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1
Couture, Réjean, Pierre Picard, Philippe Poulat, and Alexandre Prat. "Characterization of the tachykinin receptors involved in spinal and supraspinal cardiovascular regulation." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 892–902. http://dx.doi.org/10.1139/y95-123.
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The pharmacological characterization of the tachykinin receptors involved in spinal and supraspinal cardiovascular regulation is reviewed in this report. In conscious rats, substance P (SP), neurokinin A (NKA), neurokinin B (NKB), neuropeptide K (NPK), and neuropeptide γ (NPγ) were injected either intrathecally (i.t.) or intracerebroventricularly (i.c.v.), and their effects were assessed on mean arterial blood pressure (MAP) and heart rate (HR). Moreover, selective antagonists for NK1 ((±)-CP-96345 and RP-67580), NK2 (SR-48968), and NK3 (R-486) receptors were tested against the agonists. I.t. tachykinins elicited dose-dependent increases in MAP and HR (NPK > NPγ > SP > NKA > NKB). The cardiovascular response to i.t. SP, NPK, and NPγ was significantly attenuated by the prior i.t. administration of (±)-CP-96345 and RP-67580 but not by SR-48968 and R-486. By the i.c.v. route, tachykinins also elicited pressor and tachycardiac responses dose dependently (NPK > NPγ > SP > NKA > NKB). Senktide and [MePhe7]NKB, two NK3-selective agonists, were slightly more potent than NKB on both parameters. Whereas the cardiovascular response to NPK was largely blocked by (±)-CP-96345 and RP-67580, that to SP was reduced by 40–50%. This treatment had no effect on the cardiovascular response to NKA and [MePhe7]NKB. Conversely, SR-48968 reduced by 40–50% the NKA-induced cardiovascular changes without affecting the central mediated effects of NPK, SP, and [MePhe7]NKB. However, when coadministered, RP-67580 and SR-48968 abolished the effects to SP and NKA while leaving untouched those induced by [MePhe7]NKB. Finally, the central effects mediated by [MePhe7]NKB, senktide, and NKB were blocked by R-486. These findings suggest that the i.t. action of tachykinins on the rat cardiovascular system is mediated by a NK1 receptor in the spinal cord, while NK1, NK2, and NK3 receptors are likely involved in the supraspinal (hypothalamus) effects of these neuropeptides. It is also concluded that NPK is a pure and powerful NK1 agonist, in contrast to SP and NKA, which are not selective for NK1 or NK2 receptors, respectively.Key words: tachykinins, spinal cord, central cardiovascular control, tachykinin receptor antagonists.
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Phương, Đỗ Thị Mỹ. "Người kể chuyện trong truyện truyền kì trung đại Việt Nam". Tạp chí Khoa học 15, № 2 (2019): 25. http://dx.doi.org/10.54607/hcmue.js.15.2.153(2018).
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Bài viết tìm hiểu sự vận động của truyện truyền kì trung đại Việt Nam thông qua các mẫu hình người kể chuyện (NKC). Từ NKC - nhân vật đến NKC - nhân chứng, từ NKC toàn tri không giới hạn đến NKC toàn tri hạn định, từ NKC ẩn danh, giấu mặt đến NKC bộc lộ xúc cảm là những biến chuyển rõ nét trong mô thức trần thuật của truyện truyền kì từ giữa thế kỉ XVIII trở về trước và truyện truyền kì từ giữa thế kỉ XVIII trở về sau.
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Gimeno, Lourdes, Helios Martínez-Banaclocha, M. Bernardo, et al. "NKG2D Polymorphism in Melanoma Patients from Southeastern Spain." Cancers 11, no. 4 (2019): 438. http://dx.doi.org/10.3390/cancers11040438.
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Background: Natural killer (NK) and CD8+ T cells are involved in the immune response against melanoma. C-Type lectin-like NK cell receptors are located in the Natural Killer Complex (NKC) region 12p13.2-p12.3 and play a critical role in regulating the activity of NK and CD8+ T cells. An association between polymorphisms in the NKC region, including the NKG2D gene and NKG2A promoter, and the risk of cancer has been previously described. The aim of this study was to analyze the association of polymorphisms in the NKC region with cutaneous melanoma in patients from southeastern Spain. Methods: Seven single-nucleotide polymorphisms (SNPs) in the NKG2D gene (NKC3,4,7,9,10,11,12), and one SNP in the NKG2A promoter (NKC17) were genotyped by a TaqMan 5′ Nuclease Assay in 233 melanoma patients and 200 matched healthy controls. Results: A linkage disequilibrium analysis of the SNPs performed in the NKC region revealed two blocks of haplotypes (Hb-1 and Hb-2) with 14 and seven different haplotype subtypes, respectively. The third most frequent haplotype from the block Hb-2—NK3 (CAT haplotype)—was significantly more frequent on melanoma patients than on healthy controls (p = 0.00009, Pc = 0.0006). No further associations were found when NKC SNPs were considered independently. Conclusions: Our results suggest an association between NKG2D polymorphisms and the risk of cutaneous malignant melanoma.
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Hansen, Diana S., Krystal J. Evans, Marthe C. D'Ombrain, et al. "The Natural Killer Complex Regulates Severe Malarial Pathogenesis and Influences Acquired Immune Responses to Plasmodium berghei ANKA." Infection and Immunity 73, no. 4 (2005): 2288–97. http://dx.doi.org/10.1128/iai.73.4.2288-2297.2005.
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ABSTRACT The natural killer complex (NKC) is a genetic region of highly linked genes encoding several receptors involved in the control of NK cell function. The NKC is highly polymorphic, and allelic variability of various NKC loci has been demonstrated in inbred mice. Making use of BALB.B6-Cmv1r congenic mice, in which the NKC from disease-susceptible C57BL/6 mice has been introduced into the disease-resistant BALB/c background, we show here that during murine malaria infection, the NKC regulates a range of pathophysiological syndromes such as cerebral malaria, pulmonary edema, and severe anemia, which contribute to morbidity and mortality in human malaria. Parasitemia levels were not affected by the NKC genotype, indicating that control of malarial fatalities by the NKC cells does not operate through effects on parasite growth rate. Parasite-specific antibody responses and the proinflammatory gene transcription profile, as well as the TH1/TH2 balance, also appeared to be influenced by NKC genotype, providing evidence that this region, known to control innate immune responses via NK and/or NK T-cell activation, can also significantly regulate acquired immunity to infection. To date, NKC-encoded innate system receptors have been shown mainly to regulate viral infections. Our data provide evidence for critical NKC involvement in the broad immunological responses to a protozoan parasite.
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Hwang, Young Eun, Seonghun Im, Ju Hyun Cho, et al. "Semi-Biosynthetic Production of Surface-Binding Adhesive Antimicrobial Peptides Using Intein-Mediated Protein Ligation." International Journal of Molecular Sciences 23, no. 23 (2022): 15202. http://dx.doi.org/10.3390/ijms232315202.
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Microbial infections remain a global health concern, calling for the urgent need to implement effective prevention measures. Antimicrobial peptides (AMPs) have been extensively studied as potential antimicrobial coating agents. However, an efficient and economical method for AMP production is lacking. Here, we synthesized the direct coating adhesive AMP, NKC-DOPA5, composed of NKC, a potent AMP, and repeats of the adhesive amino acid 3,4-dihydroxyphenylalanine (DOPA) via an intein-mediated protein ligation strategy. NKC was expressed as a soluble fusion protein His-NKC-GyrA (HNG) in Escherichia coli, comprising an N-terminal 6× His-tag and a C-terminal Mxe GyrA intein. The HNG protein was efficiently produced in a 500-L fermenter, with a titer of 1.63 g/L. The NKC-thioester was released from the purified HNG fusion protein by thiol attack and subsequently ligated with chemically synthesized Cys-DOPA5. The ligated peptide His-NKC-Cys-DOPA5 was obtained at a yield of 88.7%. The purified His-NKC-Cys-DOPA5 possessed surface-binding and antimicrobial properties identical to those of the peptide obtained via solid-phase peptide synthesis. His-NKC-Cys-DOPA5 can be applied as a practical and functional antimicrobial coating to various materials, such as medical devices and home appliances.
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Maneechot, Sutjai, та Nisa Netinatsunton. "ความพึงพอใจของผู้รับบริการต่อการให้บริการการส่องกล้องของสถาบันโรคระบบทางเดินอาหารและตับ นันทนา-เกรียงไกร โชติวัฒนะพันธุ์ (NKC) โรงพยาบาลสงขลานครินทร์". PSU Medical Journal 5, № 1 (2025): 11–19. https://doi.org/10.31584/psumj.2025272974.
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การวิจัยนี้มีวัตถุประสงค์เพื่อศึกษา 1) ระดับความพึงพอใจของผู้รับบริการต่อบริการการส่องกล้องของสถาบัน NKC 2) ปัจจัยที่มีความสัมพันธ์กับความพึงพอใจของผู้รับบริการ วิธีการเก็บข้อมูลโดยใช้แบบสอบถามผ่าน QR Code คัดเลือกกลุ่มตัวอย่างแบบเจาะจง (Purposive sampling) คือผู้ป่วยที่มารับบริการการส่องกล้อง ระยะเวลา 4 เดือน (1 มกราคม - 30 พฤษภาคม 2567) มาตราส่วนความพึงพอใจ แบ่งเป็น 5 ระดับ น้อยที่สุดไปมากที่สุด ผลการวิจัยพบว่า กลุ่มตัวอย่างจำนวน 1,177 คน เป็นเพศชาย ร้อยละ 38.5 และเพศหญิง ร้อยละ 61.5 โดยมีอายุเฉลี่ย = 47 ปี และ S.D.=13.91 ระดับความพึงพอใจของผู้รับบริการในภาพรวมต่อการให้บริการการส่องกล้องของสถาบัน NKC ร้อยละ 97.3 ความพึงพอใจของผู้รับบริการอยู่ในระดับมากที่สุดในทุกหัวข้อ ผู้รับบริการพึงพอใจต่อ ขั้นตอนการบริการเข้าใจง่าย ไม่ยุ่งยาก ซับซ้อนร้อยละ 97.2 ต่อการให้บริการของ บุคลากรที่ให้บริการร้อยละ 98.4 ต่อความสะอาดของสถานที่ให้บริการโดยรวม ร้อยละ 98.5 และปัจจัยที่มีความสัมพันธ์กับความพึงพอใจ โดยคะแนนเฉลี่ยความพึงพอใจสูงสุดอยู่ในกลุ่ม อายุมากกว่า 60 ปี รองลงมาคือ กลุ่มอายุ 31 - 40 ปี ผู้ที่มีความพึงพอใจสูงมีโอกาสจะแนะนำญาติ หรือคนรู้จักมาใช้บริการที่สถาบัน NKC ร้อยละ 95.2 สรุป ระดับความพึงพอใจของผู้รับบริการต่อการให้บริการการส่องกล้องของสถาบัน NKC อยู่ในระดับมากที่สุด ในทุกหัวข้อ และผู้รับบริการส่วนใหญ่จะแนะนำให้ญาติหรือคนที่รู้จักมาใช้บริการ ปัจจัยที่มีความสัมพันธ์กับระดับความพึงพอใจคือกลุ่มอายุ
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Medel, Maria L. H., Gabriela G. Reyes, Luz M. Porras, et al. "Prolactin Induces IL-2 Associated TRAIL Expression on Natural Killer Cells from Chronic Hepatitis C PatientsIn vivoandIn vitro." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 7 (2019): 975–84. http://dx.doi.org/10.2174/1871530319666181206125545.
