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Drip irrigation technology is widely used due to its advantages including high efficiency water saving, ability to adapt to the terrain and so on, but the problem of emitter clogging has been always a baffled to researchers. Emitter clogging basically has three classes, respectively is physical clogging, chemical clogging and biological clogging, of which the most common is physical clogging and it is represented by sediment clogging. Studies show that even if the irrigation water after precipitation filtration, there is still have particle size of sediment particles which are less than 0.1mm get into the emitters causing emitter clogging. However, previous studies on this problem multi-use of computer simulation method to research the influence of emitter anti-clogging by emitter structures, test verification is relatively rare and most studies only from a macro perspective to observe emitters clogging, no in-depth study on the clogging mechanism. In addition, the previous researches presents the sediment particle size range which are easily lead to cause emitters clogging need further verification, sediment concentration corresponding in different size which are easily to cause emitters clogging needs to be studied in-depth. So in order to investigate the influence of sediment particle size and sediment concentration on the clogging processes of labyrinth channels emitters, periodic intermittent drip irrigation experiments were carried out using muddy water containing particles with 6 different particle ranges (all less than 0.1 mm) which were screened by means of sieving method, each particle size range of sediment are formulated to 0.5,1.0,1.5 g/L of muddy water. Each irrigation time is 30min as same as the test interval, emitters flow collect real-time and replace new pipes after the end of each group of treatment. In these experiments, the changes of flow discharges were measured under a constant pressure and after the end of the trial clogging emitters are cut to dried in the natural state, then collect the sediment which depositing in the labyrinth channel, at least the locations of sediment clogging were observed using electron microscopy and take picture to compare the difference between the status quo sediment and the clogging sediment to proven mechanisms that cause clogging of sediment particle size in different range, it also provide a theoretical basis for how to select the appropriate filter. The results show that, the sensitive sediment particle range that cause easy clogging is depending on the sediment concentration. When the sediment concentration is less than 1.3 g/L, particle size is considered as the main cause of clogging. The most easily cause clogging particle ranges are between 0.075-0.1 mm and 0.03-0.038 mm; particle ranges from 0.05-0.075 mm and 0.02-0.03 mm are lesser; while the ranges that most difficult to cause clogging are 0.038-0.05 mm and less than 0.02 mm. When the sediment concentration is greater than the critical value that between 1.2-1.3 g/L, the effect of sediment particle size on clogging is weaker and sediment concentration becomes the main factor to cause clogging. The results also appeal that sediments can easily condense into aggregates to get drippers clogged when the sediment particle size range is less than 0.038 mm. [ABSTRACT FROM AUTHOR]

Human CMV (HCMV) is a ubiquitous pathogen that indelibly shapes the NK cell repertoire. Using transcriptomic, epigenomic, and proteomic approaches to evaluate peripheral blood NK cells from healthy human volunteers, we find that prior HCMV infection promotes NK cells with a T cell-like gene profile, including the canonical markers CD3ε, CD5, and CD8β, as well as the T cell lineage-commitment transcription factor Bcl11b. Although Bcl11b expression is upregulated during NK maturation from CD56 bright to CD56 dim , we find a Bcl11b-mediated signature at the protein level for FcεRIγ, PLZF, IL-2Rβ, CD3γ, CD3δ, and CD3ε in later-stage, HCMV-induced NK cells. BCL11B is targeted by Notch signaling in T cell development, and culture of NK cells with Notch ligand increases cytoplasmic CD3ε expression. The Bcl11b-mediated gain of CD3ε, physically associated with CD16 signaling molecules Lck and CD247 in NK cells is correlated with increased Ab-dependent effector function, including against HCMV-infected cells, identifying a potential mechanism for their prevalence in HCMV-infected individuals and their prospective clinical use in Ab-based therapies., (Copyright © 2021 by The American Association of Immunologists, Inc.)

Recent studies indicate that expansion of NKG2C-positive natural killer (NK) cells is associated with human cytomegalovirus (HCMV); however, their activity in response to HCMV-infected cells remains unclear. We show that NKG2C(hi) CD57(hi) NK cells gated on CD3(neg) CD56(dim) cells can be phenotypically identified as HCMV-induced NK cells that can be activated by HCMV-infected cells. Using HCMV-infected autologous macrophages as targets, we were able to show that these NKG2C(hi) CD57(hi) NK cells are highly responsive to HCMV-infected macrophages only in the presence of HCMV-specific antibodies, whereas they are functionally poor effectors of natural cytotoxicity. We further demonstrate that NKG2C(hi) CD57(hi) NK cells are intrinsically responsive to signaling through CD16 cross-linking. Our findings show that the activity of pathogen-induced innate immune cells can be enhanced by adaptive humoral immunity. Understanding the activity of NKG2C(hi) CD57(hi) NK cells against HCMV-infected cells will be of relevance for the further development of adoptive immunotherapy.

Natural killer (NK) cells are major components of the innate immune system and are assumed to play an important role in the defense against cytomegalovirus infection. Human cytomegalovirus (HCMV) is the only virus known that shapes the NK cell receptor repertoire in humans. Assays allowing the simultaneous measurement of multiple cell parameters and the assessment of subpopulations of NK cells are suitable for monitoring the NK cell response to infected cells. Herein, we describe an autologous assay system to assess NK cell responses to HCMV-infected macrophages which is based on flow cytometry to detect CD107a expression and interferon gamma (IFNγ) secretion. Further we established a simple method to handle HCMV-infected macrophages. Our assay provides a practicable approach to investigate NK cell responses to HCMV infection in vitro.

The role of liver NK cells in virus-induced severe viral hepatitis and, subsequently, hepatic failure is not well defined. In this study, we investigated the role of liver NK cells in the development of hepatocyte necrosis in fulminant hepatic failure (FHF) and acute-on-chronic liver failure (ACLF) because of viral infection. A mouse model of FHF induced by murine hepatitis virus strain 3 (MHV-3) was used to study the role of liver NK cells. Samples from patients with hepatitis B virus-related ACLF (HBV-ACLF) were examined. After MHV-3 infection, the number of NK cells in livers of BALB/cJ mice increased markedly, peaked at 48 h postinfection, and remained at a high level until sacrifice. In peripheral blood, spleen, and bone marrow, this number decreased significantly. Expression of CD69, cytotoxic activity, and intracellular IFN-gamma and TNF-alpha production by liver NK cells at 48 h postinfection were all significantly upregulated. Depletion of NK cells 24 h post-MHV-3 infection increased the mice survival from 0 of 18 (0%) to 4 of 18 (22.2%). Highly activated liver NK cells were cytotoxic to MHV-3-infected hepatocytes and this effect was markedly inhibited by anti-Fas ligand (FasL) plus anti-NKG2D mAbs. Furthermore, the accumulation of hepatic NK cells and increased expression of FasL and natural cytotoxicity receptors (NKp30 and NKp46) on the peripheral NK cells from patients with HBV-ACLF were correlated with disease progression. These results indicate NK cells play a pivotal role in the pathogenesis of FHF and HBV-ACLF, in which process Fas/FasL and NKG2D/NKG2D ligand pathway contribute to the liver NK cell-mediated hepatocyte injury.