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Articles by A Banerjee
Total Records ( 7 ) for A Banerjee
  J. L Johnson , E. E Moore , J. L Kashuk , A Banerjee , C. C Cothren , W. L Biffl and A. Sauaia
 

Hypothesis  Transfusion of fresh frozen plasma (FFP) and platelets is independently associated with the development of multiple organ failure (MOF) in critically injured patients.

Design  Prospective cohort study.

Setting  Academic regional level I trauma center.

Patients  From 1992 to 2004, a total of 1440 critically injured patients were admitted to our surgical intensive care unit and survived at least 48 hours. Of these, 1415 had complete data on age, Injury Severity Score (ISS), and units of FFP, platelets, and packed red blood cells (PRBCs) transfused. Multiple organ failure was defined using the Denver MOF score. Multiple logistic regression analysis was used to adjust transfusion of FFP, platelets, and PRBCs for known MOF risk factors.

Main Outcome Measure  Multiple organ failure.

Results  The mean (SD) ISS was 29.3 (11.3), and the mean (SD) patient age was 37.4 (16.6) years. Among 1440 patients, 346 (24.0%) developed MOF, and 118 (8.2%) died. Multiple logistic regression analysis detected a significant interaction between units of FFP and PRBCs transfused (P < .001). Regardless of the units of PRBCs transfused, FFP transfusion was independently associated with the development of MOF. However, the deleterious effect associated with FFP transfusion was more prominent among patients receiving fewer than 6 U of PRBCs. Platelet transfusion was unassociated with MOF after adjustment for age, ISS, and FFP and PRBC transfusion.

Conclusions  Early transfusion of FFP is associated with an increased risk of postinjury MOF, even after adjusting for age, ISS, and PRBC transfusion. Caution is warranted in developing protocols for empirical FFP transfusion. Specifically, transfusion triggers for FFP should be reexamined, as well as the practice of delivering FFP in fixed ratios to the units of PRBCs transfused.

  A Banerjee , L. E Silver , C Heneghan , S. J.V Welch , L. M Bull , Z Mehta , A. P Banning and P. M. Rothwell
 

Background— Family history of premature myocardial infarction (MI) in first-degree relatives is a risk factor for MI and an indication for primary prevention. Although excess mother-to-daughter "transmission" occurs in ischemic stroke, no published studies have considered sex-of-parent/sex-of-proband interactions in the heritability of MI.

Methods and Results— In a population-based study (Oxford Vascular Study) of all patients with acute coronary syndromes (ACS), irrespective of age, family history of all acute vascular events and related risk factors were analyzed by sex and age of both probands and first-degree relatives. Premature events were categorized as occurring at age <65 years. Of 835 probands with 1 or more ACS, 623 (420 men) had incident events and complete family history data. In probands with premature ACS, maternal history of both MI and of all vascular events were more common in female than male probands (odds ratio [OR], 2.25; 95% CI, 1.02 to 4.94; P=0.04 and OR, 3.03; 95% CI, 1.47 to 6.26; P=0.002, respectively). No such effect existed for paternal history (OR, 1.00; 95% CI, 0.46 to 2.10; P=0.99 and OR, 1.19; 95% CI, 0.58 to 2.43; P=0.63, respectively). Age at ACS in probands was highly correlated with age at MI in mothers (r=0.46, P<0.001), regardless of the proband’s sex. Consequently, history of premature maternal MI was strongly associated with premature ACS and premature MI in female (OR, 10.52; 95% CI, 2.17 to 56.6; P=0.001 and OR, 7.31; 95% CI, 1.55 to 34.6; P=0.004, respectively) and male probands (OR, 3.88; 95% CI, 1.20 to 12.6; P=0.01 and OR, 3.63; 95% CI, 1.13 to 11.60; P=0.02, respectively).

Conclusions— Important sex-of-parent/sex-of-proband interactions exist in the family history of MI in patients with ACS. Greater emphasis should be placed on maternal than paternal history of MI, particularly in women aged <65 years.

  R Suriano , S. K Ghosh , A Mittelman , A Banerjee and R. K Tiwari
 

Cancer-derived heat shock protein gp96 induces a tumor-specific protective immune response primarily mediated by cytotoxic T lymphocytes (CTL) directed toward cancer-associated peptides associated with gp96. Both innate and adaptive immune responses have been demonstrated using a cell culture-based signaling mechanism. When used as an extraneous vaccine, one critical interaction which must occur for an immune response to be generated is the interaction between gp96 and the antigen presenting cell (APC) surface receptors (CD91, SR-A, TLR-2, and TLR-4). Our previous study concluded that gp96 purified from various rat and human prostate cancers is differentially glycosylated based on the amino and neutral monosaccharide content, and it was postulated that the monosaccharides may play a role in its biological activity. In this report, we report differences in the cancer-specific sialic acid content of gp96 purified from normal rat prostate compared to two rat prostate cancers, MAT-LyLu and Dunning G, as well as between two human prostate cancer cells, LnCaP and DU145. We also examined the modulatory effect of sialic acid residues on the binding of gp96 to APCs and its subsequent activation. Our results supported the contention that significant differences in the sialic acid content exist between Dunning G, MAT-LyLu, and normal rat prostate gp96, which affected its binding and biochemical activity to APCs. We therefore postulate that varied glycans of HPS96, a hitherto neglected structural component, may play a pivotal role in its anticancer activity. We suggest that construction of the glycan tree is a key to identification of the necessary and sufficient elements in the structure–function activity of HSP96.

