Miniature, Lightweight, One-Time-Opening Valve

The figure depicts the main parts of a prototype miniature, lightweight, onetime- opening valve. Like some other miniature one-time-opening valves reported in previous issues of NASA Tech Briefs, this valve is opened by melting a material that blocks the flow path. This valve is designed to remain closed at some temperature between room temperature and cryogenic temperature until the time of opening. The prototype valve includes a 1/8-in. (3-mm) aluminum tube, one end of which is plugged with a solder comprising about 37 weight percent of lead and 63 weight percent of tin. The tube and the solder both have a coefficient of thermal expansion of 23 micron/m-K at room temperature. Before plugging, the interior surface of the plug end of the tube is cleaned with a commercial flux paste developed specifically for preparing aluminum for bonding with lead/tin solder. The solder is then melted into the cleaned end of the tube, forming the plug. In a test, the plugged tube was pressurized to 1,000 psi (6.9 MPa) with helium and leak-tested. It was then cooled to a temperature of 77 K (about 196 C) and again leak-tested at the same pressure. Finally, at a lower pressure, the plugged end of the tube was heated to about 200 C (the melting temperature of the solder is 183 C), causing the solder plug to be ejected (see figure). It has been estimated that in a subsequent version of the valve, the plug could be melted by electrical heating, using a nichrome wire having a mass of only 10 g

Sparse tree-based clustering of microbiome data to characterize microbiome heterogeneity in pancreatic cancer

There is a keen interest in characterizing variation in the microbiome across cancer patients, given increasing evidence of its important role in determining treatment outcomes. Here our goal is to discover subgroups of patients with similar microbiome profiles. We propose a novel unsupervised clustering approach in the Bayesian framework that innovates over existing model-based clustering approaches, such as the Dirichlet multinomial mixture model, in three key respects: we incorporate feature selection, learn the appropriate number of clusters from the data, and integrate information on the tree structure relating the observed features. We compare the performance of our proposed method to existing methods on simulated data designed to mimic real microbiome data. We then illustrate results obtained for our motivating data set, a clinical study aimed at characterizing the tumor microbiome of pancreatic cancer patients

The Perception of Deepfake Technology Among University Students in Malaysia

It was alarming to know that a new technology (Deepfake) is paving the way to social media by demoralising popular people (celebrities) and others. It has badly affected reputation of many people without their knowledge and consent. It was decided to know about Deepfake technology at length and its extent in harming and hurting the people. A group of university students were randomly selected and administered through a questionnaire. The questionnaire comprised questions pertaining to awareness of deepfake and its consequences. The objectives of the study were to examine the emergence of Deepfake technology, the impact of Deepfake technology utility, and understanding the strategies to mitigate irresponsible usage of Deepfake technology among social media users. The descriptive data was analyzed using numbers and percentages. The major findings included its existence, impact on social media and strategies to mitigate irresponsible usage of Deepfake technology. A wider and larger diverse community using social media extensively will provide better results

Repertoire Enhancement with Adoptively Transferred Female Lymphocytes Controls the Growth of Pre-Implanted Murine Prostate Cancer

In prostate cancer, genes encoding androgen-regulated, Y-chromosome-encoded, and tissue-specific antigens may all be overexpressed. In the adult male host, however, most high affinity T cells targeting these potential tumor rejection antigens will be removed during negative selection. In contrast, the female mature T-cell repertoire should contain abundant precursors capable of recognizing these classes of prostate cancer antigens and mediating effective anti-tumor immune responses.We find that syngeneic TRAMP-C2 prostatic adenocarcinoma cells are spontaneously rejected in female hosts. Adoptive transfer of naïve female lymphocytes to irradiated male hosts bearing pre-implanted TRAMP-C2 tumor cells slows tumor growth and mediates tumor rejection in some animals. The success of this adoptive transfer was dependent on the transfer of female CD4 T cells and independent of the presence of CD25-expressing regulatory T cells in the transferred lymphocytes. We identify in female CD4 T cells stimulated with TRAMP-C2 a dominant MHC II-restricted response to the Y-chromosome antigen DBY. Furthermore, CD8 T cell responses in female lymphocytes to the immunodominant MHC I-restricted antigen SPAS-1 are markedly increased compared to male mice. Finally, we find no exacerbation of graft-versus-host disease in either syngeneic or minor-antigen mismatched allogeneic lymphocyte adoptive transfer models by using female into male versus male into male cells.This study shows that adoptively transferred female lymphocytes, particularly CD4 T cells, can control the outgrowth of pre-implanted prostatic adenocarcinoma cells. This approach does not significantly worsen graft-versus-host responses suggesting it may be viable in the clinic. Further, enhancing the available immune repertoire with female-derived T cells may provide an excellent pool of prostate cancer reactive T cells for further augmentation by combination with either vaccination or immune regulatory blockade strategies

