16 research outputs found
An approach to incompatible cross-matched red cells: Our experience in a major regional blood transfusion center at Kolkata, Eastern India
Introduction: With the increased utilization of immunohematology (IH) analyzers in the transfusion medicine, type, and screen policy is the method of choice. Still, the importance of routine crossmatching could not be overruled. Here, we tried to understand the clinical conditions and safety of red cell transfusion and their outcomes.
Materials And Methods: This prospective study was conducted by IH laboratory, Medical College Kolkata, Blood Bank from October 1, 2015 to March 31, 2016. A set of 3cc ethylenediaminetetraacetic acid and clotted blood samples of the patients were received according to sample acceptance criteria. Blood grouping by conventional tube technique followed by crossmatching was performed by column agglutination technology (CAT) in polyspecific (IgG + C3d) gel media. Any positive result was rechecked in duplicate with additional two group-specific donor units. The persistent incompatibility was further evaluated using direct anti-human globulin test, auto control, antibody screening, and antibody identification by CAT.
Results: On the evaluation of 14,387 sets of patients' sample, only 100 were found to be incompatible (0.69%). Incompatibility rate is higher in females (59%). Eighty-five of these patients were repeatedly transfused. Only 38% of incompatible crossmatch were positive on indirect anti-human globulin test/antibody screening. Antibody could be identified in 16 of them. Seventeen of 100 incompatible samples (17%) presented with panagglutination, were managed with Rh, Kell phenotype/best-matched red cell units. In these 16 patients, 23 alloantibodies were identified; allo anti-E was the most common.
Conclusion: This study showed antibody against the Rh system as the most common cause of incompatibility
Electrochemical Oxygen Evolution Catalyzed by Zn<sub>0.76</sub>Co<sub>0.24</sub>S‑Enriched ZnCo<sub>2</sub>S<sub>4</sub>/ZnCr<sub>2</sub>O<sub>4</sub> Nanostructures
Finding a suitable replacement for
expensive and scarce
precious
metal electrocatalysts for the oxygen evolution reaction (OER) remains
a challenging task. There is a need to research highly efficient and
long-lasting catalysts based on transition metals that are readily
available on Earth for electrochemical oxygen evolution. In this study,
zinc cobalt sulfide (ZnCo2S4) was derived by
hydrothermal treatment of metal salt precursors and thioacetamide,
followed by calcination at 700 °C for ZnCr2O4 to create
a ZnCo2S4/ZnCr2O4 composite
nanostructure enriched with Zn0.76Co0.24S. The
electrochemical performance of the composition-dependent ZnCo2S4/ZnCr2O4 nanostructure
enriched with Zn0.76Co0.24S was then tested
along with its constituents, and it was found that the OER activity
is not linearly proportional to the composition. We also evaluated
the OER activity at pH 7.0 in a neutral medium and the OER electrochemical
performance in an alkaline medium. Zn–Co–S is preferable
to Zn- and Cr-based thio-spinel as it increases electronic conductivity
and decreases charge transfer resistance. Both of these properties
are necessary for generating the high oxidative valency of Co species
during the OER process. The material’s unique composition and
remarkable stability make it highly desirable for future research
in this field
Intrinsic Specific Activity Enhancement for Bifunctional Electrocatalytic Activity toward Oxygen and Hydrogen Evolution Reactions via Structural Modification of Nickel Organophosphonates
A comprehensive
knowledge of the structure–activity relationship
of the framework material is decisive to develop efficient multifunctional
electrocatalysts. In this regard, two different metal organophosphonate
compounds, [Ni(Hhedp)2]·4H2O (I) and [Ni3(H3hedp)2(C4H4N2)3]·6H2O (II) have been isolated through one-pot hydrothermal strategy
by using H4hedp (1-hydroxyethane 1,1-diphosphonic acid)
and N-donor auxiliary ligand (pyrazine; C4H4N2). The structures of synthesized materials have been
established through single-crystal X-ray diffraction studies, which
confirm that compound I formed a one-dimensional molecular
chain structure, while compound II exhibited a three-dimensional
extended structure. Further, the crystalline materials have participated
as efficient electrocatalysts for the oxygen evolution and hydrogen
evolution reactions (OER and HER) as compared to the state-of-the-art
