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  1. Article: Is a self-inflicted burn part of a repeated self-harm pattern?

    Joory, K / Farroha, A / Moiemen, N

    Annals of burns and fire disasters

    2016  Volume 28, Issue 3, Page(s) 223–227

    Abstract: Self-inflicted burns (SIB) consistently account for a small proportion of burn injuries. There is a wide spectrum of SIB, from minor burns through to major life threatening burn injuries in suicidal patients who have committed self-immolation. Non-fatal ... ...

    Abstract Self-inflicted burns (SIB) consistently account for a small proportion of burn injuries. There is a wide spectrum of SIB, from minor burns through to major life threatening burn injuries in suicidal patients who have committed self-immolation. Non-fatal deliberate self-harm (DSH) is a common reason for presenting to hospital. This occurs in many forms including wounding, burning and poisoning to name a few. Such behaviours are commonly repeated, sometimes with increasing severity. DSH is a major risk factor for subsequent suicide. We had observed patterns of repeated self harm behaviours in patients presenting to our centre with SIB. Patterns of repeated DSH in those presenting with self-inflicted burns have not previously been described in the literature. In a five-year period (2008 to 2012) 84 patients presented to our burns centre with SIB. Within this population, 39 patients (46%) were identified on a national database as having been admitted to an acute National Health Service (NHS) trust somewhere in the UK with sequelae of deliberate self-harm. There had been a total of 128 additional hospital admissions. In the majority of cases (85%) another admission preceded the presentation to our service with SIB. Only four out of the 17 SIB patients (24%) who died of their injuries had previous hospital admissions with DSH. This lends weight to the need for thorough holistic assessment of any patient admitted to hospital with sequelae of deliberate self-harm in order to try and provide appropriate support and interventions for these vulnerable individuals to prevent recurrent self-harm or suicide.
    Language English
    Publishing date 2016-06-08
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 2106850-1
    ISSN 1592-9566 ; 1592-9558
    ISSN (online) 1592-9566
    ISSN 1592-9558
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: History of burns: The past, present and the future.

    Lee, Kwang Chear / Joory, Kavita / Moiemen, Naiem S

    Burns & trauma

    2014  Volume 2, Issue 4, Page(s) 169–180

    Abstract: Burn injuries are one of the most common and devastating afflictions on the human body. In this article we look back at how the treatment of burns has evolved over the centuries from a primarily topical therapy consisting of weird and wonderful topical ... ...

    Abstract Burn injuries are one of the most common and devastating afflictions on the human body. In this article we look back at how the treatment of burns has evolved over the centuries from a primarily topical therapy consisting of weird and wonderful topical concoctions in ancient times to one that spans multiple scientific fields of topical therapy, antibiotics, fluid resuscitation, skin excision and grafting, respiratory and metabolic care and nutrition. Most major advances in burn care occurred in the last 50 years, spurred on by wars and great fires. The use of systemic antibiotics and topical silver therapy greatly reduced sepsis related mortality. This along with the advent of antiseptic surgical techniques, burn depth classification and skin grafting allowed the excision and coverage of full-thickness burns which resulted in greatly improved survival rates. Advancements in the methods of assessing the surface area of burns paved way for more accurate fluid resuscitation, minimising the effects of shock and avoiding fluid over-loading. The introduction of metabolic care, nutritional support and care of inhalational injuries further improved the outcome of burn patients. We also briefly discuss some future directions in burn care such as the use of cell and pharmalogical therapies.
    Language English
    Publishing date 2014-10-25
    Publishing country England
    Document type Journal Article
    ZDB-ID 2775996-9
    ISSN 2321-3876 ; 2321-3868
    ISSN (online) 2321-3876
    ISSN 2321-3868
    DOI 10.4103/2321-3868.143620
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Smoking and glomus tumours.

    Joory, Kavita / Mikalef, Petros / Jose, Rajive Mathew

    Journal of plastic, reconstructive & aesthetic surgery : JPRAS

    2014  Volume 67, Issue 11, Page(s) 1600–1601

    MeSH term(s) Female ; Fingers ; Glomus Tumor/pathology ; Glomus Tumor/surgery ; Humans ; Magnetic Resonance Imaging ; Middle Aged ; Smoking/adverse effects
    Language English
    Publishing date 2014-11
    Publishing country Netherlands
    Document type Letter
    ZDB-ID 2217750-4
    ISSN 1878-0539 ; 1748-6815 ; 0007-1226
    ISSN (online) 1878-0539
    ISSN 1748-6815 ; 0007-1226
    DOI 10.1016/j.bjps.2014.05.057
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Vascular endothelial growth factor-C (VEGF-C) expression in normal human tissues.