Interleukin-22 Protects Intestinal Stem Cells from Immune-Mediated Tissue Damage and Regulates Sensitivity to Graft versus Host Disease

SummaryLittle is known about the maintenance of intestinal stem cells (ISCs) and progenitors during immune-mediated tissue damage or about the susceptibility of transplant recipients to tissue damage mediated by the donor immune system during graft versus host disease (GVHD). We demonstrate here that deficiency of recipient-derived IL-22 increased acute GVHD tissue damage and mortality, that ISCs were eliminated during GVHD, and that ISCs as well as their downstream progenitors expressed the IL-22 receptor. Intestinal IL-22 was produced after bone marrow transplant by IL-23-responsive innate lymphoid cells (ILCs) from the transplant recipients, and intestinal IL-22 increased in response to pretransplant conditioning. However, ILC frequency and IL-22 amounts were decreased by GVHD. Recipient IL-22 deficiency led to increased crypt apoptosis, depletion of ISCs, and loss of epithelial integrity. Our findings reveal IL-22 as a critical regulator of tissue sensitivity to GVHD and a protective factor for ISCs during inflammatory intestinal damage

Molecular Cause and Functional Impact of Altered Synaptic Lipid Signaling Due to a \u3cem\u3eprg-1\u3c/em\u3e Gene SNP

Loss of plasticity‐related gene 1 (PRG‐1), which regulates synaptic phospholipid signaling, leads to hyperexcitability via increased glutamate release altering excitation/inhibition (E/I) balance in cortical networks. A recently reported SNP in prg‐1 (R345T/mutPRG‐1) affects ~5 million European and US citizens in a monoallelic variant. Our studies show that this mutation leads to a loss‐of‐PRG‐1 function at the synapse due to its inability to control lysophosphatidic acid (LPA) levels via a cellular uptake mechanism which appears to depend on proper glycosylation altered by this SNP. PRG‐1+/− mice, which are animal correlates of human PRG‐1+/mut carriers, showed an altered cortical network function and stress‐related behavioral changes indicating altered resilience against psychiatric disorders. These could be reversed by modulation of phospholipid signaling via pharmacological inhibition of the LPA‐synthesizing molecule autotaxin. In line, EEG recordings in a human population‐based cohort revealed an E/I balance shift in monoallelic mutPRG‐1 carriers and an impaired sensory gating, which is regarded as an endophenotype of stress‐related mental disorders. Intervention into bioactive lipid signaling is thus a promising strategy to interfere with glutamate‐dependent symptoms in psychiatric diseases

NOD2 regulates hematopoietic cell function during graft-versus-host disease

Nucleotide-binding oligomerization domain 2 (NOD2) polymorphisms are independent risk factors for Crohn's disease and graft-versus-host disease (GVHD). In Crohn's disease, the proinflammatory state resulting from NOD2 mutations have been associated with a loss of antibacterial function of enterocytes such as paneth cells. NOD2 has not been studied in experimental allogeneic bone marrow transplantation (allo-BMT). Using chimeric recipients with NOD2−/− hematopoietic cells, we demonstrate that NOD2 deficiency in host hematopoietic cells exacerbates GVHD. We found that proliferation and activation of donor T cells was enhanced in NOD-deficient allo-BMT recipients, suggesting that NOD2 plays a role in the regulation of host antigen-presenting cells (APCs). Next, we used bone marrow chimeras in an experimental colitis model and observed again that NOD2 deficiency in the hematopoietic cells results in increased intestinal inflammation. We conclude that NOD2 regulates the development of GVHD through its inhibitory effect on host APC function

Mucus-degrading Bacteroides link carbapenems to aggravated graft-versus-host disease

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