskolin. The remaining activity is a pure collagen effect which is not affected by elevated levels of cAMP. (+info)Differential inhibition of collagenase and interleukin-1alpha gene expression in cultured corneal fibroblasts by TGF-beta, dexamethasone, and retinoic acid. (6/1262)
PURPOSE: Expression of the genes for collagenase and interleukin-1alpha (IL-1alpha) are induced as stromal cells become activated to the repair fibroblast phenotype after injury to the cornea. This investigation examines the mechanisms whereby expression of these genes is inhibited by transforming growth factor-beta (TGF-beta), dexamethasone (DEX), or retinoic acid (RET A). METHODS: A model of freshly isolated cultures of corneal stromal cells and early passage cultures of corneal fibroblasts was used in these studies. This model reproduces the events of stromal cell activation in the corneal wound. RESULTS: In early passage cultures of corneal fibroblasts, expression of collagenase is under obligatory control by autocrine IL-1alpha. IL-1alpha controls its own expression through an autocrine feedback loop that is dependent on transcription factor NF-kappaB. TGF-beta, DEX, and RET A were each effective inhibitors of collagenase gene expression in these cells. Furthermore, these agents have the capacity to inhibit expression of IL-1alpha and this was correlated with their ability to affect DNA-binding activity of NF-kappaB. However, TGF-beta, DEX, and RET A were also effective inhibitors of the low level of collagenase expressed by freshly isolated corneal stromal cells that cannot express IL-1alpha. CONCLUSIONS: In cells with an active IL-1alpha autocrine loop there are at least two distinct signaling pathways by which collagenase gene expression can be modulated. The results of this study demonstrate that TGF-beta, DEX, and RET A differentially inhibit collagenase and IL-1alpha gene expression. This information will be useful in the design of therapeutic modalities for fibrotic disease in the cornea and other parts of the eye. (+info)The role of macrophage cell death in tuberculosis. (7/1262)
Studies of host responses to infection have traditionally focused on the direct antimicrobial activity of effector molecules (antibodies, complement, defensins, reactive oxygen and nitrogen intermediates) and immunocytes (macrophages, lymphocytes, and neutrophils among others). The discovery of the systems for programmed cell death of eukaryotic cells has revealed a unique role for this process in the complex interplay between microorganisms and their cellular targets or responding immunocytes. In particular, cells of the monocyte/macrophage lineage have been demonstrated to undergo apoptosis following intracellular infection with certain pathogens that are otherwise capable of surviving within the hostile environment of the phagosome or which can escape the phagosome. Mycobacterium tuberculosis is a prototypical 'intracellular parasite' of macrophages, and the direct induction of macrophage apoptosis by this organism has recently been reported from several laboratories. This paper reviews the current understanding of the mechanism and regulation of macrophage apoptosis in response to M. tuberculosis and examines the role this process plays in protective immunity and microbial virulence. (+info)Ligation of Fc gamma RII (CD32) pivotally regulates survival of human eosinophils. (8/1262)
The low-affinity IgG Fc receptor, FcgammaRII (CD32), mediates various effector functions of lymphoid and myeloid cells and is the major IgG Fc receptor expressed by human eosinophils. We investigated whether FcgammaRII regulates both cell survival and death of human eosinophils. When cultured in vitro without growth factors, most eosinophils undergo apoptosis within 96 h. Ligation of FcgammaRII by anti-CD32 mAb in solution inhibited eosinophil apoptosis and prolonged survival in the absence of growth factors. Cross-linking of human IgG bound to FcgammaRII by anti-human IgG Ab or of unoccupied FcgammaRII by aggregated human IgG also prolonged eosinophil survival. The enhanced survival with anti-CD32 mAb was inhibited by anti-granulocyte-macrophage-CSF (GM-CSF) mAb, suggesting that autocrine production of GM-CSF by eosinophils mediated survival. In fact, mRNA for GM-CSF was detected in eosinophils cultured with anti-CD32 mAb. In contrast to mAb or ligands in solution, anti-CD32 mAb or human IgG, when immobilized onto tissue culture plates, facilitated eosinophil cell death even in the presence of IL-5. Cell death induced by these immobilized ligands was accompanied by DNA fragmentation and was inhibited when eosinophil beta2 integrin was blocked by anti-CD18 mAb, suggesting that beta2 integrins play a key role in initiating eosinophil apoptosis. Thus, FcgammaRII may pivotally regulate both survival and death of eosinophils, depending on the manner of receptor ligation and beta2 integrin involvement. Moreover, the FcgammaRII could provide a novel mechanism to control the number of eosinophils at inflammation sites in human diseases. (+info)Some common types of communication disorders include:
1. Speech disorders: These are conditions that affect an individual's ability to produce speech sounds correctly or fluently. Examples include stuttering, articulation disorders, and apraxia of speech.
2. Language disorders: These are conditions that affect an individual's ability to understand and use language effectively. Examples include agrammatism (difficulty with sentence structure), anomia (word-finding difficulties), and semantic-dyslexia (difficulty with word meaning).