    Joory, K D / Levick, J R / Mortimer, P S / Bates, D O

    Lymphatic research and biology

    2006  Volume 4, Issue 2, Page(s) 73–82

    Abstract: Objective: To characterize vascular endothelial growth factor-C (VEGF-C) protein expression in normal human tissues by immunohistochemistry (IHC). VEGF-C is a growth factor for lymphatic endothelial cells. VEGF-C mRNA and protein are expressed in a ... ...

    Abstract Objective: To characterize vascular endothelial growth factor-C (VEGF-C) protein expression in normal human tissues by immunohistochemistry (IHC). VEGF-C is a growth factor for lymphatic endothelial cells. VEGF-C mRNA and protein are expressed in a variety of cancerous tissues, but the localization of VEGF-C protein in many normal human tissues has not been clearly demonstrated to date. We therefore performed an immunohistochemical survey of the distribution of intracellular VEGF-C protein in a range of normal human tissue types.
    Methods: Five microm sections were cut from archived human tissues. Sections were dewaxed, rehydrated, and subjected to microwave pretreatment. They were incubated with VEGF-C antibody before detection with biotinylated secondary antibody using 'Elite' avidin-biotin enzyme complex and diaminobenzidine substrate. The primary antibody recognized the C-terminus of the VEGF-C propeptide that is cleaved before secretion and hence only cellular protein was detected. Negative controls used the same concentration of normal goat IgG.
    Results: Staining manifested as small punctate cytoplasmic granules. Strong expression was observed in large intestine epithelium, and mammary duct epithelium, skeletal and cardiac muscle, thyroid, ovary, and the prostate. Weaker expression was also detected in the hepatocytes close to the terminal hepatic venules of the liver, vascular smooth muscle, and placenta. No expression was consistently detected in spleen or thymus.
    Conclusions: Intracellular VEGF-C protein is widely expressed in many normal human adult tissues. Its expression in cancer is not therefore per se indicative of a prolymphangiogenic change. To demonstrate the latter, a quantitative change in expression level is required.
    MeSH term(s) Female ; Humans ; Immunohistochemistry ; Lymphoid Tissue/metabolism ; Mesoderm/metabolism ; Muscles/metabolism ; Ovary/metabolism ; Placenta/metabolism ; Reference Values ; Vascular Endothelial Growth Factor C/metabolism
    Chemical Substances Vascular Endothelial Growth Factor C
    Language English
    Publishing date 2006
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2147953-7
    ISSN 1557-8585 ; 1539-6851
    ISSN (online) 1557-8585
    ISSN 1539-6851
    DOI 10.1089/lrb.2006.4.73
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5921: Show issues Location:
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  5. Article: Chemokine-mediated migration of melanoma cells towards lymphatics--a mechanism contributing to metastasis.

    Shields, J D / Emmett, M S / Dunn, D B A / Joory, K D / Sage, L M / Rigby, H / Mortimer, P S / Orlando, A / Levick, J R / Bates, D O

    Oncogene

    2007  Volume 26, Issue 21, Page(s) 2997–3005

    Abstract: The mechanisms that cause tumors such as melanomas to metastasize into peripheral lymphatic capillaries are poorly defined. Non-mutually-exclusive mechanisms are lymphatic endothelial cell (LEC) chemotaxis and proliferation in response to tumor cells ( ... ...

