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Human Trafficking

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3341. Policies to prevent firearm trafficking Full Text available with Trip Pro

Policies to prevent firearm trafficking 17446245 2007 09 04 2018 11 13 1353-8047 13 2 2007 Apr Injury prevention : journal of the International Society for Child and Adolescent Injury Prevention Inj. Prev. Policies to prevent firearm trafficking. 78-9 Vernick Jon S JS Johns Hopkins Center for Gun Policy and Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. jvernick@jhsph.edu Webster Daniel W DW eng Journal Article Review England Inj Prev 9510056 1353-8047 IM (...) Commerce legislation & jurisprudence Crime prevention & control Firearms legislation & jurisprudence Humans Licensure Public Policy United States 24 2007 4 21 9 0 2007 9 5 9 0 2007 4 21 9 0 ppublish 17446245 13/2/78 10.1136/ip.2007.015487 PMC2610592 J Urban Health. 2006 Sep;83(5):778-87 16937085 Inj Prev. 2006 Dec;12(6):365-72 17170183 J Law Med Ethics. 2006 Winter;34(4):765-75 17199819 Inj Prev. 1999 Dec;5(4):259-63 10628912 Inj Prev. 2006 Aug;12(4):225-30 16887943 Inj Prev. 2003 Jun;9(2):147-50

2007 Injury Prevention

3342. Thrifty Tbc1d1 and Tbc1d4 proteins link signalling and membrane trafficking pathways Full Text available with Trip Pro

Thrifty Tbc1d1 and Tbc1d4 proteins link signalling and membrane trafficking pathways Establishing a complete pathway which links occupancy of the insulin receptor to GLUT4 translocation has been particularly elusive because of the complexities involved in studying both signalling and membrane trafficking processes. However, Lienhard's group has now discovered two related molecules that could function in this linking role. These proteins, Tbc1d4 (also known as AS160) and now Tbc1d1, as reported (...) in this issue of the Biochemical Journal, have been demonstrated to be Rab GAPs (GTPase-activating proteins) that link upstream to Akt (protein kinase B) and phosphoinositide 3-kinase and downstream to Rabs involved in trafficking of GLUT4 vesicles. The data from Leinhard and colleagues suggest that high levels of Rab GAP activity lead to suppression of GLUT4 translocation and this observation has wide significance and is likely to be relevant to the recent discovery that mutations in the Tbc1d1 gene lead

2007 Biochemical Journal

3343. Israeli transplant surgeon is arrested for suspected organ trafficking Full Text available with Trip Pro

Israeli transplant surgeon is arrested for suspected organ trafficking 17494004 2007 05 22 2012 03 06 1756-1833 334 7601 2007 May 12 BMJ (Clinical research ed.) BMJ Israeli transplant surgeon is arrested for suspected organ trafficking. 973 Sarig Merav M eng News England BMJ 8900488 0959-8138 AIM IM Humans Israel Kidney Transplantation legislation & jurisprudence Tissue and Organ Procurement legislation & jurisprudence 2007 5 12 9 0 2007 5 23 9 0 2007 5 12 9 0 ppublish 17494004 334/7601/973

2007 BMJ : British Medical Journal

3344. Copper Trafficking and Extracellular Superoxide Dismutase Activity: Kinky Hair, Kinky Vessels Full Text available with Trip Pro

Copper Trafficking and Extracellular Superoxide Dismutase Activity: Kinky Hair, Kinky Vessels 18768396 2008 11 13 2018 11 13 1524-4563 52 5 2008 Nov Hypertension (Dallas, Tex. : 1979) Hypertension Copper trafficking and extracellular superoxide dismutase activity: kinky hair, kinky vessels. 811-2 10.1161/HYPERTENSIONAHA.108.117770 Rudolph Volker V Rudolph Tanja K TK Freeman Bruce A BA eng R01 HL058115 HL NHLBI NIH HHS United States R01 HL064937 HL NHLBI NIH HHS United States HL58115 HL NHLBI (...) NIH HHS United States R01 HL64937 HL NHLBI NIH HHS United States Editorial Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Comment 2008 09 02 United States Hypertension 7906255 0194-911X 0 Cation Transport Proteins 31C4KY9ESH Nitric Oxide 789U1901C5 Copper EC 1.15.1.1 Superoxide Dismutase EC 3.6.1.- Adenosine Triphosphatases EC 3.6.3.54 ATP7A protein, human EC 3.6.3.54 Copper-transporting ATPases IM Hypertension. 2008 Nov;52(5):945-51 18768397 Adenosine Triphosphatases

