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Extracellular ATP reduces HIV-1 transfer from immature dendritic cells to CD4+ T lymphocytes
Corinne Barat, Caroline Gilbert, Michael Imbeault, Michel J Tremblay
Retrovirology , 2008, DOI: 10.1186/1742-4690-5-30
Abstract: In this study, we show that extracellular ATP reduces HIV-1 transfer from immature monocyte-derived DCs (iDCs) to autologous CD4+ T cells. This observed decrease in viral replication was related to a lower proportion of infected CD4+ T cells following transfer, and was seen with both X4- and R5-tropic isolates of HIV-1. Extracellular ATP had no effect on direct CD4+ T cell infection as well as on productive HIV-1 infection of iDCs. These observations indicate that extracellular ATP affects HIV-1 infection of CD4+ T cells in trans with no effect on de novo virus production by iDCs. Additional experiments suggest that extracellular ATP might modulate the trafficking pathway of internalized virions within iDCs leading to an increased lysosomal degradation, which could be partly responsible for the decreased HIV-1 transmission.These results suggest that extracellular ATP can act as a factor controlling HIV-1 propagation.Dendritic cells (DCs) are crucial in generating a virus-specific immune response since they are recognized as the most potent antigen-presenting cells of the immune system, yet they also play a pivotal role in establishment and dissemination of HIV-1 infection. Indeed, HIV-1 exploits the migratory ability of DCs to gain access to CD4+ T lymphocytes in lymphoid tissues. DCs, particularly immature DCs (iDCs) that reside in peripheral mucosal tissues, are among the first target cells for the virus. The reported low levels of CD4 and chemokine co-receptors CXCR4 and CCR5 on DCs are probably responsible for their weaker susceptibility to productive HIV-1 infection in vitro as compared to CD4+ T cells [1,2]. It has been demonstrated that interactions between the external HIV-1 envelope and C-type lectin receptors such as DC-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN) [3,4], mannose receptor (MR) (CD206) and galactosyl ceramide [5] result in an efficient capture of viral particles. Following interactions with the viral entity, DCs
Kefir induces cell-cycle arrest and apoptosis in HTLV-1-negative malignant T-lymphocytes
Katia Maalouf, Elias Baydoun, Sandra Rizk
Cancer Management and Research , 2011, DOI: http://dx.doi.org/10.2147/CMAR.S15109
Abstract: induces cell-cycle arrest and apoptosis in HTLV-1-negative malignant T-lymphocytes Original Research (3441) Total Article Views Authors: Katia Maalouf, Elias Baydoun, Sandra Rizk Published Date February 2011 Volume 2011:3 Pages 39 - 47 DOI: http://dx.doi.org/10.2147/CMAR.S15109 Katia Maalouf1, Elias Baydoun2, Sandra Rizk1 1Department of Natural Sciences, Lebanese American University, Beirut, Lebanon; 2Department of Biology, American University of Beirut, Beirut, Lebanon Background: Adult lymphoblastic leukemia (ALL) is a malignancy that occurs in white blood cells. The overall cure rate in children is 85%, whereas it is only 40% in adults. Kefir is an important probiotic that contains many bioactive ingredients, which give it unique health benefits. It has been shown to control several cellular types of cancer. Purpose: The present study investigates the effect of a cell-free fraction of kefir on CEM and Jurkat cells, which are human T-lymphotropic virus type I (HTLV-1)-negative malignant T-lymphocytes. Methods: Cells were incubated with different kefir concentrations. The cytotoxicity of the compound was evaluated by determining the percentage viability of cells. The effect of all the noncytotoxic concentrations of kefir on the proliferation of CEM and Jurkat cells was then assessed. The levels of transforming growth factor-alpha (TGF-α), transforming growth factor- beta1 (TGF-β1), matrix metalloproteinase-2 (MMP-2), and MMP-9 mRNA upon kefir treatment were then analyzed using reverse transcriptase polymerase chain reaction (RT-PCR). Finally, the growth inhibitory effects of kefir on cell-cycle progression/apoptosis were assessed by Cell Death Detection (ELISA) and flow cytometry. Results: The maximum cytotoxicity recorded after 48-hours treatment with 80 μg/μL kefir was only 42% and 39% in CEM and Jurkat cells, respectively. The percent reduction in proliferation was very significant, and was dose-, and time-dependent. In both cell lines, kefir exhibited its antiproliferative effect by downregulating TGF-α and upregulating TGF- β1 mRNA expression. Upon kefir treatment, a marked increase in cell-cycle distribution was noted in the preG1 phase of CEM and Jurkat cells, indicating the proapoptotic effect of kefir, which was further confirmed by Cell Death Detection ELISA. However, kefir did not affect the mRNA expression of metalloproteinases needed for the invasion of leukemic cell lines. Conclusion: In conclusion, kefir is effective in inhibiting proliferation and inducing apoptosis of HTLV-1-negative malignant T-lymphocytes. Therefore, further in vivo investigation is highly recommended.