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Background:Natural killer cells (NKC) are a major component of the innate immune response to HCV, mediating their effects through TRAIL and IFN-γ. However, their function is diminished in chronic HCV patients (HCVp). Prolactin is an immunomodulatory hormone capable of activating NKC.Objective:The study aims to explore if hyperprolactinemia can activate NKC in HCVp.Methods:We treated twelve chronic HCVp (confidence level =95%, power =80%) for 15 days with Levosulpiride plus Cimetidine to induce mild hyperprolactinemia. Before and after treatment, we determined TRAIL and NKG2D expression on peripheral blood NKC, along with cytokine profiles, viral loads and liver function. We also evaluated in vitro effects of prolactin and/or IL-2 on NKC TRAIL or NKG2D expression and IFN-γ levels on cultured blood mononuclear cells from 8 HCVp and 7 healthy controls.Results:The treatment induced mild hyperprolactinemia and increased TRAIL expression on NKC as well as the secretion of IL-1ra, IL-2, PDGF and IFN-γ. Viral loads decreased in six HCVp. IL-2 and TRAIL together explained the viral load decrease. In vitro, prolactin plus IL-2 synergized to increase TRAIL and NKG2D expression on NKC from HCVp but not in controls.Conclusion:Levosulpiride/Cimetidine treatment induced mild hyperprolactinaemia that was associated with NKC activation and Th1-type cytokine profile. Also, an increase in TRAIL and IL-2 was associated with viral load decrease. This treatment could potentially be used to reactivate NKC in HCVp.
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Dons’koi, Boris, Oksana Onyshchuk, Iryna Kononenko, et al. "Accentuated Peripheral Blood NK Cytotoxicity Forms an Unfavorable Background for Embryo Implantation and Gestation." Diagnostics 12, no. 4 (2022): 908. http://dx.doi.org/10.3390/diagnostics12040908.
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Problem Many studies have demonstrated the negative impact of high rates of NK cytotoxicity (NKc) on reproductive processes, but there is no agreement as to the appropriateness and feasibility of using the NKc for routine diagnostic in IVF patients. This study conducted a retrospective analysis of embryo transfer (ET) success rates and live birth rates (LBR) in patients with different NKc values. Method of study 1854 cycles of ET were selected and divided into three groups according to NKc levels, and randomized by anamnesis and age: normal (nNKc, n = 871), elevated (eNKc, n = 759), and reduced NKc (rNKc, n = 123). ET with donors’ embryos (n = 101) were analyzed separately. NKc-to-K562 was measured in PBMC (peripheral blood mononuclear cells) by flow cytometry before ET. The patients did not obtain any additional treatments. Results Patients with eNKc, in addition to having reduced clinical pregnancy rates (OR1.59, p < 0.0001), had increased levels of subsequent pregnancy failures (OR2.545, p < 0.0001) when compared to nNKc patients. As a result, patients with eNKc had almost half the LBR than patients with nNKc (OR2.2, p < 0.0001). In patients with rNKc, LBR was also lowered. eNKc was equally unfavorable for implantation and delivery in cryo- or fresh cycles. Markedly, eNKc was much more unfavorable for reproduction than slightly elevated NKc. The donor’s embryos were implanted irrespective of the recipient’s NKc levels, but the later stages of pregnancy were worse in patients with eNKc. Conclusions Our findings highlighted the negative impact of high levels of NK cytotoxicity on pregnancy outcomes.
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Syamsiro, Mochamad, Nurcaya Putra Anwar, Siti Rochmah Ika, Agus Mulyono, Feri Febria Laksana, and Fadmi Rina. "Rancang Bangun dan Uji Eksperimental Performa Burner Biomassa Berbahan Bakar Limbah Nyamplung (Calophyllum Inophyllum) dan Pelet Kayu." JURNAL SAINS TEKNOLOGI & LINGKUNGAN 11, no. 1 (2025): 1–12. https://doi.org/10.29303/jstl.v11i1.702.
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As a tropical country, Indonesia has abundant biomass potential because plants grow all year. Among the several types of biomass, nyamplung kernel cake (NKC) has a high potential for use as an energy source. The goal of this research was to develop a biomass burner and evaluate its performance using NKC and wood pellets (WP) as comparisons. The burner performance test is designed to investigate the effect of air mass flow rate on combustion flame, heat release rate, and thermal efficiency for both types of biomass. The thermal efficiency of the burner was calculated using the water boiling test (WBT). The results revealed that using NKC resulted in a longer combustion flame at air flow rates of 146 and 219 g/s. The higher the air flow rate, the longer the flame. The combustion of NKC and WP produced the longest flame, measuring 80 cm with an air mass flow rate of 290 g/s. The experiment also demonstrated that WP produced a higher temperature than NKC. The highest combustion temperature was produced by WP, reaching 818.1°C with an air mass flow rate of 290 g/s. From the two types of biomass evaluated, WP combustion produced more heat than NKC. The highest heat release rate of 35.46 kW was achieved with an air mass flow rate of 290 g/s. The burning of NKC resulted in the maximum thermal efficiency, 30.35% at an air mass flow rate of 219 g/.
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Ellis, James L. "Neurokinin receptors subserving bronchoconstriction." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 923–26. http://dx.doi.org/10.1139/y95-127.
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Tachykinin receptor subtypes were initially defined using agonist potency ratios for the endogenous ligands substance P (SP), neurokinin (NK) A, and NKB. On this basis it was suggested that there are three tachykinin receptor subtypes. These subtypes were designated NK1, NK2, and NK3, where SP is most potent at NK1 receptors, NKA is most potent at NK2 receptors, and NKB is most potent at NK3 receptors. Recently analogs of the endogenous ligands that show greater selectivity (about 1000-fold) for the different receptor subtypes have been developed. In addition selective antagonists, which are either nonpeptides or modified peptides, for the receptor subtypes have been developed. This minireview concentrates on the wealth of new knowledge concerning the tachykinin receptor subtypes subserving bronchoconstriction in several mammalian species, including man, provided by the use of these selective agonists and antagonists.Key words: neurokinins, bronchoconstriction, substance P, neurokinin A, receptor subtypes.
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Goicoa, Maria Aranzazu, I. J. Ballart, M. Fernanda Palacios, et al. "Effect of Indomethacin and Thymostimulin on Natural Killer Activity of Thalassemic Patients and Normal Subjects." International Journal of Immunopathology and Pharmacology 5, no. 1 (1992): 23–30. http://dx.doi.org/10.1177/039463209200500103.
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To evaluate whether indomethacin (IM) and thymostimulin (TP-1) could revert the alterations of natural killer cytotoxicity (NKC) observed in patients and carriers of Thalassemia Major (TM), 14 TM patients, 10 TM carriers, 16 normal controls, and 4 polytransfused patients were studied. In vitro, IM induced an increase in NKC of normal controls and TM carriers (Δ CI: + 5.98±2.49 and + 9.77±6.82 respectively), but not in TM patients (-0.32±1.45) or other polytransfused recipients. The addition of IM to Concanavalin A (Con A) also resulted in an increase of NKC in normal controls and TM carriers, similar to that induced by each substance separately in normal controls, or by IM alone in TM carriers. Similarly, TP-1 (50 μg/ml) induced increases of NKC in normal subjects (+ 4.66±3.62), but not in TM patients (-1.1±2.43). The impairment in NKC observed in TM and polytransfused patients, and the absence of response to Con A in both, TM patients and carriers, do not seem to be mediated by an excessive production of prostaglandins. The lack of response not only to Con A, but also to TP-1 could indicate a quantitative or qualitative defect in T cells, that affects NKC regulation, or a deficient response of NK cells to modulators produced by T lymphocytes.
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Nakazawa, Tsutomu, Takayuki Morimoto, Ryosuke Maeoka, et al. "Characterization of CISH-knockout NK cells derived from human peripheral blood and evaluated the antitumor effects in allogeneic glioblastoma." Journal of Immunology 212, no. 1_Supplement (2024): 0739_6154. http://dx.doi.org/10.4049/jimmunol.212.supp.0739.6154.
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Abstract Background: Glioblastoma (GBM) is the most common malignant brain tumor. Allogeneic natural killer cells (NKCs) have gained considerable attention as promising immunotherapeutic tools against cancer, where gene-edited NKCs would result in effective anti-cancer treatment. This study focused on the immune checkpoint molecule cytokine-inducible SH2-containing protein (CISH) as a critical negative regulator in NKCs. Methods: We generated human primary CISH-deleted NKCs (NKC dCISH) by combining our specific NKC expansion method and CRISPR/Cas9. The genome-edited NKCs underwent microarray analysis. The anti-GBM activity of the genome-edited NKCs was evaluated in vitro and further detected in vivo antitumor effects using xenograft brain tumor mice. Results: We successfully induced NKC dCISH derived from human peripheral blood. Gene set enrichment analysis (GSEA) using microarrays revealed that the enriched genes were involved in effector functions in NKC dCISH. CISH deletion enhanced NKC-mediated apoptosis induction against allogeneic GBM cells and spheroids. Intracranial administration of the allogeneic CISH-deleted NKCs prolonged the overall survival of xenograft brain tumor mice. Conclusion: CISH deletion enhanced NKCs' effector functions and NKC-mediated antitumor effects in allogeneic GBM. The genome-editing NKCs could be a promising immunotherapeutic alternative for patients with GBM.
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Savitz, Jonathan, Chibing Tan, Ashlee Taylor, Wayne Drevets, and Kent Teague. "Abnormalities in regulatory T cells and natural killer cells in major depressive disorder (P3127)." Journal of Immunology 190, no. 1_Supplement (2013): 43.25. http://dx.doi.org/10.4049/jimmunol.190.supp.43.25.