    Abstract The mechanisms that cause tumors such as melanomas to metastasize into peripheral lymphatic capillaries are poorly defined. Non-mutually-exclusive mechanisms are lymphatic endothelial cell (LEC) chemotaxis and proliferation in response to tumor cells (chemotaxis-lymphangiogenesis hypothesis) or LECs may secrete chemotactic agents that attract cancer cells (chemotactic metastasis hypothesis). Using migration assays, we found evidence supporting both hypotheses. Conditioned medium (CM) from metastatic malignant melanoma (MMM) cell lines attracted LEC migration, consistent with the lymphangiogenesis hypothesis. Conversely, CM from mixed endothelial cells or LECs, but not blood endothelial cells, attracted MMM cells but not non-metastatic melanoma cells, consistent with the chemotactic metastasis hypothesis. MMM cell lines expressed CCR7 receptors for the lymphatic chemokine CCL21 and CCL21 neutralizing antibodies prevented MMM chemotaxis in vitro. To test for chemotactic metastasis in vivo tumor cells were xenotransplanted into nude mice approximately 1 cm from an injected LEC depot. Two different MMM grew directionally towards the LECs, whereas non-metastatic melanomas did not. These observations support the hypothesis that MMM cells grow towards regions of high LEC density owing to chemotactic LEC secretions, including CCL21. This chemotactic metastasis may contribute to the close association between metastasizing tumor cells and peri-tumor lymphatic density and promote lymphatic invasion.
    MeSH term(s) Animals ; Biomarkers, Tumor/analysis ; Cell Movement/physiology ; Cells, Cultured ; Chemokines/physiology ; Endothelium, Lymphatic/metabolism ; Endothelium, Lymphatic/pathology ; Humans ; Ki-67 Antigen/analysis ; Lymphatic Metastasis/pathology ; Melanoma, Experimental/metabolism ; Melanoma, Experimental/pathology ; Melanoma, Experimental/secondary ; Mice ; Mice, Nude ; Neoplasm Transplantation/pathology
    Chemical Substances Biomarkers, Tumor ; Chemokines ; Ki-67 Antigen
    Language English
    Publishing date 2007-05-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/sj.onc.1210114
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    Zs.A 2218: Show issues Location:
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  6. Article: VEGF-C promotes survival in podocytes.

    Foster, R R / Satchell, S C / Seckley, J / Emmett, M S / Joory, K / Xing, C Y / Saleem, M A / Mathieson, P W / Bates, D O / Harper, S J

    American journal of physiology. Renal physiology

    2006  Volume 291, Issue 1, Page(s) F196–207

    Abstract: Vascular endothelial growth factor (VEGF)-A is an autocrine survival factor for podocytes, which express two VEGF receptors, VEGF-R1 and VEGF-R3. As VEGF-A is not a known ligand for VEGF-R3, the aim of this investigation was to examine whether VEGF-C, a ... ...

    Abstract Vascular endothelial growth factor (VEGF)-A is an autocrine survival factor for podocytes, which express two VEGF receptors, VEGF-R1 and VEGF-R3. As VEGF-A is not a known ligand for VEGF-R3, the aim of this investigation was to examine whether VEGF-C, a known ligand for VEGF-R3, served a function in podocyte biology and whether this was VEGF-R3 dependent. VEGF-C protein expression was localized to podocytes in contrast to VEGF-D, which was expressed in parietal epithelial cells. Intracellular calcium ([Ca2+]i) experiments demonstrated that VEGF-C induced a 0.74+/-0.09-fold reduction in [Ca2+]i compared with baseline in human conditionally immortalized podocytes (hCIPs; P<0.05, one sample t-test, n=8). Cytotoxicity experiments revealed that in hCIPs VEGF-C reduced cytotoxicity to 81.4+/-1.9% of serum-starved conditions (P<0.001, paired t-test, n=16), similar to VEGF-A (82.8+/-4.5% of serum-starved conditions, P<0.05, paired t-test). MAZ51 (a VEGF-R3 kinase inhibitor) inhibited the VEGF-C-induced reduction in cytotoxicity (106.2+/-2.1% of serum-starved conditions), whereas MAZ51 by itself had no cytotoxic effects on hCIPs. VEGF-C was also shown to induce a 0.5+/-0.13-fold reduction in levels of MAPK phosphorylation compared with VEGF-A and VEGF-A-Mab treatment (P<0.05, ANOVA, n=4), yet had no effect on Akt phosphorylation. Surprisingly, immunoprecipitation studies detected no VEGF-C-induced autophosphorylation of VEGF-R3 in hCIPs but did so in HMVECs. Moreover, SU-5416, a tyrosine kinase inhibitor, blocked the VEGF-C-induced reduction in cytotoxicity (106+/-2.8% of serum-starved conditions) at concentrations specific for VEGF-R1. Together, these results suggest for the first time that VEGF-C acts in an autocrine manner in cultured podocytes to promote survival, although the receptor or receptor complex activated has yet to be elucidated.
    MeSH term(s) Calcium/analysis ; Calcium/metabolism ; Cell Line ; Cell Survival/drug effects ; Cell Survival/physiology ; Endothelial Cells/chemistry ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/physiology ; Humans ; Immunoprecipitation ; Indoles/pharmacology ; Kidney Glomerulus/chemistry ; Mitogen-Activated Protein Kinase Kinases/analysis ; Mitogen-Activated Protein Kinase Kinases/physiology ; Naphthalenes/pharmacology ; Phosphorylation ; Podocytes/chemistry ; Podocytes/cytology ; Podocytes/drug effects ; Podocytes/physiology ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-akt/analysis ; Proto-Oncogene Proteins c-akt/physiology ; Pyrroles/pharmacology ; Receptors, Vascular Endothelial Growth Factor/analysis ; Receptors, Vascular Endothelial Growth Factor/physiology ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Vascular Endothelial Growth Factor A/analysis ; Vascular Endothelial Growth Factor A/physiology ; Vascular Endothelial Growth Factor C/physiology ; Vascular Endothelial Growth Factor D/analysis ; Vascular Endothelial Growth Factor D/physiology
    Chemical Substances 3-(4-dimethylamino-naphthalen-1-ylmethylene)-1,3-dihydro-indol-2-one ; Indoles ; Naphthalenes ; Protein Kinase Inhibitors ; Pyrroles ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor C ; Vascular Endothelial Growth Factor D ; Semaxinib (71IA9S35AJ) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2006-03-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 1931-857X ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 1931-857X ; 0363-6127
    DOI 10.1152/ajprenal.00431.2005
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    Uc I Zs.89: Show issues Location:
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  7. Article: Effect of iron deficiency on placental transfer of iron and expression of iron transport proteins in vivo and in vitro.