Cytokeratin 18 expression in immature Sertoli cells: co-localization with interstitial lymphocytic infiltrates.  [cached]
Roland Kruse,Sibylle Eigelshoven,Anna Kaiser,Thomas Ruzicka
Folia Histochemica et Cytobiologica , 2009, DOI: 10.5603/4371
Abstract: Although multiple interactions of seminiferous tubules and the interstitial testicular tissue are known, correlation of cytokeratin 18 expressing Sertoli cells with interstitial changes has still not yet been reported. Considering this fact, we focused our investigation on changes of the adjacent interstitial tissue. A total sample of 51 testicular biopsies (from infertile patients) showing mixed atrophy was examined immunohistochemically with antibodies against cytokeratin 18, vimentin, L26/CD20, CD4 and CD8. Twenty-one of the 51 cases showed single seminiferous tubules with Sertoli cells expressing cytokeratin 18. These 21 tubules consistently exhibit either spermatogenic arrest at the level of spermatogonia or only immature Sertoli cells. In the adjacent interstitial tissue of 8 of the 21 cytokeratin 18 positive tubules (39%) striking inflammatory infiltrates--predominantly expressing L26/CD20 typical for B lymphocytes and CD8 typical for T suppressor lymphocytes--were detected. These findings underline that tubules with cytokeratin 18 expressing Sertoli cells exhibit early spermatogenic arrest or only few remaining Sertoli cells. Additionally, we observed a remarkable co-localization of these tubules with lymphocytic infiltrates of the adjacent interstitial tissue.
Kefir induces cell-cycle arrest and apoptosis in HTLV-1-negative malignant T-lymphocytes  [cached]
Katia Maalouf,Elias Baydoun,Sandra Rizk
Cancer Management and Research , 2011,
Abstract: Katia Maalouf1, Elias Baydoun2, Sandra Rizk11Department of Natural Sciences, Lebanese American University, Beirut, Lebanon; 2Department of Biology, American University of Beirut, Beirut, LebanonBackground: Adult lymphoblastic leukemia (ALL) is a malignancy that occurs in white blood cells. The overall cure rate in children is 85%, whereas it is only 40% in adults. Kefir is an important probiotic that contains many bioactive ingredients, which give it unique health benefits. It has been shown to control several cellular types of cancer.Purpose: The present study investigates the effect of a cell-free fraction of kefir on CEM and Jurkat cells, which are human T-lymphotropic virus type I (HTLV-1)-negative malignant T-lymphocytes.Methods: Cells were incubated with different kefir concentrations. The cytotoxicity of the compound was evaluated by determining the percentage viability of cells. The effect of all the noncytotoxic concentrations of kefir on the proliferation of CEM and Jurkat cells was then assessed. The levels of transforming growth factor-alpha (TGF-α), transforming growth factor- beta1 (TGF-β1), matrix metalloproteinase-2 (MMP-2), and MMP-9 mRNA upon kefir treatment were then analyzed using reverse transcriptase polymerase chain reaction (RT-PCR). Finally, the growth inhibitory effects of kefir on cell-cycle progression/apoptosis were assessed by Cell Death Detection (ELISA) and flow cytometry.Results: The maximum cytotoxicity recorded after 48-hours treatment with 80 μg/μL kefir was only 42% and 39% in CEM and Jurkat cells, respectively. The percent reduction in proliferation was very significant, and was dose-, and time-dependent. In both cell lines, kefir exhibited its antiproliferative effect by downregulating TGF-α and upregulating TGF- β1 mRNA expression. Upon kefir treatment, a marked increase in cell-cycle distribution was noted in the preG1 phase of CEM and Jurkat cells, indicating the proapoptotic effect of kefir, which was further confirmed by Cell Death Detection ELISA. However, kefir did not affect the mRNA expression of metalloproteinases needed for the invasion of leukemic cell lines.Conclusion: In conclusion, kefir is effective in inhibiting proliferation and inducing apoptosis of HTLV-1-negative malignant T-lymphocytes. Therefore, further in vivo investigation is highly recommended.Keywords: apoptosis, cancer, CEM, Jurkat, kefir, leukemia
Exchange Bias following Kinetic Arrest  [PDF]
Praveen Chaddah
Physics , 2015,
Abstract: Exchange bias is often observed when anti-ferromagnetic and ferromagnetic phases coexist. The coexistence of two competing magnetic phases can persist to the lowest temperatures if the disorder-broadened 1st order transition separating them is interrupted, as is proposed in the kinetic arrest phenomenon. The fractions of coexisting phases can, in this phenomenon, be tuned by following different cooling protocols. We discuss predicted behaviours of exchange bias resulting from the kinetic arrest phenomenon. Specifically, for appropriate values of cycling field Hmax and measuring temperature T0 there will be no exchange bias under cooling in zero field, while it will manifest with increasing cooling field, and then saturate.