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Abstract Major depressive disorder (MDD) is associated with increased levels of acute phase proteins, pro-inflammatory cytokines, and monocytosis, indicative of immune activation. However, in apparent contrast to evidence of depression-associated inflammation, a reduction in natural killer cell (NKC) activity is also a well-replicated finding, leading to the hypothesis that MDD is an “immunosuppressive” disorder. Here used FACS analysis to identify key subtypes of T cells and NKC in 36 healthy controls (HC) and 34 physically healthy, unmedicated patients with MDD matched for age and body mass index. After controlling for group differences in gender, we found a greater percentage of monocytes and Treg cells (relative to total live cells) in the MDD group. In addition, there was a smaller percentage of putative regulatory NKC (CD56+CD16-) but not cytotoxic NKC (CD56+CD16+) or NK T-cells (NKT) in the MDD patients. In wild-type mice, a microglia-driven, T cell-dependent protective response has been shown to be restricted by Treg cells, raising the possibility that the elevation of Treg cells in the MDD group may impair the resolution of acute pathophysiological changes leading to chronic inflammation. The depression-associated reduction in putative regulatory NKC but not effector NKC favors the hypothesis that MDD is associated with inflammation rather than immunosuppression.
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Edwards, B. S., R. R. Hoffman, and M. S. Curry. "Calcium mobilization-associated and independent cytosolic acidification elicited in tandem with Na+/H+ exchanger activation in target cell-adherent human NK cells." Journal of Immunology 150, no. 11 (1993): 4766–76. http://dx.doi.org/10.4049/jimmunol.150.11.4766.
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Abstract Flow cytometry was used to identify mechanisms by which human NK cells regulate intracellular pH (pHi) and to investigate the relationship between NK cell pHi and cytolytic function. Temporally resolved determinations of pHi were simultaneously made in NK cells that formed conjugates with target cells (NKC) and unconjugated NK cells (NKU) on the basis of the red/orange fluorescence emission ratio of the pH indicator seminapthylrhodafluor-1. Two pHi regulatory mechanisms were identified in NK cells: 1) a HCO3-/Cl- antiport that promoted pHi changes in response to variation of extracellular HCO3- and Cl- but not Na+ ion concentrations, was sensitive to stilbene derivatives 4,4'-diisothiocyanatostilbene sulfonic acid and 4-acetamido-4'-isothyocyanotostilbene-2-2'-disulfonic acid, and exhibited similar activity in NKC and NKU, and 2) a Na+/H+ exchanger that promoted pHi changes in response to extracellular Na+ ion concentration changes and was sensitive to dimethylamiloride (DMA), permeable to Na+ and Li+ but not K+ or N-methyl-D-glucamine, and quiescent in NKU but activated in target cell-adherent NKC. When Na+/H+ exchange was blocked with 10 microM DMA, the pHi of NKC bound to NK-sensitive K562 target cells progressively decreased for 3 to 4 min, then stabilized at 0.1 to 0.15 pH units below the pHi of NKU. A significant temporal decline in NKC pHi also occurred in the nominal absence of extracellular Ca2+ (0.07 +/- 0.02 pH units) and when NKC formed conjugates with NK-resistant B lymphoblastoid target cells that failed to mobilize NK cell Ca2+ (0.07 +/- 0.01 pH units) (mean +/- SD). However, the magnitude of the NKC cytosolic acidification response was consistently reduced (42 +/- 4 and 44 +/- 6%, respectively) under these Ca2+ flux response-limiting conditions. Thus, adhesion to target cells triggered two pHi-related responses in NK cells: 1) a decline in pHi which exhibited both Ca2+ mobilization-dependent and -independent components, and 2) Na+/H+ exchanger activation by which acid production was neutralized. Manipulations of HCO3- and DMA that clamped NKC pHi at values ranging from 6.8 to 7.2 failed to significantly influence NK cell cytolytic function. By contrast, isosmotic replacement of extracellular Na+ with NMDG resulted in a 57 +/- 22% inhibition of NK cell-mediated cytolysis (n = 8, p &lt; 0.01). NKC pHi declined to 6.8 to 6.9 under these conditions, but this was not the apparent basis of impaired cytolysis because sustained elevation of NKC pHi by addition of dimethylamine failed to significantly reverse inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)
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Daniel, E. E., M. B. Parrish, E. G. Watson, J. E. Fox-Threlkeld, D. Regoli, and K. D. Rainsford. "The tachykinin receptors inducing contractile responses of canine ileum circular muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 1 (1995): G161—G170. http://dx.doi.org/10.1152/ajpgi.1995.268.1.g161.
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This study sought to determine which tachykinin receptors were involved in contractile responses of circular muscle to tachykinins infused into isolated segments of canine ileum. Selective agonists for neurokinin receptors NK1 and NK2 as well as for substance P (SP) and neurokinin A (NKA) were infused, and selective antagonists against NK1, NK2, and NK3 receptors were tested. The responses to a submaximal concentration of NKA were reduced by a selective NK2 antagonist, SR-48968, and abolished by a combination of this antagonist with an NK1 antagonist, either CP-96,345 or RP-67580. The selective NK2 agonist, [Nle10]NKA-(4-10), had low potency. We concluded that NKA acted on typical NK2 receptors and that is action was potentiated by its additional action on NK1 receptors. Neither the contractile responses to SP nor those to [Sar9,Met(O2)11]SP given in submaximal concentrations were inhibited by CP-96,345 or RP-67580, either alone or together with SR-48968. Indeed, the two NK1-selective antagonists potentiated responses to the selective NK1 agonist, [Sar9,Met(O2)11]SP, an effect attributed to previously demonstrated prejunctional inhibitory action of the agonist. The selective NK3 agonist, succinyl-[Asp6,N-Me-Phe8]SP-(6-11), was not effective as a contractile agent, even after block of nitric oxide synthase with N omega-nitro-L-arginine. The selective NK3 antagonist, R-487, was also ineffective in blocking responses to SP. Studies with an antagonist to H1 histamine receptors suggested that contractile actions of SP did not involve histamine release from mast cells. We concluded that, in addition to typical NK1 and NK2 receptors activated by NKA and a prejunctional inhibitory receptor activated by SP and [Sar9,Met(O2)11]SP, another tachykinin receptor existed on canine ileum to initiate contractions. It is not a typical NK1, NK2, or NK3 receptor.
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Al-Sharafi, Butheinah A., and Abdallah A. Gunaid. "Effect of Habitual Khat Chewing on Glycemic Control, Body Mass Index, and Age at Diagnosis of Diabetes in Patients with Type 2 Diabetes Mellitus in Yemen." Clinical Medicine Insights: Endocrinology and Diabetes 8 (January 2015): CMED.S26045. http://dx.doi.org/10.4137/cmed.s26045.
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Khat chewing is common in Yemen. We conducted this study to see if it affected diabetes control in patients with type 2 diabetes mellitus (DM). We studied 1540 patients with type 2 DM attending an endocrinology clinic in Sana'a, Yemen, of which 997 were khat chewers (KC) and 543 were non-khat chewers (NKC). The patients answered a questionnaire regarding khat chewing. Hemoglobin A1c (HbA1c) and body mass index (BMI) were measured. KC had a higher mean HbA1c of 9.8 (95% confidence interval (95% CI) 9.6–10) than the NKC, with a mean of 9.1 (95% CI 8.9–9.4) (adjusted odds ratios (AOR) 1.74, P < 0.001) after multivariate regression analysis. KC also had a lower mean BMI, 26.9 (95% CI 26.6–27.2), than the NKC, mean BMI 27.6 (95% CI 27.1–28) ( P < 0.01). The mean age at diagnosis of DM among the KC group was 43.3 (10.1) and among the NKC group was 45.9 (11.8) (AOR 1.4 P < 0.008) after multivariate regression analysis. KC patients had a higher mean HbA1c, a lower BMI, and a younger age at diagnosis of type 2 DM when compared with NKC.
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Brown, Michael G., Jun Zhang, Ying Du, Janis Stoll, Wayne M. Yokoyama, and Anthony A. Scalzo. "Localization on a Physical Map of the NKC-Linked Cmv1 Locus Between Ly49b and the Prp Gene Cluster on Mouse Chromosome 6." Journal of Immunology 163, no. 4 (1999): 1991–99. http://dx.doi.org/10.4049/jimmunol.163.4.1991.
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Abstract The Cmv1 locus controls NK cell-mediated resistance to infection with murine CMV. Our recent genetic analysis of backcross mice demonstrated that the NK gene complex (NKC)-linked Cmv1 locus should reside between the Ly49 and Prp gene clusters on distal mouse chromosome 6. We have aligned yeast artificial chromosome (YAC) inserts in a contig spanning the interval between the Ly49 and Prp gene clusters. This YAC contig includes 13 overlapping YAC inserts that span more than 2 megabases (Mb) in C57BL/6 (B6) mice. Since we have identified genomic clones that span the Ly49-Prp gene region, we hypothesize that at least one should contain the Cmv1 locus. To narrow the Cmv1 critical region, we developed novel NKC genetic markers and used these to genotype informative backcross and intra-NKC recombinant congenic mouse DNA samples. These data suggest that Cmv1 resides on a single YAC insert within an interval that corresponds to a physical distance of ∼390 kb. This high resolution, integrated physical and genetic NKC map will facilitate identification of Cmv1 and other NKC-linked loci that regulate NK cell-mediated immunity.
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Steinle, Alexander, Veronika Stejfova, Sabrina Kuttruff, Birgit Schittek, and Jessica Spreu. "CLEC2A Is a Novel Skin-Specific, Stimulatory Ligand of Human NK Cells (39.8)." Journal of Immunology 182, no. 1_Supplement (2009): 39.8. http://dx.doi.org/10.4049/jimmunol.182.supp.39.8.
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Abstract The Natural Killer Gene Complex (NKC) encodes for numerous C-type lectin-like receptors (CTLR) variably expressed on lymphocytes and myeloid cells. Well-known representatives of NKC-encoded CTLR are NKG2D, CD69, and Ly49 molecules. However, the NKC also contains a considerable number of genes which are barely characterized. Recently, we described the CLEC2A gene encoding for a new member of the human CLEC2 family of NKC-encoded CTLR. CLEC2A, in contrast to other human CLEC2 family members such as CD69/CLEC2C and AICL/CLEC2B, is virtually not expressed by peripheral leukocytes, but its expression appears restricted to skin. We now report that CLEC2A encodes for a non-disulfide-linked, homodimeric surface CTLR which is expressed on freshly isolated skin cells. Addressing a potential immune-associated function, we find that CLEC2A stimulates cytotoxicity and cytokine release of human NK cells. However, we failed to ascertain CLEC2A engagement by known activating NK receptors. Instead, we identified a hitherto undescribed NKC-encoded CTLR (NKp65) that specifically interacts with CLEC2A and activates NK cytotoxicity. In summary, we define CLEC2A as a skin-specific and NK cell-stimulating CTLR engaging NKp65, a novel activating CTLR which may allow for dedicated immunosurveillance of human skin. This work was supported by funds (SFB 685/A1) of the German Research Foundation (DFG).