3. Reading disorders: These are conditions that affect an individual's ability to read and spell written words. Examples include dyslexia and other reading disabilities.
4. Hearing impairments: These are conditions that affect an individual's ability to hear or process sound. Examples include conductive hearing loss, sensorineural hearing loss, and auditory processing disorders.
5. Cognitive communication disorders: These are conditions that affect an individual's ability to think, reason, and understand language. Examples include traumatic brain injury, dementia, and neurodegenerative diseases such as Alzheimer's and Parkinson's.
The symptoms of communication disorders can vary depending on the specific condition and the individual affected. Some common symptoms include:
* Difficulty articulating words or sounds
* Slurred or slow speech
* Difficulty understanding spoken language
* Difficulty with word-finding
* Difficulty with reading and spelling
* Difficulty with comprehending written text
* Difficulty with nonverbal communication such as gestures and facial expressions
Communication disorders can be diagnosed by a speech-language pathologist (SLP) through a series of tests and assessments. Treatment options for communication disorders vary depending on the specific condition and the individual affected, but may include:
* Speech and language therapy to improve articulation, fluency, and comprehension skills
* Cognitive therapy to improve memory, attention, and problem-solving skills
* Use of technology such as hearing aids or communication devices
* Counseling and support for individuals and their families.
It is important to seek professional help if you or someone you know is experiencing difficulty with communication. With appropriate diagnosis and treatment, individuals with communication disorders can improve their communication skills and lead fulfilling lives.
Glucose-6-phosphate isomerase
Teleost leptins
Cell biology
Stuart C. Sealfon
Wnt signaling pathway
Biology
Granulin
Purinergic signalling
Autocrine signaling
Paracrine signaling
Macrophage polarization
Sardul Singh Guraya
Connexin
Endocrinology
List of MeSH codes (G04)
Folliculostellate cell
Prolactin
Keiko Torii
Annexin A2
C-C chemokine receptor type 7
LYVE1
Cell signaling
Endocrine system
Lymphatic endothelium
Juxtacrine signalling
Microfluidic cell culture
Neovascularization
Allograft inflammatory factor 1
Adipogenesis
ABCB5
VIPR1
Keith W. Kelley
Perlecan
Protein moonlighting
Protein Wnt-5a
Health effects of tobacco
Signal transduction
CXCL9
C-Met
Succinic acid
HPG80
Cancer stem cell
Antineoplastic resistance
Pericyte
Induced stem cells
Mechanotransduction
Fibroblast growth factor
PELP-1
β-arrestin1/YAP/mutant p53 complexes orchestrate the endothelin A receptor signaling in high-grade serous ovarian cancer |...
MH DELETED MN ADDED MN
The Tie-2 ligand Angiopoietin-2 destabilizes quiescent endothelium through an internal autocrine loop mechanism | Journal of...
Autocrine and paracrine regulation of interleukin-8 expression in lung cancer cells | NTU Scholars
DeCS
Int Med - Digestv & Liver Dis - Research output - University of Texas Southwestern Medical Center
Pesquisa | Portal Regional da BVS
Pharmacogenomics of EGFR-targeted therapies in non-small cell lung cancer: EGFR and beyond | Cancer Communications | Full Text
Download Essentials Of Business Communication Book Only Eighth Edition
Corticotrophs. Medical search
Dr. Jou, Yuh-Shan 周玉山 博士 HIGHLIGHT DETAIL 重要成果詳細內容
Characterization and oncolytic virus targeting of FAP-expressing tumor-associated pericytes in glioblastoma | Acta...
Behind The Scenes: Hypertrophy!
IGF-1 Des Muscle Building Human Growth Hormone Peptide High Purity Peptides
Pesquisa | Portal Regional da BVS
MH DELETED MN ADDED MN
c) Show thatJozxio,z f(e,y) dx dy = 0. (Hint: Read E… - SolvedLib
Senotherapy Protects against Cisplatin-Induced Ovarian Injury by Removing Senescent Cells and Alleviating DNA Damage
EMF-Portal | Literature search results
Find Research outputs - Yonsei University
Postdoctoral Fellow - Oliver Wessely Lab (Cleveland)
Jennifer Richer's research topics | Colorado PROFILES
Ebook Americas Most Wanted Recipes Just Desserts Sweet Indulgences From Your Familys Favorite Restaurants Americas Most Wanted...
These final results showed that siCD81 would turn out to be effective equipment | PDGF Receptor
Barry Behr, Ph.D., H.C.L.D.'s Profile | Stanford Profiles
51 Drugstore: Cialis fiyat 20 mg purchase online!
RegenerativeMedicine.net - Article Archives
Frontiers | Pituitary Adenylate Cyclase Activating Polypeptide Has Inhibitory Effects on Melanoma Cell Proliferation and...
The power of bioinformatics and analyzing biological data to unlock the mysteries of life.