Activation of the Syk tyrosine kinase is insufficient for downstream signal transduction in B lymphocytes
Robert C Hsueh, Adrienne M Hammill, Jamie A Lee, Jonathan W Uhr, Richard H Scheuermann
BMC Immunology , 2002, DOI: 10.1186/1471-2172-3-16
Abstract: A mutant form of Syk carrying a combination of a K395A substitution in the kinase domain and substitutions of three phenylalanines (3F) for the three C-terminal tyrosines was expressed in a murine B cell lymphoma cell line, BCL1.3B3 to interfere with normal Syk regulation as a means to examine the Syk activation step in BCR signaling. Introduction of this kinase-inactive mutant led to the constitutive activation of the endogenous wildtype Syk enzyme in the absence of receptor engagement through a 'dominant-positive' effect. Under these conditions, Syk kinase activation occurred in the absence of phosphorylation on Syk tyrosine residues. Although Syk appears to be required for BCR-induced apoptosis in several systems, no increase in spontaneous cell death was observed in these cells. Surprisingly, although the endogenous Syk kinase was enzymatically active, no enhancement in the phosphorylation of cytoplasmic proteins, including phospholipase Cγ2 (PLCγ2), a direct Syk target, was observed.These data indicate that activation of Syk kinase enzymatic activity is insufficient for Syk-dependent signal transduction. This observation suggests that other events are required for efficient signaling. We speculate that localization of the active enzyme to a receptor complex specifically assembled for signal transduction may be the missing event.The B cell antigen receptor (BCR) is a multi-subunit complex that acts as a key sensor regulating the response of lymphocytes to their environment (reviewed in [1-7]). In mature B cells, activation through the BCR stimulates cellular proliferation and differentiation. In immature B cells, activation through the BCR induces either a state of unresponsiveness, termed anergy, or death by apoptosis, depending on the physical nature and concentration of the antigen [8-25]. In some B cell lymphomas, activation through the BCR can induce cell cycle arrest and apoptosis in vitro and tumor dormancy in vivo [19,26-28]. The core of the multi-subuni
Fes cycling
Berkelmans Rik
Journal of Automatic Control , 2008, DOI: 10.2298/jac0802073b
Abstract: Many research with functional electrical stimulation (FES) has been done to regain mobility and for health benefits. Better results have been reported for FES-cycling than for FES-walking. The majority of the subjects during such research are people with a spinal cord injury (SCI), cause they often lost skin sensation. Besides using surface stimulation also implanted stimulators can be used. This solves the skin sensation problem, but needs a surgery. Many physiological effects of FES-cycling has been reported, e.g., increase of muscles, better blood flow, reduction of pressure ulcers, improved self-image and some reduction of bone mineral density (BMD) loss. Also people with an incomplete SCI benefit by FES-cycling, e.g. cycling time without FES, muscle strength and also the walking abilities increased. Hybrid exercise gives an even better cardiovascular training. Presently 4 companies are involved in FES-cycling. They all have a stationary mobility trainer. Two of them also use an outdoor tricycle. One combined with voluntary arm cranking. By optimizing the stimulation parameters the power output and fatigue resistance will increase, but will still be less compared to voluntary cycling.
CARDIAC ARREST
LIAQUAT ALI
The Professional Medical Journal , 2006,
Abstract: We present hereby a case report of 65 years old female scheduled for laparotomy for excision ofhydatid cyst liver diagnosed on ultrasonography and CT scan, but on laparotomy unexpectedly it turned out to bepheochromocytoma right adrenal and was further complicated by rupture of tumour, avulsion of inferior vena cava,massive haemorrhage, leading to cardiac arrest. Detailed in this report is the management of unexpectedpheochromocytoma, treatment of acute severe haemorrhage with massive transfusion and resuscitation and revivalof patient from cardiac arrest with CPR.
Assessing Cycling Participation in Australia  [PDF]
Chris Rissel,Cameron Munro,Adrian Bauman
Sports , 2013, DOI: 10.3390/sports1010001
Abstract: Planning and evaluating cycling programs at a national or state level requires accurate measures of cycling participation. However, recent reports of cycling participation have produced very different estimates. This paper examines the reported rates of cycling in five recent population surveys of cycling. Three surveys (one national and two from Sydney) asking respondents when they last rode a bicycle generated cycling participation (cycled in the past year) estimates of 29.7%, 34.1% and 28.9%. Two other national surveys which asked participants to recall (unprompted) any physical activity done for exercise, recreation or sport in the previous 12 months, estimated cycling in the past year as 11.1% and 6.5%. While unprompted recall of cycling as a type of physical activity generates lower estimates of cycling participation than specific recall questions, both assessment approaches produced similar patterns of cycling by age and sex with both approaches indicating fewer women and older adults cycling. The different question styles most likely explain the substantial discrepancies between the estimates of cycling participation. Some differences are to be expected due to sampling variability, question differences, and regional variation in cycling.
Coherence properties of cycling chaos  [PDF]
T. A. Levanova,G. V. Osipov,A. Pikovsky
Physics , 2013, DOI: 10.1016/j.cnsns.2014.01.011
Abstract: Cycling chaos is a heteroclinic connection between several chaotic attractors, at which switching between the chaotic sets occur at growing time intervals. Here we characterize the coherence properties of these switchings, considering nearly periodic regimes that appear close to the cycling chaos due to imperfections or to instability. Using numerical simulations of coupled Lorenz, Roessler, and logistic map models, we show that the coherence is high in the case of imperfection (so that asymptotically the cycling chaos is very regular), while it is low close to instability of the cycling chaos.
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