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Anyanwu, Ebere, Andrew W. Campbell, Joseph Jones, John E. Ehiri, and Akpan I. Akpan. "The Neurological Significance of Abnormal Natural Killer Cell Activity in Chronic Toxigenic Mold Exposures." Scientific World JOURNAL 3 (2003): 1128–37. http://dx.doi.org/10.1100/tsw.2003.98.
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Toxigenic mold activities produce metabolites that are either broad-spectrum antibiotics or mycotoxins that are cytotoxic. Indoor environmental exposure to these toxigenic molds leads to adverse health conditions with the main outcome measure of frequent neuroimmunologic and behavioral consequences. One of the immune system disorders found in patients presenting with toxigenic mold exposure is an abnormal natural killer cell activity. This paper presents an overview of the neurological significance of abnormal natural killer cell (NKC) activity in chronic toxigenic mold exposure. A comprehensive review of the literature was carried out to evaluate and assess the conditions under which the immune system could be dysfunctionally interfered with leading to abnormal NKC activity and the involvement of mycotoxins in these processes. The functions, mechanism, the factors that influence NKC activities, and the roles of mycotoxins in NKCs were cited wherever necessary. The major presentations are headache, general debilitating pains, nose bleeding, fevers with body temperatures up to 40�C (104�F), cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, vertigo/dizziness, and in some cases, seizures. Although sleep is commonly considered a restorative process that is important for the proper functioning of the immune system, it could be disturbed by mycotoxins. Most likely, mycotoxins exert some rigorous effects on the circadian rhythmic processes resulting in sleep deprivation to which an acute and transient increase in NKC activity is observed. Depression, psychological stress, tissue injuries, malignancies, carcinogenesis, chronic fatigue syndrome, and experimental allergic encephalomyelitis could be induced at very low physiological concentrations by mycotoxin-induced NKC activity. In the light of this review, it is concluded that chronic exposures to toxigenic mold could lead to abnormal NKC activity with a wide range of neurological consequences, some of which were headache, general debilitating pains, fever, cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, and seizures.
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Kavinilavan, R., P. Mekala, MJ Raja, M. Arthanari Eswaran, and S. Nagajothi. "Immunomodulatory effect of Nilavembu Kudineer Choornam in backyard chicken." Journal of Phytopharmacology 14, no. 2 (2025): 104–9. https://doi.org/10.31254/phyto.2025.14205.
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Aim and Objective: The study aimed to evaluate the immunomodulatory effects of Nilavembu Kudineer Choornam (NKC) on humoral, cell-mediated, and nonspecific immunity in unsexed backyard chickens. Materials and Methods: Seventy-two unsexed backyard chickens were randomly assigned to six groups (n=12 per group): control, vaccine control (Newcastle disease oral pellet vaccine), positive control (levamisole at 30 mg/kg), and three treatment groups receiving NKC decoction at 0.5, 1.0, and 2.0 mL/kg. All groups, except the control, were vaccinated at the end of the 1st, 4th, and 8th weeks. Levamisole and NKC were administered via drinking water for five days prior to immunological assessments. Humoral immunity was assessed by immunizing the birds with sheep red blood cells at the end of the 11th and 12th weeks, followed by haemagglutination titre measurements at the end of the 13th and 16th weeks. Cell-mediated immunity was evaluated using a delayed hypersensitivity reaction to phytohemagglutinin-P at the 16th week. Nonspecific immunity was assessed via a carbon clearance test at the 16th week. Results: The haemagglutination titres at the 13th week ranged from 5.80 ± 0.49 to 6.60 ± 0.60, and at the 16th week, from 4.50 ± 0.27 to 5.05 ± 0.20. The highest titres were observed in the NKC 1.0 mL/kg group, followed by the levamisole group. For cell-mediated immunity, the delayed hypersensitivity test showed significantly greater skin thickness (0.20 ± 0.01 to 0.34 ± 0.04 mm) in the treatment groups compared to the control. The carbon clearance test demonstrated enhanced phagocytic activity in all treatment groups (0.024 ± 0.001 to 0.013 ± 0.001) relative to controls. Conclusion: Administration of NKC at 1.0 mL/kg for five days before vaccination significantly enhanced humoral, cell-mediated, and nonspecific immune responses, comparable to levamisole. NKC shows potential as a natural immunomodulator in poultry, enhancing immune responses and offering a viable alternative to synthetic immunostimulants.
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Fan, Ying Fang, Shi Yi Zhang, and Surendra P. Shah. "Influence of Nanoclay on Concrete Subjected to Freeze-Thaw Cycles and Bond Behavior between Rebar and Concrete." Key Engineering Materials 711 (September 2016): 256–62. http://dx.doi.org/10.4028/www.scientific.net/kem.711.256.
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This paper explores the effects of nanokaolinite clay (NKC) on the behavior of cement-based materials concrete. The resistance of NKC modified cement-based materials to freezing-thaw cycles and the corrosion processes of rebar embedded in the concrete were investigated. Ordinary Portland cement was partially substituted with NKC in ratios of 0%, 1%, 3%, and 5% by weight. The Rapid Freeze-Thaw Cabinet was used to measure the resistance of ordinary Portland cement concrete and concrete with clay to deterioration caused by repeated cycles of freezing and thawing, compressive strength were measured at regular intervals. The corrosion conditions of the rebar embedded in the concrete were studied by an electrochemical accelerated penetration system, pullout tests were performed to assess the bond properties including bond-slip curve, ultimate bond strength between concrete and rebar before and after corrosion. It is revealed that the introduction of NKC improves the freeze-thaw resistivity values and bond behavior in the concrete specimens compared to the control concrete; the corrosion of the rebar embedded in the concrete is impeded efficiently.
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Lewis, D. E., B. E. Gilbert, and V. Knight. "Influenza virus infection induces functional alterations in peripheral blood lymphocytes." Journal of Immunology 137, no. 12 (1986): 3777–81. http://dx.doi.org/10.4049/jimmunol.137.12.3777.
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Abstract This report describes alterations in functional responses to lectin-induced stimulation of peripheral blood lymphocytes and in the natural killer cell (NKC) activity, of college students, obtained during an outbreak of influenza A/Philippines/2/82(H3N2) virus infection. These results are compared with similar observations in college students with an acute, febrile, noninfluenzal respiratory illness that occurred during the same outbreak. The lymphopenia typical of influenza during acute illness was shown to be due to a reduction in both T and B cells without alteration in the CD4:CD8 ratio. In addition, phytohemagglutinin and concanavalin A responses were reduced and NKC activity was increased, while pokeweed mitogen reactivity was unaltered at the time of admission to the study. Patients with noninfluenzal illness showed early polymorphonuclear leukocytosis and a similar lymphopenia. Lymphocyte functions were virtually unchanged during acute illness in noninfluenza patients. The relatively specific alterations in lymphocyte responses to lectin-induced stimulation in influenza patients may indicate that the peripheral T cells are incapable of activation via the CD3 or CD2 activation pathways. In addition, increased NKC activity in the periphery may be reflective of increased NKC activity in the lung. Influenza-infected individuals with higher NKC activity at the time of admission to the study also took longer to recover. Finally, the early lymphopenia and the later neutropenia in the influenza-infected patient may represent migration of these cells from the circulation to the infected respiratory tract as a consequence of infection.
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Geppetti, P., C. Bertrand, E. Bacci, O. Huber, and J. A. Nadel. "Characterization of tachykinin receptors in ferret trachea by peptide agonists and nonpeptide antagonists." American Journal of Physiology-Lung Cellular and Molecular Physiology 265, no. 2 (1993): L164—L169. http://dx.doi.org/10.1152/ajplung.1993.265.2.l164.
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The tachykinin receptors mediating mucus secretion and smooth muscle contraction were studied in the ferret trachea in vitro. Substance P (SP) and the selective agonist for NK1 receptor ([Sar9,Met(O2)11]SP), but not selective agonists for NK2 ([Ala5,beta-Ala8]neurokinin A-(4–10)) and NK3 ([MePhe7]neurokinin B) receptors, induced secretion of macromolecules in a concentration-dependent fashion. The nonpeptide NK1 receptor antagonist, CP-96,345, but not the nonpeptide NK2 receptor antagonist, SR-48968, inhibited SP-induced secretion. Both neurokinin A (NKA) and [Ala5,beta-Ala8]NKA-(4-10), but not NK1 and NK3 selective agonists, evoked a concentration-dependent smooth muscle contraction. SR-48968, but not CP-96,345, inhibited in a concentration-dependent manner the response to NKA. CP-96,345 and SR-48968 did not affect the concentration-dependent increase in macromolecule secretion or smooth muscle contraction by carbachol. These findings indicate that NK1 receptors mediate secretion of macromolecules and NK2 receptors mediate smooth muscle contraction, in response to tachykinins in the ferret trachea in vitro.
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Brown, Michael G., Anthony A. Scalzo, Laurie R. Stone, et al. "Natural killer gene complex (Nkc) allelic variability in inbred mice: evidence for Nkc haplotypes." Immunogenetics 53, no. 7 (2001): 584–91. http://dx.doi.org/10.1007/s002510100365.
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Gao, Zhongli, and Norton P. Peet. "Recent Advances in Neurokinin Receptor Antagonists." Current Medicinal Chemistry 6, no. 5 (1999): 375–88. http://dx.doi.org/10.2174/0929867306666220320220251.
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The structurally related neuropeptides, substance P (SP), neurokinin A (NKA), and neurokinin B (NKB), which belong to a family of molecules termed tachykinins and are widely distributed in the central and peripheral nervous systems, influence the function of many tissues. SP and NKA have links to the fol)owing chronic diseases: asthma, inflammatory bowel disorders, rheumatoid arthritis, pain and psychiatric disorders. These peptides exert their effects through three G-protein coupled receptor sub types, namely, the NK1, NK2, and NK3 receptors. Non-peptide antagonists of these receptors may provide opportunities for disease treatments. In this review, the very recent advances in nonpeptide neurokinin receptor antagonists will be described with an emphasis on structure-activity relationships which have been developed.