2008 Hypertension

3345. Prolactin Activation of Srcs Accelerates Receptor Internalization, Modulating Trafficking and Signaling in Breast Cancer Cells. Full Text available with Trip Pro

Prolactin Activation of Srcs Accelerates Receptor Internalization, Modulating Trafficking and Signaling in Breast Cancer Cells. Despite the growing body of evidence supporting prolactin (PRL) actions in human breast cancer, little is known regarding PRL regulation of its own receptor in these cells. Ligand-initiated endocytosis is a key process in the regulation of receptor availability and signaling cascades that may lead to oncogenic actions. Although exposure to exogenous PRL accelerates (...) for optimal phosphorylation of ERK1/2 and Akt, but not for Janus kinase 2 or signal transducer and activator of transcription 5, indicating that internalization selectively modulates signaling cascades. Together, these data indicate that SFKs are key mediators of ligand-initiated lPRLR internalization, down-regulation, and signal transduction in breast cancer cells, and underscore the importance of target cell context in receptor trafficking and signal transduction.

2008 Molecular Endocrinology

3346. Phosphorylation-dependent interaction with 14-3-3 regulates Bad trafficking in retinal ganglion cells. Full Text available with Trip Pro

Phosphorylation-dependent interaction with 14-3-3 regulates Bad trafficking in retinal ganglion cells. To focus on the proteomic analysis of 14-3-3 proteins and to determine their cellular localization and functional role during glaucomatous neurodegeneration.Complementary proteomic approaches were used to identify phosphorylated proteins in a chronic pressure-induced rat model of glaucoma. To detect interacting proteins, specific protein complexes were eluted using coimmunoprecipitation (...) and recombinant protein-based affinity pull-down for subsequent mass spectrometric analysis. Western blot analysis was performed for validation of the proteomic findings, and immunohistochemical analysis of rat eyes and human donor eyes determined the cellular localization of 14-3-3 proteins. In addition, in vivo treatment experiments were conducted using JNK and protein phosphatase inhibitors.Findings of mass spectrometry, Western blotting, and tissue immunolabeling revealed the presence of different 14-3-3

2008 Investigative Ophthalmology & Visual Science

3347. Organ trafficking and transplant tourism: a commentary on the global realities. Full Text available with Trip Pro

Organ trafficking and transplant tourism: a commentary on the global realities. The extent of organ sales from commercial living donors (CLDs) or vendors has now become evident. At the Second Global Consultation on Human Transplantation of the World Health Organization's (WHO) in March 2007, it was estimated that organ trafficking accounts for 5-10% of the kidney transplants performed annually throughout the world. Patients with sufficient resources in need of organs may travel from one country

2008 American Journal of Transplantation

3348. Melanocytes derived from patients with Hermansky-Pudlak Syndrome types 1, 2, and 3 have distinct defects in cargo trafficking. Full Text available with Trip Pro

unaffected in all three HPS genotypes. These data demonstrate that the three initially identified subtypes of human HPS exhibit distinct defects in the trafficking of various melanocyte-specific proteins. (...) Melanocytes derived from patients with Hermansky-Pudlak Syndrome types 1, 2, and 3 have distinct defects in cargo trafficking. Hermansky-Pudlak Syndrome (HPS) is a genetically heterogeneous disorder in which mutations in one of several genes interrupts biogenesis of melanosomes, platelet dense bodies, and lysosomes. Affected patients have oculocutaneous albinism, a bleeding diathesis, and sometimes develop granulomatous colitis or pulmonary fibrosis. In order to assess the role of HPS genes

2005 Journal of Investigative Dermatology

3349. Point mutation in the HCN4 cardiac ion channel pore affecting synthesis, trafficking, and functional expression is associated with familial asymptomatic sinus bradycardia. Full Text available with Trip Pro