Graduate Theses & Dissertations | digitalcollections.trentu.ca
Paracrine6
- Cytokines are protein mediators of intercellular stress communication with autocrine, paracrine, and endocrine modes of action. (diabetesjournals.org)
- In this study, we focused on the paracrine and autocrine regulation of interleukin (IL)-8 expression in sensitized lung cancer cells after interacting with macrophages. (ntu.edu.tw)
- Our results highly suggest that both autocrine and paracrine regulation are involved in IL-8 expression of lung cancer cells cocultured with macrophage. (ntu.edu.tw)
- Electrical stimulation of sympathetic neurons induces autocrine/paracrine effects of NGF mediated by TrkA [med. (emf-portal.org)
- As the kidney ages, the cells establish new autocrine and paracrine signaling loops. (careeraddict.com)
- These neurons then secrete CPE/NF-α1 to protect them from glutamate- induced cell death in an autocrine/paracrine manner. (nih.gov)
Signaling6
- Endothelial Autocrine Signaling through CXCL12/CXCR4/FoxM1 Axis Contributes to Severe Pulmonary Arterial Hypertension. (nih.gov)
- Endothelial autocrine signaling is essential to maintain vascular homeostasis. (nih.gov)
- There is limited information about the role of endothelial autocrine signaling in regulating severe pulmonary vascular remodeling during the onset of pulmonary arterial hypertension (PAH). (nih.gov)
- In this study, we employed the first severe pulmonary hypertension (PH) mouse model, Egln1Tie2Cre (Tie2Cre-mediated disruption of Egln1) mice, to identify the novel autocrine signaling mediating the pulmonary vascular endothelial cell (PVEC) proliferation and the pathogenesis of PAH. (nih.gov)
- This makes IGF-1 a good protagonist at targeting tissues to spur cell to cell communication (growth) or in a more autocrine cell signaling process that facilitates cell division. (bulkingcyclesteroids.com)
- Besides helping us refine techniques to improve gene transfer efficiency into murine stem cells, these studies also provided insight into the possible roles of autocrine growth factor production in myeloproliferative diseases and leukemias, and further work defined a possible intracellular autocrine pathway for IL-3 signaling. (nih.gov)
Endothelial cell1
- However, autocrine Ang-2-mediated endothelial-cell detachment cannot be blocked by soluble Tie-2. (biologists.com)
Vascular1
- Intercellular communication of blood, vascular and heart cells. (nih.gov)
Interactions2
- 2014. Effector CD4 T cell transition to memory requires late cognate interactions that induce autocrine IL-2. (ucf.edu)
- In 2004 he oversaw the relocation of administrative and extramural offices, and NIAAA intramural laboratories to newly-built quarters on Fishers Lane in Rockville, MD. The new buildings have been a welcome upgrade for NIAAA staff and have helped to improve communications and interactions across NIAAA intramural and extramural divisions. (nih.gov)
Ovarian1
- Gene ontology analysis further revealed that combining senotherapies enhanced ovarian cell differentiation, development, and communication. (hindawi.com)
Cell4
- Mode of communication wherein a bound hormone affects the function of the cell type that produced the hormone. (nih.gov)
- Information of cell-cell communication within the kidney was obtained using receptor-ligand pairing resources. (bvsalud.org)
- Since its half-life is about a day, the IGF-1 LR3 will circulate the body, for around 24 hours, binding to receptors and activating cell communication that improves muscle growth and fat loss. (bulkingcyclesteroids.com)
- The successful applicant should demonstrate a commitment to research, a collaborative work ethic, strong written and verbal communication skills and experience in cell and/or molecular biology. (careeraddict.com)
Nature Communications1
- Nature Communications 5:5377 doi: 10.1038/ncomms6377. (ucf.edu)
Manner1
- Ang-2 is mainly produced by endothelial cells and therefore acts primarily in an autocrine manner. (biologists.com)
Identify1
- Taken together, the data demonstrate for the first time the antagonistic Ang-1/Ang-2 concept in a defined cellular model and identify Ang-2 as a rapidly acting autocrine regulator of the endothelium that acts through an internal autocrine loop mechanism. (biologists.com)
Cells1
- This study firstly demonstrated the communication between proximal tubular epithelial cells (PTECs) and mesangial cells (MCs) through exosome transmission. (bvsalud.org)
Metabolic2
- and c ) whether preestablished insulin resistance alters the metabolic responses of adipocytes exposed to PCB126 and the communication between adipocytes and myotubes. (nih.gov)
- These hormones regulate the body's growth, and are involved in cell to cell communication, control metabolic activity, sleep-wake homeostasis, and altered regulation or dysregulation of adaptive response in various physiologic and pathophysiologic states. (medscape.com)
Cell Communication1
- Information of cell-cell communication within the kidney was obtained using receptor-ligand pairing resources. (bvsalud.org)
Function1
- Mode of communication wherein a bound hormone affects the function of the cell type that produced the hormone. (nih.gov)