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Dissen, E., J. C. Ryan, W. E. Seaman, and S. Fossum. "An autosomal dominant locus, Nka, mapping to the Ly-49 region of a rat natural killer (NK) gene complex, controls NK cell lysis of allogeneic lymphocytes." Journal of Experimental Medicine 183, no. 5 (1996): 2197–207. http://dx.doi.org/10.1084/jem.183.5.2197.
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Natural Killer (NK) cells can recognize and kill MHC-incompatible normal bone marrow-derived cells. Presently characterized MHC-binding receptors on NK cells, including the Ly-49 family in the mouse, transmit inhibitory signals upon binding to cognate class I MHC ligands. Here we study in vivo NK-mediated lysis of normal allogeneic lymphocytes in crosses between alloreactivity-competent PVG rats and alloreactivity-deficient DA rats. NK cells from both strains are able to lyse standard tumor targets. We identify an autosomal dominant locus, Nka, that controls NK-mediated alloreactivity. Individuals carrying the dominant PVG allele in single dose were fully competent in eliminating allogeneic target cells, suggesting that Nka encodes or regulates a gene product inducing or activating alloreactivity. By linkage analysis and pulsed field gel electrophoresis, a natural killer gene complex (NKC) on rat chromosome 4 is described that contains the rat NKR-P1 and Ly-49 multigene families plus a rat NKG2D homologue. Nka maps within the NKC, together with the most telomeric Ly-49 family members, but separate from NKG2D and the NKR-P1 family. The Nka-encoded response, moreover, correlates with the expression of transcripts for Ly-49 receptors in NK cell populations, as Northern blot analysis demonstrated low expression of Ly-49 genes in DA NK cells, in contrast to high expression in alloreactivity-competent PVG, (DA X PVG)F1, and PVG.1AVI NK cells. The low Ly-49 expression in DA is not induced by MHC haplotype, as demonstrated by high expression of Ly-49 in the DA MHC-congenic PVG.1AVI strain. Finally, we have cloned and characterized the first four members of the rat Ly-49 gene family. Their cytoplasmic domains demonstrate substantial heterogeneity, consistent with the hypothesis that different Ly-49 family members may subserve different signaling functions.
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Jewett, A., and B. Bonavida. "Target-induced inactivation and cell death by apoptosis in a subset of human NK cells." Journal of Immunology 156, no. 3 (1996): 907–15. http://dx.doi.org/10.4049/jimmunol.156.3.907.
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Abstract Interaction of sensitive target cells with NK cells results in both positive and negative signaling. Positive signaling results in the induction of NK cytotoxicity and sensitization for IL-2-mediated proliferation and secretion of cytokines. Negative signaling prevents the NK cells from recycling for cytotoxicity. Functional inactivation is restricted to the NK-target conjugate subset sparing the nonconjugating free NK subset. The mechanism of target-induced inactivation of NK cells was examined in cell-sorted and purified conjugates. The conjugates were subdivided into two fractions; in one fraction the NK cells were dissociated from the target (NKDC), and in the other fraction the conjugates were not disturbed (NKC). After coculture overnight with IL-2, the cytotoxic function of NKC was not augmented although a subpopulation proliferated and secreted TNF-alpha and IFN-gamma into the supernatant. In contrast, NKDC cytotoxic activity was enhanced by IL-2, but proliferated poorly and did not secrete TNF-alpha or IFN-gamma following IL-2 activation. The phenotype of the inactive NKC was found to be CD16dim/- CD692+ CD11b2+. Target-mediated inactivation correlated with target cell sensitivity to NK cytotoxicity. Furthermore, a significant fraction of NK cells in the NKC was programmed for cell death by apoptosis. Altogether, these results demonstrate that sensitive targets inactivate NK cells for cytotoxicity resulting in loss of NK cells. Furthermore, the results suggest that signaling for cytotoxic function by target cells is not linked to signaling for proliferation and secretion of cytokines by NK cells.
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Marceau, François, Brigitte Tremblay, Réjean Couture, and Domenico Regoli. "Prostacyclin release induced by neurokinins in cultured human endothelial cells." Canadian Journal of Physiology and Pharmacology 67, no. 2 (1989): 159–62. http://dx.doi.org/10.1139/y89-026.
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The effects of neurokinins (NK) and related peptides on the secretion of 6-keto-prostaglandin F1α, a stable metabolite of prostacyclin, were measured. These peptides enhanced three- to five-fold the basal secretion rate with the following rank order of potency (based on threshold concentrations for a significant output): substance P (SP) ≥ NKA > SP 4–11 ≥ [pGlu6]SP 6–11 = SP7–11. NKB and SP 1–9 were inactive. Ac[Arg6, Sar9, Met(O2)11]SP, a NK1 receptor selective agonist, was more potent than other selective agonists for the NK2 and NK3 receptor subtypes. These results suggest that the NK receptors, which mediate the release of prostacyclin from human endothelial cells, belong to the NK1 subtype.Key words: neurokinins, substance P fragments, selective agonists, prostacyclin release, human endothelial cells.
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Naper, Christian, James C. Ryan, Mary C. Nakamura, Doris Lambracht, Bent Rolstad, and John T. Vaage. "Identification of an Inhibitory MHC Receptor on Alloreactive Rat Natural Killer Cells." Journal of Immunology 160, no. 1 (1998): 219–24. http://dx.doi.org/10.4049/jimmunol.160.1.219.
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Abstract Studies of allogeneic lymphocyte cytotoxicity have shown that the rat NK allorecognition repertoire is controlled by genetic elements in both the MHC (RT1) and the NK gene complex (NKC). DA rats, possessing NK cells that are unable to lyse allogeneic lymphoblasts, were immunized with alloreactive NK cells from MHC-matched PVG.1AV1 rats, and two mAb, STOK1 and STOK2, were generated. STOK1 and STOK2 stained identical subsets of NKR-P1+ T and NK cells from certain strains of rats. Relative numbers varied markedly in a panel of MHC congenic strains, however, implicating a role for self MHC genes in their development. Both STOK1 and STOK2 immunoprecipitated a 110-kDa disulfide-linked homodimeric molecule, with extensive N-linked glycosylations, encoded by a gene that mapped to the NKC. NK cells expressing this glycoprotein displayed an increased ability to lyse allogeneic lymphoblasts, while syngeneic targets were spared. However, blockade of the STOK2 Ag with F(ab′)2 of STOK2 permitted the NK lysis of syngeneic targets, but did not affect NK allorecognition. These results indicate that mAb STOK1 and STOK2 identify an NKC-encoded MHC receptor in the rat that acts as a negative regulator of cytotoxicity.
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Hwang, Young Eun, Seonghun Im, Hyun Kim, et al. "Adhesive Antimicrobial Peptides Containing 3,4-Dihydroxy-L-Phenylalanine Residues for Direct One-Step Surface Coating." International Journal of Molecular Sciences 22, no. 21 (2021): 11915. http://dx.doi.org/10.3390/ijms222111915.
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Bacterial colonization and transmission via surfaces increase the risk of infection. In this study, we design and employ novel adhesive antimicrobial peptides to prevent bacterial contamination of surfaces. Repeats of 3,4-dihydroxy-L-phenylalanine (DOPA) were added to the C-terminus of NKC, a potent synthetic antimicrobial peptide, and the adhesiveness and antibacterial properties of the resulting peptides are evaluated. The peptide is successfully immobilized on polystyrene, titanium, and polydimethylsiloxane surfaces within 10 min in a one-step coating process with no prior surface functionalization. The antibacterial effectiveness of the NKC-DOPA5-coated polystyrene, titanium, and polydimethylsiloxane surfaces is confirmed by complete inhibition of the growth of Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus aureus within 2 h. The stability of the peptide coated on the substrate surface is maintained for 84 days, as confirmed by its bactericidal activity. Additionally, the NKC-DOPA5-coated polystyrene, titanium, and polydimethylsiloxane surfaces show no cytotoxicity toward the human keratinocyte cell line HaCaT. The antimicrobial properties of the peptide-coated surfaces are confirmed in a subcutaneous implantation animal model. The adhesive antimicrobial peptide developed in this study exhibits potential as an antimicrobial surface-coating agent for efficiently killing a broad spectrum of bacteria on contact.
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Richardson, Eleanor, Jeremy S. Lewis, Jo Gibson, et al. "Role of the kinetic chain in shoulder rehabilitation: does incorporating the trunk and lower limb into shoulder exercise regimes influence shoulder muscle recruitment patterns? Systematic review of electromyography studies." BMJ Open Sport & Exercise Medicine 6, no. 1 (2020): e000683. http://dx.doi.org/10.1136/bmjsem-2019-000683.
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ObjectiveTo investigate the influence of trunk and lower limb motion on electromyography (EMG) muscle activity and recruitment patterns around the shoulder.DesignSystematic review.Data sourcesMEDLINE, CINAHL, PEDro, AMED, PubMed, Cochrane Central Register of Controlled trials, Cochrane Database of Systematic reviews, SportsDiscuss and PROSPERO.Eligibility criteriaStudies investigating both multiregional kinetic chain (KC) shoulder exercises and localised non-kinetic chain (nKC) shoulder exercises in healthy subjects under the same experimental conditions were included in this review.ResultsKC exercises produced greater EMG activation levels in 5 of 11 studies for the lower trapezius. Of the remaining studies, five found no difference between the exercise types and one favoured nKC exercises. KC exercises produced greater EMG activation levels in 5 of 11 studies for the serratus anterior. Of the remaining studies, three reported the opposite and three found no significant difference between the exercise types. nKC exercises produced greater EMG activation in infraspinatus in three of four studies. KC exercises produced the lowest trapezius muscle ratios in all studies. Studies investigating the upper trapezius, middle trapezius, supraspinatus, subscapularis, biceps brachii, latifissimus dorsi, pectoralis major, deltoid, and trapezius and serratus anterior ratios showed inconsistency.ConclusionThis review found evidence that integrating the KC during shoulder rehabilitation may increase axioscapular muscle recruitment, produce lower trapezius muscle ratios and reduce the demands on the rotator cuff. Stepping appears preferable to squatting.PROSPERO registration numberCRD42015032557, 2015.
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Shehata, Hesham, Kristin Lampe, Kasper Hoebe, and Claire Chougnet. "Skewed homeostasis of natural killer cells in aging decreases their capacity to eliminate target cells (HEM3P.290)." Journal of Immunology 192, no. 1_Supplement (2014): 51.19. http://dx.doi.org/10.4049/jimmunol.192.supp.51.19.