Point mutation in the HCN4 cardiac ion channel pore affecting synthesis, trafficking, and functional expression is associated with familial asymptomatic sinus bradycardia. The hyperpolarization-activated nucleotide-gated channel--HCN4 plays a major role in the diastolic depolarization of sinus atrial node cells. Mutant HCN4 channels have been found to be associated with inherited sinus bradycardia.Sixteen members of a family with sinus bradycardia were evaluated. Evaluation included a clinical (...) mutation, G480R, in the ion channel pore domain in all affected family members. Function analysis, including expression of HCN4 wild-type and G480R in Xenopus oocytes and human embryonic kidney 293 cells, revealed that mutant channels were activated at more negative voltages compared with wild-type channels. Synthesis and expression of the wild-type and mutant HCN4 channel on the plasma membrane tested in human embryonic kidney 293 cells using biotinylation and Western blot analysis demonstrated

2007 Circulation

3350. Most LQT2 mutations reduce Kv11.1 (hERG) current by a class 2 (trafficking-deficient) mechanism. Full Text available with Trip Pro

Most LQT2 mutations reduce Kv11.1 (hERG) current by a class 2 (trafficking-deficient) mechanism. The KCNH2 or human ether-a-go-go related gene (hERG) encodes the Kv11.1 alpha-subunit of the rapidly activating delayed rectifier K+ current (IKr) in the heart. Type 2 congenital long-QT syndrome (LQT2) results from KCNH2 mutations that cause loss of Kv11.1 channel function. Several mechanisms have been identified, including disruption of Kv11.1 channel synthesis (class 1), protein trafficking (...) (class 2), gating (class 3), or permeation (class 4). For a few class 2 LQT2-Kv11.1 channels, it is possible to increase surface membrane expression of Kv11.1 current (IKv11.1). We tested the hypotheses that (1) most LQT2 missense mutations generate trafficking-deficient Kv11.1 channels, and (2) their trafficking-deficient phenotype can be corrected.Wild-type (WT)-Kv11.1 channels and 34 missense LQT2-Kv11.1 channels were expressed in HEK293 cells. With Western blot analyses, 28 LQT2-Kv11.1 channels

2006 Circulation

3351. Kinetics of metastatic breast cancer cell trafficking in bone. Full Text available with Trip Pro

Kinetics of metastatic breast cancer cell trafficking in bone. In vivo studies have focused on the latter stages of the bone metastatic process (osteolysis), whereas little is known about earlier events, e.g., arrival, localization, and initial colonization. Defining these initial steps may potentially identify the critical points susceptible to therapeutic intervention.MDA-MB-435 human breast cancer cells engineered with green fluorescent protein were injected into the cardiac left ventricle

2006 Clinical Cancer Research

3352. Transmembrane S1 mutations in CNGA3 from achromatopsia 2 patients cause loss of function and impaired cellular trafficking of the cone CNG channel. Full Text available with Trip Pro

Transmembrane S1 mutations in CNGA3 from achromatopsia 2 patients cause loss of function and impaired cellular trafficking of the cone CNG channel. Achromatopsia 2, an inherited retinal disorder resulting in attenuation or loss of cone function, is caused by mutations in the alpha subunit of the cone cyclic nucleotide-gated (CNG) channel gene CNGA3. Examination of mutations that cluster in the first transmembrane segment of the protein may provide insight into its role in CNG channel structure (...) , function, biogenesis, and pathophysiology.The human CNGA3 gene was tagged at the C terminus with green fluorescent protein. Four mutations, Y181C, N182Y, L186F, and C191Y, were expressed in human embryonic kidney cells. Protein expression was evaluated with immunoblot analysis and cellular localization was determined by immunocytochemistry. Channel function was evaluated by patch-clamp electrophysiology.All the mutations result in loss of channel function, as determined by the failure of cGMP

2005 Investigative Ophthalmology & Visual Science

3353. Heparan sulfate domains on cultured activated glomerular endothelial cells mediate leukocyte trafficking. Full Text available with Trip Pro