  P. C Eckels , A Banerjee , E. E Moore , N. J. D McLaughlin , L. M Gries , M. R Kelher , K. M England , F Gamboni Robertson , S. Y Khan and C. C. Silliman
 

Receptor signaling is integral for adhesion, emigration, phagocytosis, and reactive oxygen species production in polymorphonuclear neutrophils (PMNs). Priming is an important part of PMN emigration, but it can also lead to PMN-mediated organ injury in the host. Platelet-activating factor (PAF) primes PMNs through activation of a specific G protein-coupled receptor. We hypothesize that PAF priming of PMNs requires clathrin-mediated endocytosis (CME) of the PAF receptor (PAFr), and, therefore, amantadine, known to inhibit CME, significantly antagonizes PAF signaling. PMNs were isolated by standard techniques to >98% purity and tested for viability. Amantadine (1 mM) significantly inhibited the PAF-mediated changes in the cellular distribution of clathrin and the physical colocalization [fluorescence resonance energy transfer positive (FRET+)] of early endosome antigen-1 and Rab5a, known components of CME and similar to hypertonic saline, a known inhibitor of CME. Furthermore, amantadine had no effect on the PAF-induced cytosolic calcium flux; however, phosphorylation of p38 MAPK was significantly decreased. Amantadine inhibited PAF-mediated changes in PMN physiology, including priming of the NADPH oxidase and shape change with lesser inhibition of increases in CD11b surface expression and elastase release. Furthermore, rimantadine, an amantadine analog, was a more potent inhibitor of PAF priming of the N-formyl-methionyl-leucyl-phenylalanine-activated oxidase. PAF priming of PMNs requires clathrin-mediated endocytosis that is inhibited when PMNs are pretreated with either amantadine or rimantadine. Thus, amantadine and rimantadine have the potential to ameliorate PMN-mediated tissue damage in humans.

  S Uchiyama , A. F Carlin , A Khosravi , S Weiman , A Banerjee , D Quach , G Hightower , T. J Mitchell , K. S Doran and V. Nizet
 

In humans, Streptococcus pneumoniae (SPN) is the leading cause of bacterial meningitis, a disease with high attributable mortality and frequent permanent neurological sequelae. The molecular mechanisms underlying the central nervous system tropism of SPN are incompletely understood, but include a primary interaction of the pathogen with the blood–brain barrier (BBB) endothelium. All SPN strains possess a gene encoding the surface-anchored sialidase (neuraminidase) NanA, which cleaves sialic acid on host cells and proteins. Here, we use an isogenic SPN NanA-deficient mutant and heterologous expression of the protein to show that NanA is both necessary and sufficient to promote SPN adherence to and invasion of human brain microvascular endothelial cells (hBMECs). NanA-mediated hBMEC invasion depends only partially on sialidase activity, whereas the N-terminal lectinlike domain of the protein plays a critical role. NanA promotes SPN–BBB interaction in a murine infection model, identifying the protein as proximal mediator of CNS entry by the pathogen.

  C. N Jenne , A Enders , R Rivera , S. R Watson , A. J Bankovich , J. P Pereira , Y Xu , C. M Roots , J. N Beilke , A Banerjee , S. L Reiner , S. A Miller , A. S Weinmann , C. C Goodnow , L. L Lanier , J. G Cyster and J. Chun
 

During a screen for ethylnitrosourea-induced mutations in mice affecting blood natural killer (NK) cells, we identified a strain, designated Duane, in which NK cells were reduced in blood and spleen but increased in lymph nodes (LNs) and bone marrow (BM). The accumulation of NK cells in LNs reflected a decreased ability to exit into lymph. This strain carries a point mutation within Tbx21 (T-bet), which generates a defective protein. Duane NK cells have a 30-fold deficiency in sphingosine-1-phosphate receptor 5 (S1P5) transcript levels, and S1P5-deficient mice exhibit an egress defect similar to Duane. Chromatin immunoprecipitation confirms binding of T-bet to the S1pr5 locus. S1P-deficient mice exhibit a more severe NK cell egress block, and the FTY720-sensitive S1P1 also plays a role in NK cell egress from LNs. S1P5 is not inhibited by CD69, a property that may facilitate trafficking of activated NK cells to effector sites. Finally, the accumulation of NK cells within BM of S1P-deficient mice was associated with reduced numbers in BM sinusoids, suggesting a role for S1P in BM egress. In summary, these findings identify S1P5 as a T-bet–induced gene that is required for NK cell egress from LNs and BM.

  I Isomura , S Palmer , R. J Grumont , K Bunting , G Hoyne , N Wilkinson , A Banerjee , A Proietto , R Gugasyan , W Li , A McNally , R. J Steptoe , R Thomas , M. F Shannon and S. Gerondakis
 

During thymopoiesis, a unique program of gene expression promotes the development of CD4 regulatory T (T reg) cells. Although Foxp3 maintains a pattern of gene expression necessary for T reg cell function, other transcription factors are emerging as important determinants of T reg cell development. We show that the NF-B transcription factor c-Rel is highly expressed in thymic T reg cells and that in c-rel–/– mice, thymic T reg cell numbers are markedly reduced as a result of a T cell–intrinsic defect that is manifest during thymocyte development. Although c-Rel is not essential for TGF-β conversion of peripheral CD4+CD25 T cells into CD4+Foxp3+ cells, it is required for optimal homeostatic expansion of peripheral T reg cells. Despite a lower number of peripheral T reg cells in c-rel–/– mice, the residual peripheral c-rel–/– T reg cells express normal levels of Foxp3, display a pattern of cell surface markers and gene expression similar to those of wild-type T reg cells, and effectively suppress effector T cell function in culture and in vivo. Collectively, our results indicate that c-Rel is important for both the thymic development and peripheral homeostatic proliferation of T reg cells.

 
 
 
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