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Abstract Natural killer cells (NKCs) are critical in eliminating tumors and viral infections, both of which occur at a high incidence in the elderly. Previous studies showed that aged NKCs are less cytotoxic in vitro and are less mature than young NKCs. However, the mechanisms by which aging influences NKC homeostasis and function remain poorly understood. We found that aged mice had a significant decrease in frequency of mature and educated NKCs in all lymphoid organs and aged NKCs were less efficient at eliminating allogeneic and B16 melanoma targets in vivo. This phenomenon could be explained by the impaired degranulation, particularly by mature NKCs of aged mice. Administration of exogenous IL-15 or depleting Tregs or CD8+ T cells, which may compete for IL-15, did not augment aged NKC maturation. However, T-bet and Eomes which regulate NKC maturation, were significantly decreased in bone marrow (BM) NKCs of aged mice, indicating that there may be a block in progressive differentiation of immature to mature NKCs in aging. Consistent with reports supporting T-bet mediated Granzyme B (GZB) expression, the proportion of GZB+ NKCs was significantly reduced in aged mice. The homeostatic proliferation of BM aged NKCs was also greatly diminished compared to young NKCs. Overall, our results suggest that aged BM NKCs may not respond well to maturation signals and that this impaired maturation is linked to their defective cytotoxicity.
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Thompson, G. W., D. B. Hoover, J. L. Ardell, and J. A. Armour. "Canine intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 5 (1998): R1683—R1689. http://dx.doi.org/10.1152/ajpregu.1998.275.5.r1683.
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To determine whether intrinsic cardiac neurons involved in cardiac regulation possess neurokinin (NK) receptor subtypes, we administered selective NK receptor agonists individually (100 μM; 0.1 ml) into the coronary arterial blood supply of right atrial intrinsic cardiac neurons of 18 anesthetized dogs. The selective NK1 receptor agonist [Sar9,Met(O2)11]-substance P depressed the spontaneous activity of right atrial neurons (26.7 ± 6.7 to 13.0 ± 4.0 impulses/min; P < 0.05) in 11 dogs and augmented such activity in the other 5 dogs (8.0 ± 3.1 to 27.8 ± 8.7 impulses/min; P < 0.05). Local administration of the selective NK2 receptor agonist [β-Ala8]-NKA-(4—10) depressed right atrial neuronal activity (27.3 ± 6.4 to 14.7 ± 3.8 impulses/min; P < 0.05), whereas the selective NK3 receptor agonist senktide augmented such activity (18.9 ± 6.4 to 53.1 ± 12.0 impulses/min; P < 0.05). Left ventricular chamber pressure fell when selective NK1 and NK2 receptor agonists were administered. Increases in heart rate and right ventricular intramyocardial systolic pressure occurred when the selective NK3 receptor agonist was studied. Administration of a selective NK1or NK2 receptor antagonist altered neuronal activity, with no subsequent change in activity occurring after administration of its respective receptor agonist. Receptor autoradiography demonstrated tachykinin receptors associated with ventral right atrial intrinsic cardiac neurons. It is concluded that intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors and that some intrinsic cardiac neurons receive tonic input via endogenously released NKs.
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Astudillo, Beatriz, Domingo A. Martín, Jorge L. Costafreda, Leticia Presa, Miguel A. Sanjuán, and José Luis Parra. "Improvement of the Mechanical Properties of Mortars Manufactured with Partial Substitution of Portland Cement by Kaolinitic Clays." Buildings 13, no. 7 (2023): 1647. http://dx.doi.org/10.3390/buildings13071647.
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Presently, the search for urgent solutions to mitigate climate change has become a global priority. One of the most important challenges is the characterization, standardization, and technology of sustainable natural raw materials, which will significantly improve the quality of common types of cement, the production process of which emits large amounts of greenhouse gases into the atmosphere. This work is focused on the study of natural kaolinitic clays (NKC) from the eastern part of the Iberian Peninsula and its main objective is to define and normalize their properties as natural pozzolanic materials. This research consists of an initial study to determine the morphological and chemical properties using SEM and XRF. Furthermore, the physical properties of the samples were studied, such as thermic treatment (TT), Blane particle finesse (BPF), real density (RD) and apparent density (AD), porosity (P), volume stability (VS) and start and final setting time (SFST). On the other hand, technological analyses were carried out as follows: chemical analysis (CATQ), pozzolanicity (CAP), mechanical compression strength tests at 7, 28, and 90 days (MCST) as well as the ultrasonic pulse velocity (UPV). XRF results indicated that the SiO2 content (49.9–51.0%) of kaolinitic clay in its natural state (NKC) increases to 57.41 and 58.10%, respectively, when calcined (CKC). The chemical analysis of pozzolanicity established that the NKC does not show pozzolanic activity during the first 8 and 15 days; however, once calcinated, its pozzolanic reactivity increases substantially. On the other hand, the results of the mechanical stress tests (MCST) indicate an exponential increase in mechanical resistance from 7 to 90 days, which is higher in mortars made with CKC; similarly, and according to the results of the calculation of the Resistant Activity Index (RAI), it shows that the substitutions of Portland cement (PC) by NKC are effective between the ranges of 10 and 25%, while in the case of the substitution of PC by CKC, all formulations (10, 25 and 40%) are effective. This research establishes that the kaolinitic clays of the east of the Iberian Peninsula can be considered quality pozzolanic materials, capable of partially replacing Portland cement. The results presented here could be used as guidelines for the understanding and application of natural pozzolanic materials contributing to the improvement of types of cement, mortars, and concretes, which would positively affect the quality and preservation of the environment as well as the sustainability of eco-efficient construction materials.
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Wang, Qiurong, Qi Zhang, Na Kang, et al. "Abstract 888: NKC and KIR humanized mice: a powerful tool to develop NK-targeting drugs." Cancer Research 85, no. 8_Supplement_1 (2025): 888. https://doi.org/10.1158/1538-7445.am2025-888.
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Abstract Natural killer (NK) cells are leukocytes within the innate immune system, acting as a first line of defense against cancer and virally infected cells. NK cell responses—whether “killing” or “tolerant”—are regulated by interactions between activating and inhibitory receptors and their ligands. Currently, there remains a need for comprehensive in vivo models featuring humanized NK cell receptors, including key proteins encoded by the KIR and NKC gene clusters. Killer cell immunoglobulin-like receptors (KIR) form a highly polymorphic gene cluster expressed by NK and certain T cell subtypes, while the Natural Killer Gene Complex (NKC) encodes several C-type lectin-like receptors, such as the NKG2 family, found across various immune cells. To introduce a novel NK gene cluster-related in vivo model, Biocytogen has used advanced gene-editing technology to humanize ∼150,000 base pairs of KIR gene cluster DNA (B-hKIR mice) and 0.9 million base pairs of NKC gene cluster DNA (B-hNKC mice) on a C57BL/6 background. In this combined B-hNKC/hKIR mouse model, 29 functional genes have been modified.The immunophenotype of B-hNKC/hKIR mice is consistent with that of wild-type C57BL/6 mice. Human proteins NKG2A, NKG2C, CD94, NKG2D, and CD161 are detectable on NK cells, while human CLEC9A is observed on CD8a+ and CD103+ dendritic cells in the spleen. Human CLEC12A is expressed on T cells, macrophages, monocytes, and dendritic cells, and human LOX1 is present on activated macrophages, monocytes, and neutrophils in the bone marrow. Additionally, human CD69 is expressed on activated T cells, B cells, NK cells, macrophages, monocytes, neutrophils, and dendritic cells in the spleen. In B-hKIR mice, human KIR2DL1, KIR2DL3, and KIR3DL2 are detectable on NK cells, and mRNA for human KLRF2, CLEC2A, TMEM52B, CLEC1A, and CLEC2D is also expressed in B-hNKC/hKIR mice.This B-hNKC/hKIR mouse model provides an advanced platform for NK-targeted research and serves as a valuable in vivo system for preclinical studies. Citation Format: Qiurong Wang, Qi Zhang, Na Kang, Huizhen Zhao, Lili Liu, Jiawei Yao, Yanshuang Li. NKC and KIR humanized mice: a powerful tool to develop NK-targeting drugs [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 888.
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Vogler, Isabel, and Alexander Steinle. "Vis-à-Vis in the NKC: Genetically Linked Natural Killer Cell Receptor/Ligand Pairs in the Natural Killer Gene Complex (NKC)." Journal of Innate Immunity 3, no. 3 (2011): 227–35. http://dx.doi.org/10.1159/000324112.
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Noveral, J. P., and M. M. Grunstein. "Tachykinin regulation of airway smooth muscle cell proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 3 (1995): L339—L343. http://dx.doi.org/10.1152/ajplung.1995.269.3.l339.
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The tachykinins, substance P (SP) and neurokinins A (NKA) and B (NKB), have been identified in the respiratory tract and implicated in mediating neurogenic inflammation of the airways. To the extent that these neuropeptides may be involved in the pathogenesis of asthma, a condition associated with hyperplasia of airway smooth muscle (ASM), we examined the mitogenic effects and mechanisms of action of tachykinins in cultured rabbit ASM cells. SP was found to elicit dose-dependent (10(-14) to 10(-4) M) stimulation of ASM cell proliferation, with a mean (+/- SE) maximal increase in cell number of 169 +/- 6.1% of control. In contrast, NKA and NKB had little and no effect on ASM cell growth, respectively. Because SP is nonselective in its binding to the tachykinin receptors, to identify the specific NK receptor subtype(s) mediating the promitogenic action of SP, in separate studies we found that 1) the NK1-receptor-specific agonist, [beta-Ala4, Sar9, Met(O2)11]SP-(4-11) induced stimulation of ASM cell growth similar in magnitude to that elicited by SP; 2) in contrast, neither the NK1- nor NK2-receptor-specific agonists, [beta-Ala8]NKA-(4-10) and [MePhe7]NKB, respectively, had any effect on ASM cell growth; and 3) the promitogenic action of SP was inhibited by the NK1-receptor antagonist, GR-82,334. Moreover, in extended experiments, we found that the phospholipase C and phospholipase A2 inhibitors, neomycin and quinacrine, respectively, each inhibited SP-induced ASM cell proliferation by approximately 45%. Collectively, these observations provide new evidence that the tachykinin SP induces ASM cell proliferation, and that this action is mediated by transmembrane signaling coupled to selective activation of the NK1 receptor.
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Morimoto, Takayuki, Tsutomu Nakazawa, Ryosuke Matsuda, et al. "Antitumor Effects of Intravenous Natural Killer Cell Infusion in an Orthotopic Glioblastoma Xenograft Murine Model and Gene Expression Profile Analysis." International Journal of Molecular Sciences 25, no. 4 (2024): 2435. http://dx.doi.org/10.3390/ijms25042435.