Heparan sulfate domains on cultured activated glomerular endothelial cells mediate leukocyte trafficking. Heparan sulfate (HS) proteoglycans by playing key roles in the leukocyte-endothelial interactions are thought to mediate inflammatory cell influx in proliferative glomerulonephritis. Here, we evaluated the specific features within glomerular endothelial HS that promote leukocyte adhesion. Mouse and human glomerular endothelial cells activated by tumor necrosis factor (TNF)-alpha (...) of endothelial HS or addition of sulfated heparinoids. Specific antibodies that block N- and 6-O-sulfated HS domains on activated mouse endothelial cells reduced the number of rolling and firmly adhering leukocytes under dynamic flow conditions, while they increased the average leukocyte-rolling velocity. Our study shows that N- and 6-O-sulfated domains in HS on activated glomerular endothelium are crucial for leukocyte trafficking and are possible therapeutic targets.

2007 Kidney International

3354. Genetic variation in Mon1a affects protein trafficking and modifies macrophage iron loading in mice. (Abstract)

Genetic variation in Mon1a affects protein trafficking and modifies macrophage iron loading in mice. We undertook a quantitative trait locus (QTL) analysis in mice to identify modifier genes that might influence the severity of human iron disorders. We identified a strong QTL on mouse chromosome 9 that differentially affected macrophage iron burden in C57BL/10J and SWR/J mice. A C57BL/10J missense allele of an evolutionarily conserved gene, Mon1a, cosegregated with the QTL in congenic mouse (...) lines. We present evidence that Mon1a is involved in trafficking of ferroportin, the major mammalian iron exporter, to the surface of iron-recycling macrophages. Differences in amounts of surface ferroportin correlate with differences in cellular iron content. Mon1a is also important for trafficking of cell-surface and secreted molecules unrelated to iron metabolism, suggesting that it has a fundamental role in the mammalian secretory apparatus.

2007 Nature Genetics

3355. Caveolin-1 regulates cellular trafficking and function of the glucagon-like Peptide 1 receptor. Full Text available with Trip Pro

Caveolin-1 regulates cellular trafficking and function of the glucagon-like Peptide 1 receptor. The glucagon-like peptide 1 receptor (GLP-1R) mediates important effects on beta-cell function and glucose homeostasis and is one of the most promising therapeutic targets for type 2, and possibly type 1, diabetes. Yet, little is known regarding the molecular and cellular mechanisms that regulate its function. Therefore, we examined the cellular trafficking of the GLP-1R and the relation between (...) receptor localization and signaling activity. In resting human embryonic kidney 293 and insulinoma MIN6 cells, a fully functional green fluorescent protein-tagged GLP-1R was localized both at the cell membrane and in highly mobile intracellular compartments. Real-time confocal fluorescence microscopy allowed direct visualization of constitutive cycling of the receptor. Overexpression of K44A-dynamin increased the number of functional receptors at the cell membrane. Immunoprecipitation, sucrose

2006 Molecular Endocrinology

3356. Corticotropin-releasing hormone receptor (CRHR)1 and CRHR2 are both trafficking and signaling receptors for urocortin. Full Text available with Trip Pro

Corticotropin-releasing hormone receptor (CRHR)1 and CRHR2 are both trafficking and signaling receptors for urocortin. Transport of urocortin, a potent satiety peptide, occurs at the blood-brain barrier of the mouse. Endocytosis of urocortin by the cerebral microvessel endothelial cells composing the blood-brain barrier is a rate-limiting step of this transport, but the cellular mechanisms involved have not been fully elucidated. The presence of both CRH receptors R1 and R2 in isolated cerebral (...) microvessels shown in this study suggested that both subtypes might mediate urocortin transport. The roles of these two receptors in the endocytosis and signal transduction of urocortin were tested by overexpression studies in human embryonic kidney 293 cells. Both receptors led to a significant increase of binding and endocytosis of radiolabeled urocortin. CRHR1-mediated urocortin endocytosis was blocked by astressin (antagonist for both CRHRs), whereas CRHR2-mediated urocortin endocytosis was also

2007 Molecular Endocrinology

3357. Disease-causing missense mutations in NPHS2 gene alter normal nephrin trafficking to the plasma membrane. Full Text available with Trip Pro