electrocatalyst RuO2. The electrocatalytic OER and HER
performances show that compound II displayed better electrocatalytic
performances toward OER (η10 = 305 mV) and HER (η10 = 230 mV) in alkaline (1 M KOH) and acidic (0.5 M H2SO4) media, respectively. Substantially, the specific
activity has been assessed in order to measure the inherent electrocatalytic
activity of the title electrocatalyst, which displays an enrichment
of fourfold higher activity of compound II (0.64 mA/cm2) than compound I (0.16 mA/cm2) for
the OER experiments. Remarkably, inclusion of an auxiliary pyrazine
ligand into the metal organophosphonate structure (compound II) not only offers higher dimensionality along with significant
enhancement of the overall bifunctional electrocatalytic performances
but also improves the long-term stability, which is noteworthy for
the family of hybrid framework materials
Europium Molybdate/Molybdenum Disulfide Nanostructures with Efficient Electrocatalytic Activity for the Hydrogen Evolution Reaction
The design of hybrid nanostructures of molybdenum disulfide
(MoS2) has been extensively explored as potent electrocatalysts
for hydrogen generation reactions. Here, we report the in situ synthesis
of a nanocomposite containing europium molybdate [Eu2(MoO4)3] and molybdenum disulfide (MoS2)
for an enhanced electrochemical hydrogen evolution reaction (HER).
The characteristic X-ray diffraction (XRD) peaks of both 2H–MoS2 and α-Eu2(MoO4)3 confirm
the formation of the nanocomposite. The nanoflower (NF) architecture
of MoS2 coupled with flakes of europium molybdate is observed
in the transmission electron microscopy (TEM) and scanning electron
microscopy (SEM) images, which lead to an enhanced surface area of
the nanocomposite. Raman and X-ray photoelectron spectroscopy (XPS)
studies reveal a variation in the layer thickness of MoS2 and a significant interfacial electronic interaction between Eu2(MoO4)3 and MoS2. As evident
from the small onset potential of −0.05 V vs reversible hydrogen
electrode (RHE) and a lower overpotential value of 186 mV (at a current
density of 10 mA/cm2), the nanocomposite outperforms pristine
MoS2 nanoflowers in terms of electrocatalytic HER. The
charge-transfer resistance of the nanocomposite (80.02 Ω) is
significantly low compared to pristine MoS2 (158.37 Ω),
thus confirming the enhanced interfacial charge transfer. The Tafel
slope value of the nanocomposite (189 mV/dec) is notably less than
that of pristine MoS2 (313 mV/dec), indicating the enhanced
HER activity of the nanocomposite. The fabrication of lanthanide-containing
MoS2 nanocomposites appears to be promising for an efficient
electrocatalytic activity for the hydrogen evolution reaction
Neem leaf glycoprotein prevents post-surgical sarcoma recurrence in Swiss mice by differentially regulating cytotoxic T and myeloid-derived suppressor cells
<div><p>Post-surgical tumor recurrence is a common problem in cancer treatment. In the present study, the role of neem leaf glycoprotein (NLGP), a novel immunomodulator, in prevention of post-surgical recurrence of solid sarcoma was examined. Data suggest that NLGP prevents tumor recurrence after surgical removal of sarcoma in Swiss mice and increases their tumor-free survival time. In NLGP-treated tumor-free mice, increased cytotoxic CD8<sup>+</sup> T cells and a decreased population of suppressor cells, especially myeloid-derived suppressor cells (MDSCs) was observed. NLGP-treated CD8<sup>+</sup> T cells showed greater cytotoxicity towards tumor-derived MDSCs and supernatants from the same CD8<sup>+</sup> T cell culture caused upregulation of FasR and downregulation of cFLIP in MDSCs. To elucidate the role of CD8<sup>+</sup> T cells, specifically in association with the downregulation in MDSCs, CD8<sup>+</sup> T cells were depleted <i>in vivo</i> before NLGP immunization in surgically tumor removed mice and tumor recurrence was noted. These mice also exhibited increased MDSCs along with decreased levels of Caspase 3, Caspase 8 and increased cFLIP expression. In conclusion, it can be stated that NLGP, by activating CD8<sup>+</sup> T cells, down regulates the proportion of MDSCs. Accordingly, suppressive effects of MDSCs on CD8<sup>+</sup> T cells are minimized and optimum immune surveillance in tumor hosts is maintained to eliminate the residual tumor mass appearing during recurrence.</p></div
CD8<sup>+</sup> T cells downregulate MDSCs in Fas dependent pathway.