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Despite standard multimodality treatment, containing maximum safety resection, temozolomide, radiotherapy, and a tumor-treating field, patients with glioblastoma (GBM) present with a dismal prognosis. Natural killer cell (NKC)-based immunotherapy would play a critical role in GBM treatment. We have previously reported highly activated and ex vivo expanded NK cells derived from human peripheral blood, which exhibited anti-tumor effect against GBM cells. Here, we performed preclinical evaluation of the NK cells using an in vivo orthotopic xenograft model, the U87MG cell-derived brain tumor in NOD/Shi-scid, IL-2RɤKO (NOG) mouse. In the orthotopic xenograft model, the retro-orbital venous injection of NK cells prolonged overall survival of the NOG mouse, indirectly indicating the growth-inhibition effect of NK cells. In addition, we comprehensively summarized the differentially expressed genes, especially focusing on the expression of the NKC-activating receptors’ ligands, inhibitory receptors’ ligands, chemokines, and chemokine receptors, between murine brain tumor treated with NKCs and with no agents, by using microarray. Furthermore, we also performed differentially expressed gene analysis between an internal and external brain tumor in the orthotopic xenograft model. Our findings could provide pivotal information for the NK-cell-based immunotherapy for patients with GBM.
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Kohl, S., L. S. Loo, F. S. Schmalstieg, and D. C. Anderson. "The genetic deficiency of leukocyte surface glycoprotein Mac-1, LFA-1, p150,95 in humans is associated with defective antibody-dependent cellular cytotoxicity in vitro and defective protection against herpes simplex virus infection in vivo." Journal of Immunology 137, no. 5 (1986): 1688–94. http://dx.doi.org/10.4049/jimmunol.137.5.1688.
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Abstract The role of the Mac-1, LFA-1, p150,95 leukocyte glycoprotein family in mediating antiviral host defense was investigated by utilizing mononuclear cells (MC) obtained from eight patients with a genetic deficiency of Mac-1, LFA-1, and p150,95, and normal MC incubated with subunit-specific monoclonal antibodies (MAb) directed against these glycoproteins. As shown with an in vitro chromium-release cytotoxicity assay to herpes simplex virus (HSV)-infected Chang liver target cells, MC of these patients with the severe phenotype or normal MC preincubated with a combination of MAb against Mac-1 glycoprotein subunits were deficient in antibody-dependent cellular cytotoxicity (ADCC). When used individually, MAb directed at LFA-1-alpha or -beta also inhibited ADCC and natural killer cytotoxicity (NKC). In a single cell agarose assay, MC of Mac-1-deficient patients formed fewer effector-target cell conjugates in the presence of specific anti-HSV antibody. To investigate the in vitro contributions of these glycoproteins to cytotoxic host defense mechanisms, two in vivo adoptive transfer models were explored in which neonatal mice are protected against a lethal HSV challenge by normal human MC plus anti-HSV antibody (in vivo ADCC) or human interferon-alpha (NKC stimulated in vivo). In each model, MC from patients with "severe" or "moderate" phenotypes of Mac-1 deficiency, or normal MC incubated with a combination of anti-LFA-alpha, Mac-1-alpha, p150,95-alpha plus -beta MAb failed to protect neonatal mice against lethal HSV infection. These studies further indicate requirements for adhesion-dependent mechanisms in the mediation of MC-ADCC, and suggest that Mac-1-dependent cellular adhesive properties are necessary for normal cytotoxic functions in vivo in experimental models of human ADCC or interferon-stimulated NKC. These findings, in addition to the recognized occurrence of severe or even lethal viral infections in some Mac-1-deficient patients, suggest that glycoproteins of the Mac-1 family may be important determinants of antiviral host defense.
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Ma, Xiaoyang, Jeon-Kyung Kim, Yoon-Jung Shin, et al. "Alleviation of Cognitive Impairment-like Behaviors, Neuroinflammation, Colitis, and Gut Dysbiosis in 5xFAD Transgenic and Aged Mice by Lactobacillus mucosae and Bifidobacterium longum." Nutrients 15, no. 15 (2023): 3381. http://dx.doi.org/10.3390/nu15153381.
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Neuropsychiatric disorders including Alzheimer’s disease (AD) may cause gut inflammation and dysbiosis. Gut inflammation-suppressing probiotics alleviate neuropsychiatric disorders. Herein, to understand whether anti-inflammatory probiotics Lactobacillus mucosae NK41 and Bifidobacterium longum NK46, which suppressed tumor necrosis factor (TNF)-α expression in lipopolysaccharide (LPS)-stimulated macrophages, could alleviate cognitive impairment, we first examined their effects on cognitive function, gut inflammation, and gut microbiota composition in 5xFAD-transgenic mice. Oral administration of NK41 or NK46 decreased cognitive impairment-like behaviors, hippocampal amyloid-β (Aβ), TNF-α and interleukin (IL)-1β expression, hippocampal NF-κB+Iba1+ cell population, and Aβ accumulation, while hippocampal brain-derived neurotropic factor (BDNF) and IL-10 expression and BDNF+NeuN+ cell population increased. They also decreased TNF-α and IL-1β expression and NF-κB+CD11c+ cell population in the colon. They also reduced fecal and blood LPS levels and gut Proteobacteria and Verrucomicrobia populations (including Akkkermansiaceae), which are positively associated with hippocampal TNF-α and fecal LPS levels and negatively correlated with hippocampal BDNF level. However, they increased Odoribactericeae, which positively correlated with BDNF expression level and TNF-α to IL-10 expression ratio. The combination of NK41 and NK46 (4:1, NKc), which potently inhibited TNF-α expression in LPS-stimulated macrophages, additively alleviated cognitive impairment-like behaviors in 5xFAD-transgenic or aged mice. NKc increased hippocampal BDNF+NeuN+ cell population and BDNF expression in 5xFAD-transgenic or aged mice, while hippocampal TNF-α and IL-1β expression decreased. NKc also decreased TNF-α and IL-1β expression in the colon and LPS levels in the blood and feces. These findings suggest that gut bacteria and its product LPS may be closely connected with occurrence of cognitive impairment and neuroinflammation and the combination of NK41 and NK46 can additively alleviate cognitive impairment and neuroinflammation by inducing NF-κB-suppressed BDNF expression and suppressing LPS-producing gut bacteria.
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MacNaughton, W., B. Moore, and S. Vanner. "Cellular pathways mediating tachykinin-evoked secretomotor responses in guinea pig ileum." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 5 (1997): G1127—G1134. http://dx.doi.org/10.1152/ajpgi.1997.273.5.g1127.
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This study characterized tachykinin-evoked secretomotor responses in in vitro submucosal and mucosal-submucosal preparations of the guinea pig ileum using combined intracellular and Ussing chamber recording techniques. Superfusion of endogenous tachykinins substance P (SP), neurokinin A (NKA), and neurokinin B depolarized single submucosal neurons and evoked increased short-circuit current ( I sc) responses in Ussing chamber preparations. The NK1-receptor agonist [Sar9,Met(O2)11]SP [50% effective concentration (EC50) = 2 nM] depolarized all submucosal neurons examined. The NK3-receptor agonist senktide (EC50 = 20 nM) depolarized ∼50% of neurons examined, whereas the NK2-receptor agonist [Ala5,β-Ala8]NKA-(4—10) had no effect on membrane potential. [Sar9,Met(O2)11]SP and senktide evoked similar increases in I sc that were tetrodotoxin sensitive (91 and 100%, respectively) and were selectively blocked by the NK1antagonist CP-99,994 and the NK3antagonist SR-142801, respectively. Capsaicin-evoked increases in I sc were significantly inhibited (54%, P < 0.05) by CP-99,994 but not by SR-142801. Neither antagonist inhibited slow excitatory postsynaptic potentials. These findings suggest that tachykinin-evoked secretion in guinea pig ileum is mediated by NK1 and NK3 receptors on submucosal secretomotor neurons and that capsaicin-sensitive nerves release tachykinin(s) that activate the NK1 receptors.
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Celo, Sokol. "Neutrality in Internationalized R&D-Portfolios: An NKC-Application." Academy of Management Proceedings 2019, no. 1 (2019): 15495. http://dx.doi.org/10.5465/ambpp.2019.15495abstract.
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Idris, Azza H., Koho Iizuka, Hamish R. C. Smith, Anthony A. Scalzo, and Wayne M. Yokoyama. "Genetic Control Of Natural Killing and In Vivo Tumor Elimination by the Chok Locus." Journal of Experimental Medicine 188, no. 12 (1998): 2243–56. http://dx.doi.org/10.1084/jem.188.12.2243.
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The molecular mechanisms underlying target recognition during natural killing are not well understood. One approach to dissect the complexities of natural killer (NK) cell recognition is through exploitation of genetic differences among inbred mouse strains. In this study, we determined that interleukin 2–activated BALB/c-derived NK cells could not lyse Chinese hamster ovary (CHO) cells as efficiently as C57BL/6-derived NK cells, despite equivalent capacity to kill other targets. This strain-determined difference was also exhibited by freshly isolated NK cells, and was determined to be independent of host major histocompatibility haplotype. Furthermore, CHO killing did not correlate with expression of NK1.1 or 2B4 activation molecules. Genetic mapping studies revealed linkage between the locus influencing CHO killing, termed Chok, and loci encoded within the NK gene complex (NKC), suggesting that Chok encodes an NK cell receptor specific for CHO cells. In vivo assays recapitulated the in vitro data, and both studies determined that Chok regulates an NK perforin–dependent cytotoxic process. These results may have implications for the role of NK cells in xenograft rejection. Our genetic analysis suggests Chok is a single locus that affects NK cell–mediated cytotoxicity similar to other NKC loci that also regulate the complex activity of NK cells.
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Bai, T. R., D. Zhou, T. Weir, et al. "Substance P (NK1)- and neurokinin A (NK2)-receptor gene expression in inflammatory airway diseases." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 3 (1995): L309—L317. http://dx.doi.org/10.1152/ajplung.1995.269.3.l309.