Disease-causing missense mutations in NPHS2 gene alter normal nephrin trafficking to the plasma membrane. Podocin is a membrane-integrated protein that is located at the glomerular slit diaphragm and directly interacts with nephrin. The gene encoding podocin, NPHS2, is mutated in patients with autosomal-recessive steroid-resistant nephrotic syndrome (SRN). In order to study a potential pathomechanism of massive proteinuria in patients with SRN, we have investigated the trafficking (...) and subcellular localization of five common disease-causing missense mutants of human podocin.Site-directed mutagenesis was applied to generate cDNA constructs encoding five different missense mutations of human podocin (P20L, G92C, R138Q, V180M, and R291W). To identify the subcellular localization of each mutant in transfected human embryonic kidney (HEK)293 cells, we have generated and characterized a rabbit polyclonal antibody against the human podocin. Specificity of the antibody was determined by light

2004 Kidney International

3358. Increased adhesion molecule and chemokine receptor expression on CD8+ T cells trafficking to cerebrospinal fluid in HIV-1 infection. Full Text available with Trip Pro

Increased adhesion molecule and chemokine receptor expression on CD8+ T cells trafficking to cerebrospinal fluid in HIV-1 infection. The central nervous system (CNS) is a recognized target for human immunodeficiency virus type 1 (HIV-1). CD8(+) T cells may mediate viral clearance from the CNS but also may contribute to immune-mediated neuronal damage.Using 4- and 6-color flow cytometry, we investigated the role of adhesion molecules (very late antigen [VLA]-4 [ alpha 4 beta 1 integrin (...) ] and leukocyte function antigen [LFA]-1 [ alpha L beta 2 integrin]) and chemokine receptors (CXCR3 and CCR5) in CD8(+) T cell migration to cerebrospinal fluid (CSF) during HIV-1 infection.CD8(+) T cells trafficking to CSF were uniformly VLA-4(high), LFA-1(high). CCR5 expression was significantly enhanced in T cells from CSF, compared with those from blood (P<.001), including HIV-1-specific CD8(+) T cells, and most T cells from CSF expressed both CXCR3 and CCR5. Interferon-inducible protein (IP)-10 (CXCL10

2004 Journal of Infectious Diseases

3359. Two common PFIC2 mutations are associated with the impaired membrane trafficking of BSEP/ABCB11. (Abstract)

of these two mutants in human embryonic kidney 293 and Madin-Darby canine kidney II cells, respectively. Introduction of E297G and D482G mutations into the human BSEP gene by site-directed mutagenesis resulted in a significant reduction in the BSEP expression level, which was associated with impaired membrane trafficking. Most of the D482G BSEP and some of the E297G BSEP underwent only core glycosylation and appeared to be predominantly located in the endoplasmic reticulum. The inhibition of proteasome (...) Two common PFIC2 mutations are associated with the impaired membrane trafficking of BSEP/ABCB11. Progressive familial intrahepatic cholestasis type 2 (PFIC2) is caused by a mutation in the bile salt export pump (BSEP/ABCB11) gene. However, the mechanisms for the deficiency in the function of two mutations (E297G and D482G), which are frequently found in European patients, have not yet been identified. In the present study, we examined the transport activity and cellular localization

2005 Hepatology

3360. Defective trafficking of nephrin missense mutants rescued by a chemical chaperone. (Abstract)

. Because sodium 4-phenylbutyrate has been shown to function as a chemical chaperone and to correct the cellular trafficking of several mislocalized or misfolded mutant plasma membrane proteins, the effects of this compound on the missense mutants identified in patients with congenital nephrotic syndrome of the Finnish type were investigated. This study was performed using human embryonic kidney 293 cells stably expressing wild-type or missense nephrin mutants trapped in the ER. Immunofluorescence (...) Defective trafficking of nephrin missense mutants rescued by a chemical chaperone. The nephrin gene (NPHS1) is mutated in congenital nephrotic syndrome of the Finnish type. Most mutations found in non-Finnish patients are missense mutations. The most common consequence of missense mutations in congenital nephrotic syndrome is a defect in intracellular transport and retention of the mutant proteins in the endoplasmic reticulum (ER), possibly as a result of misfolding and unfavored conformation

2004 Journal of the American Society of Nephrology

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