<p>(A) Percentage of Annexin V-PI<sup>+</sup> MDSCs within the blood of PBS, NLGP, CD8<sup>+</sup> T cell depleted NLGP immunized mice (n = 6). (B) Flow cytometric assessment of Gr1<sup>+</sup>FasR<sup>+</sup> MDSCs in post-surgery PBS-, NLGP-treated mice with or without CD8<sup>+</sup> T cell depletion. (C) Expression of FasL within CD8<sup>+</sup> T cells in mice with tumor surgery in PBS and NLGP immunized mice. (D) Flow cytometric assessment of Caspase 3 within Gr1<sup>+</sup> MDSCs in PBS, NLGP and CD8 depleted NLGP immunized mice. (E) Protein level expression of Caspase 3, Caspase 8 and cFLIP within MDSCs from PBS, NLGP and CD8 depleted NLGP immunized surgically tumor removed mice. (n = 6, in each group). (F) Experimental design with MDSCs and CD8<sup>+</sup> T cells. (G1) Expression of FasL within NLGP-treated CD8<sup>+</sup> T cells. (G2) Expression of cFLIP and FasR within MDSCs in the presence and absence of supernatants from NLGP-treated CD8<sup>+</sup> T cells, with or without IFNγ neutralization. (H) Assessment of the cytotoxic potential of NLGP-treated CD8<sup>+</sup> T cells towards tumor-derived MDSCs, in the presence of Brefeldin A and Concanamycin A. (**<i>p</i><0.001,*<i>p</i><0.01). (n = 3, in each group). Bar diagrams along with representative figures are present in each case (A-C).</p
Recurrent tumor growth and survival of Swiss mice with post-surgery NLGP treatment.
<p>(A) Experimental design showing sarcoma inoculation, NLGP treatment and blood collection. (B) Recurrent tumor growth curve in pre- and post-surgery phases of mice with or without NLGP treatment (n = 9). (C) Representative photographs of tumor free and tumor bearing mice in the NLGP and PBS groups, respectively, in the post-surgical period. (D) Survival of mice undergoing surgery followed by NLGP treatment (n = 9) (**<i>p</i><0.001).</p
Primer list<sup>*</sup>.
<p>Primer list<sup><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0175540#t001fn001" target="_blank">*</a></sup>.</p
CD8<sup>+</sup> T cells play an important role in NLGP mediated prevention of tumor recurrence.
<p>(A1) Status of CD8<sup>+</sup> T cells in PBS and NLGP immunized mice after tumor inoculation (n = 9). (B1) Percent positive CD8<sup>+</sup> T cells in PBS and NLGP immunized mice after surgery (n = 9). A representative figure in both cases is shown in right upper corner panel (A2, B2). (C) Expression of CD69 on CD8<sup>+</sup> T cells in post-surgical PBS- and NLGP-treated mice (n = 9). (D) Flow cytometric analysis of Granzyme B on CD8<sup>+</sup> T cells in post-surgical PBS- and NLGP-treated mice (n = 9). Bar diagrams along with representative figures in right panel are shown (C,D). (E) Experimental design showing sarcoma inoculation, CD8<sup>+</sup> T cell depletion, NLGP immunization and blood collection. (F) Circulating CD8<sup>+</sup> T cell status following <i>in vivo</i> depletion of same cells. (G) Table showing number of recurrent tumor bearing and tumor free mice. (H) Tumor growth curve of recurrent tumor bearing mice in CD8<sup>+</sup> T cell depleted NLGP immunized mice (n = 6). (I) Survivability curve in NLGP-treated post-surgery mice with or without CD8<sup>+</sup> T cell depletion (n = 6). (J) RT-PCR analysis of the expression of IFNγ, Perforin and Granzyme B gene expression profile in partial CD8<sup>+</sup> T cell depleted post-surgery NLGP-treated mice. The bar diagram represents the mean ± SD of three individual observations from each group at each time point (**<i>p</i><0.001,*<i>p</i><0.01).</p