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The tachykinin neuropeptides substance P and neurokinin (NK) A have been postulated to participate in the inflammatory reaction in airways of smokers and asthmatics. We have examined the hypothesis that the expression of one or more of the three cloned tachykinin receptors (NK1, NK2, and NK3) is increased in inflammatory airway disorders, which could result in augmentation of the effect of released tachykinin neuropeptides. NK1 receptor and NK2 receptor but not NK3-receptor mRNA were detected by ribonuclease protection assay in RNA from both cartilaginous and membranous bronchi and subpleural lung. In lung samples containing membranous airways, NK2-receptor mRNA expression was increased fourfold in asthmatics compared with nonsmoking controls, whereas NK1-receptor mRNA levels were similar in the two groups. NK1- and NK2-receptor mRNA expression was increased twofold in smokers without airflow obstruction compared with nonsmokers, whereas NK1-receptor mRNA expression was significantly lower in patients with chronic obstructive pulmonary disease compared with smoking controls. In situ hybridization indicated NK1-receptor mRNA was expressed in submucosal glands and airway epithelial cells, whereas NK2-receptor and NK3-receptor mRNA were not detected. These observations have implications for the pathophysiology and treatment of both asthma and tobacco smoke-induced airway inflammation.
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Porrata, Luis, David James Inwards, Stephen M. Ansell, et al. "Sustained Natural Killer Cell Recovery Post-Autologous Peripheral Blood Hematopoietic Stem Cell Transplantation Predicts Survival in Non-Hodgkin's Lymphoma." Blood 128, no. 22 (2016): 4641. http://dx.doi.org/10.1182/blood.v128.22.4641.4641.
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Abstract Abstract Our group recently reported a Phase III clinical trial (Porrata et al. Biology of Blood and Marrow Transplantation 2016; 22: 1017-1023) demonstrating that the infusion of the autograft-absolute lymphocyte count (A-ALC) and autograft natural killer cells (A-NKC) are survival prognostic factors in non-Hodgkin lymphoma (NHL) patients treated with autologous peripheral blood hematopoietic stem cell transplantation (APBHSCT). A limitation of our Phase III clinical trial was the short-term follow-up of just two years. Therefore, we evaluated longer follow-up and assessed the role of the infused A-ALC, infused A-NKC, and peripheral blood absolute natural killer cell count (ANKC) recovery on survival post-APBHSCT. Of the 122 patients that participated in the Phase III trial, 111 patients were able to complete APBHSCT and included in the current study. With a median follow-up of 57.2 months (range: 2.1-84.6 months), superior overall survival (OS) and progression-free survival (PFS) was observed in patients infused with an A-ALC ≥ 0.5 x 109 lymphocytes/kg [OS: HR = 0.429, 95%CI, 0.128-0.828, p < 0.01; and PFS: HR = 0.456, 95% CI, 0.177-0.863, p < 0.01] and an A-NKC ≥ 0.09 x 109 cells/kg [OS: HR = 1.58e-3, 95% CI, 1.046e-6-0.179, p < 0.003; and PFS: HR= 1.58e-3, 95% CI, 7.81e-7-0.064, p < 0.003]. Furthermore, patients that maintained an ANKC ≥ 250 cells/µl at 3 months, 6 months, 9 months and 12 months post-APBHSCT also experienced superior OS (Figure 1A) and PFS (Figure 1B)[OS and PFS times in months were evaluated from infusion date of stem cells]. In the multivariate analysis a sustained ANKC ≥ 250 cells/µl was an independent predictor for OS (HR = 0.013, 95% CI, 0.001-0.063, p < 0.0001) and PFS (HR = 0.014, 95% CI, 0.001-0.067, p < 0.0001). This study is an extension of our Phase III clinical trial showing that sustained innate immunity by measuring the ANKC correlated with superior clinical outcomes; thus providing a platform to develop innate immunity immunotherapeutic strategists directing to improve clinical outcomes post-APBHSCT in NHL patients. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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Gay, J., J. Fioramonti, R. Garcia-Villar, X. Emonds-Alt, and L. Bueno. "Involvement of tachykinin receptors in sensitisation to cow’s milk proteins in guinea pigs." Gut 44, no. 4 (1999): 497–503. http://dx.doi.org/10.1136/gut.44.4.497.
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BACKGROUNDThere is growing evidence for a pivotal role for tachykinins in gut neuroimmune interactions.AIMSTo determine whether NK1, NK2, and NK3 tachykinin receptors are involved in milk protein induced allergic sensitisation.METHODSEight groups of 12 Dunkin-Hartley guinea pigs (250–300 g) were used. Four groups were sensitised to milk proteins for three weeks. During this period, these animals were injected intraperitoneally each day with NK1 (SR 140333; 0.3 mg/kg), NK2 (SR 48968; 5 mg/kg), or NK3 (SR 142801; 5 mg/kg) receptor antagonist or vehicle. The fifth group had water available instead of milk and was used as a non-sensitised control. The three other groups received the NK receptor antagonists for three weeks but were not sensitised to milk proteins.RESULTSSensitised animals treated with NK1 and NK3 receptor antagonists had both lower IgE and IgG serum titres, evaluated by passive cutaneous anaphylaxis, and lower specific IgG serum titres, determined by enzyme linked immunosorbent assay (ELISA), than vehicle treated animals. Sensitisation induced an increase in intestinal mast cell number which was abolished by treatment with the NK1 receptor antagonist. Antigenic challenge-induced jejunal hypersecretion was also blocked by treatment with the NK1 receptor antagonist.CONCLUSIONIn guinea pigs, NK1 and NK3 but not NK2 receptors are involved in sensitisation to cow’s milk. However, NK1 but not NK3 receptor antagonists abolish both the hypermastocytosis induced by food allergy and the hypersecretion induced by antigenic challenge, suggesting different roles for NK1 and NK3 receptors in the mechanisms of sensitisation to β-lactoglobulin.
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Theoharis, Vasilis, Ioannis Toliopoulos, Yannis Simos, et al. "Inhibition of platelet aggregation and stimulation of natural killer cells functionality by administration of flavonoids." South Asian Journal of Experimental Biology 1, no. 2 (2011): 94–100. http://dx.doi.org/10.38150/sajeb.1(2).p94-100.
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Platelets play an important role in homeostasis, inflammation and regulation of immune response. Natural Killer cells (NKC) on the other hand are the first line of defense of the immune system against viruses, bacteria and cancer cells. Platelets directly protect tumor cells from NK lysis. Thus, platelet aggregation around migrating cancer cells as well as the response of the immune system constitutes important mechanisms, which influence the progression of malignant diseases. The present study was designed to evaluate the possible effects of flavonoids (genistein, apigenin and quercetin) on the stimulation of the immune system and the inhibition of platelet aggregation. Two experimental protocols were used: a) ex vivo aggregation of human platelets, production of thromboxane A2 (TXA2) and estimation of the expression of the platelet membranic receptor GpIIb/IIIa, and b) functional activity of human NK lymphocytes against K562 target cells in vitro. All substances were found to induce a dose dependent inhibition of platelet aggregation and to reduce production of TXA2 in platelets. There was a decrease in the number of the GpIIb/IIIa receptors on the platelets surface membrane. Flow cytometry analysis revealed that all substances powerfully reinforce cytotoxic activity of NKC against K562 cells. These results show that flavonoids increase the susceptibility of tumor cells to NK cells by decreasing platelet aggregation and stimulating the NK lymphocyte activity.
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Zhou, Yanqing, Yiwen Tang, and Zhibing Li. "An Improved Two-Shot Tracking Algorithm for Dynamics Analysis of Natural Killer Cells in Tumor Contexts." Bioengineering 11, no. 6 (2024): 540. http://dx.doi.org/10.3390/bioengineering11060540.
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Natural killer cells (NKCs) are non-specific immune lymphocytes with diverse morphologies. Their broad killing effect on cancer cells has led to increased attention towards activating NKCs for anticancer immunotherapy. Consequently, understanding the motion characteristics of NKCs under different morphologies and modeling their collective dynamics under cancer cells has become crucial. However, tracking small NKCs in complex backgrounds poses significant challenges, and conventional industrial tracking algorithms often perform poorly on NKC tracking datasets. There remains a scarcity of research on NKC dynamics. In this paper, we utilize deep learning techniques to analyze the morphology of NKCs and their key points. After analyzing the shortcomings of common industrial multi-object tracking algorithms like DeepSORT in tracking natural killer cells, we propose Distance Cascade Matching and the Re-Search method to improve upon existing algorithms, yielding promising results. Through processing and tracking over 5000 frames of images, encompassing approximately 300,000 cells, we preliminarily explore the impact of NKCs’ cell morphology, temperature, and cancer cell environment on NKCs’ motion, along with conducting basic modeling. The main conclusions of this study are as follows: polarized cells are more likely to move along their polarization direction and exhibit stronger activity, and the maintenance of polarization makes them more likely to approach cancer cells; under equilibrium, NK cells display a Boltzmann distribution on the cancer cell surface.
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Herawati, Titin, and Theresia Tri Suharni. "Fermentasi Etanol dengan Bahan Baku Produk Sakarifikasi Singkong oleh Aspergillus niger dengan Menggunakan Isolat Saccharomyces spp. (NKB dan NKC)." Biogenesis: Jurnal Ilmiah Biologi 1, no. 1 (2013): 1–8. http://dx.doi.org/10.24252/bio.v1i1.441.
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Ungwiwatkul, Sunisa, and Aiya Chantarasiri. "Study on the Potential for Biodiesel Production of Microalgal Consortia from Brackish Water Environment in Rayong Province, Thailand." International Journal of Renewable Energy Development 11, no. 4 (2022): 1060–67. http://dx.doi.org/10.14710/ijred.2022.45547.
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Microalgae are photoautotrophic microorganisms that can be grown in a wide variety of water environments. They are the most promising biodiesel source, with the potential to replace fossil diesel. In this study, microalgae samples were collected from the brackish water environment of three locations in Rayong province, Thailand including Phra Chedi Klang Nam (PKC), Noen Kho Canal (NKC), and Raksamae Bridge (RSM), and induced to form multi-algae communities or microalgal consortia (MC). All consortia were cultured and analyzed for their ability to produce biomass and lipid. The result was found that the biomass concentration of MC-RSM was 0.65 ± 0.05 mg.L-1, which is higher than 1.2 and 1.5-times of MC-PCK and MC-NKC, respectively. The most common microalgae species found under all cultures were green algae (Chlorophyta) and diatom (Bacillariophyta), and the dominant species was the green algae, Chlorella sp. The lipid content of all samples ranged from 28.07 ± 0.60 to 33.21 ± 0.79% of dry weight, and the highest value was noticed in the MC-RSM sample. The fatty acid composition of fatty acid methyl ester (FAME) was also evaluated as feasibility for biodiesel production. FAME profiles of each sample showed high amounts of saturated fatty acids (SFAs) ranging from 67.82%-71.31% of total fatty acids. The majority of the SFAs in all were palmitic acid (C16:0) followed by myristic acid (C14:0, and stearic acid (C18:0). Therefore, all microalgal consortia showed great fatty acid profiles and these have the potential for use as feedstock for biodiesel production.