    Gambling, L / Danzeisen, R / Gair, S / Lea, R G / Charania, Z / Solanky, N / Joory, K D / Srai, S K / McArdle, H J

    The Biochemical journal

    2001  Volume 356, Issue Pt 3, Page(s) 883–889

    Abstract: Maternal iron deficiency during pregnancy induces anaemia in the developing fetus; however, the severity tends to be less than in the mother. The mechanism underlying this resistance has not been determined. We have measured placental expression of ... ...

    Abstract Maternal iron deficiency during pregnancy induces anaemia in the developing fetus; however, the severity tends to be less than in the mother. The mechanism underlying this resistance has not been determined. We have measured placental expression of proteins involved in iron transfer in pregnant rats given diets with decreasing levels of iron and examined the effect of iron deficiency on iron transfer across BeWo cell layers, a model for placental iron transfer. Transferrin receptor expression was increased at both mRNA and protein levels. Similarly, expression of the iron-responsive element (IRE)-regulated form of the divalent metal transporter 1 (DMT1) was also increased. In contrast, the non-IRE regulated isoform showed no change in mRNA levels. Protein levels of DMT1 increased significantly. Iron efflux is thought to be mediated by the metal transporter protein, IREG1/ferroportin1/MTP1, and oxidation of Fe(II) to Fe(III) prior to incorporation into fetal transferrin is carried out by the placental copper oxidase. Expression of IREG1 was not altered by iron deficiency, whereas copper oxidase activity was increased. In BeWo cells made iron deficient by treatment with desferrioxamine ('deferioxamine'), iron accumulation from iron-transferrin increased, in parallel with increased expression of the transferrin receptor. At the same time, iron efflux also increased, showing a higher flux of iron from the apical to the basolateral side. The data show that expression of placental proteins of iron transport are up-regulated in maternal iron deficiency, resulting in an increased efficiency of iron flux and a consequent minimization of the severity of fetal anaemia.
    MeSH term(s) Anemia, Iron-Deficiency/metabolism ; Animals ; Base Sequence ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cation Transport Proteins ; Cell Line ; DNA Primers ; Female ; In Vitro Techniques ; Iron/metabolism ; Iron-Binding Proteins ; Membrane Proteins/metabolism ; Placenta/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats ; Transferrin/metabolism
    Chemical Substances Carrier Proteins ; Cation Transport Proteins ; DNA Primers ; Iron-Binding Proteins ; Membrane Proteins ; RNA, Messenger ; Transferrin ; metal transporting protein 1 ; solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2 ; Iron (E1UOL152H7)
    Language English
    Publishing date 2001-02-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2969-5
    ISSN 1470-8728 ; 0264-6021 ; 0006-2936 ; 0306-3275
    ISSN (online) 1470-8728
    ISSN 0264-6021 ; 0006-2936 ; 0306-3275
    DOI 10.1042/0264-6021:3560883
    Database MEDical Literature Analysis and Retrieval System OnLINE

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