Treatment of Escherichia coli contaminated water with different pulse-powered NTP configurations and analysis for post treatment efficacy.

A cost-effective and energy efficient method for water sterilization is a challenging demand in the present scenario where scarcity of pure water is rising. Non-Thermal Plasma (NTP) finds promising applications in environmental processes and has advantages over conventional water treatment methods. Escherichia coli contaminated water treatment using multiple pin plasma reactor and atmospheric pressure plasma jet reactor was undertaken in this work.

Long noncoding RNA uc.230/CUG-binding protein 1 axis sustains intestinal epithelial homeostasis and response to tissue injury.

Intestinal epithelial integrity is commonly disrupted in patients with critical disorders, but the exact underlying mechanisms are unclear. Long noncoding RNAs transcribed from ultraconserved regions (T-UCRs) control different cell functions and are involved in pathologies. Here, we investigated the role of T-UCRs in intestinal epithelial homeostasis and identified T-UCR uc.

Astrocyte-derived microparticles initiate a neuroinflammatory cycle due to carbon monoxide poisoning.

We hypothesized that carbon monoxide (CO) establishes an inflammatory cycle mediated by microparticles (MPs). Mice exposed to a CO protocol (1000 ​ppm for 40 ​min and then 3000 ​ppm for 20 ​min) that causes neuroinflammation exhibit NF-κB activation in astrocytes leading to generation of MPs expressing thrombospondin-1(TSP-1) that collect in deep cervical lymph nodes draining the brain glymphatic system. TSP-1 bearing MPs gain access to the blood stream where they activate neutrophils to generate a new family of MPs, and also stimulate endothelial cells as documented by leakage of intravenous 2000 ​kDa dextran.

HIV-1 Vpr-Induced Proinflammatory Response and Apoptosis Are Mediated through the Sur1-Trpm4 Channel in Astrocytes.

Successful treatment of HIV-infected patients with combinational antiretroviral therapies (cART) can now prolong patients' lives to nearly normal life spans. However, the new challenge faced by many of those HIV-infected patients is chronic neuroinflammation and neurotoxicity that often leads to HIV-associated neurocognitive disorders (HAND). However, the mechanism of neuropathogenesis underlying HAND, especially in those who are under cART, is not well understood.

Long Noncoding RNA uc.173 Promotes Renewal of the Intestinal Mucosa by Inducing Degradation of MicroRNA 195.

Background And Aims: The mammalian intestinal epithelium self-renews rapidly and homeostasis is preserved via tightly controlled mechanisms. Long noncoding RNAs transcribed from ultraconserved regions (T-UCRs) control different cell functions, but little is known about their role in maintaining the integrity of the intestinal epithelium. We searched for T-UCRs that regulate growth of the intestinal mucosa and investigated the mechanism by which T-UCR uc.

Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice.

Gene-associated with retinoid-interferon induced mortality-19 (GRIM-19), a STAT3-inhibitory protein, was isolated as a growth-suppressive gene product using a genome-wide expression knockdown screen. We and others have shown a loss of expression and occurrence of mutations in the GRIM-19 gene in a variety of primary human cancers, indicating its potential role as tumor suppressor. To help investigate its role in tumor development in vivo, we generated a genetically modified mouse in which Grim-19 can be conditionally inactivated.

GRIM-19 mutations fail to inhibit v-Src-induced oncogenesis.

The non-receptor tyrosine kinase Src is a major player in multiple physiological responses including growth, survival and differentiation. Overexpression and/or oncogenic mutation in the Src gene have been documented in human tumors. The v-Src protein is an oncogenic mutant of Src, which promotes cell survival, migration, invasion and division.

Tumor-derived mutations in the gene associated with retinoid interferon-induced mortality (GRIM-19) disrupt its anti-signal transducer and activator of transcription 3 (STAT3) activity and promote oncogenesis.

The signal transducer and activator of transcription 3 (STAT3) protein is critical for multiple cytokine and growth factor-induced biological responses in vivo. Its transcriptional activity is controlled by a transient phosphorylation of a critical tyrosine. Constitutive activation of STAT3 imparts resistance to apoptosis, promotes cell proliferation, and induces de novo micro-angiogenesis, three of the six cardinal hallmarks of a typical cancer cell.

Identification of a structural motif in the tumor-suppressive protein GRIM-19 required for its antitumor activity.

We have previously isolated GRIM-19, a novel growth suppressor, using a genetic method. GRIM-19 ablates cell growth by inhibiting the transcription factor signal transducer and activator of transcription 3 (STAT3). Up-regulation of STAT3 and growth promotion were observed in a number of human tumors.

GRIM-19 and p16(INK4a) synergistically regulate cell cycle progression and E2F1-responsive gene expression.

GRIM-19 (Gene associated with Retinoid-IFN-induced Mortality-19) was originally isolated as a growth suppressor in a genome-wide knockdown screen with antisense libraries. Like classical tumor suppressors, mutations, and/or loss of GRIM-19 expression occur in primary human tumors; and it is inactivated by viral gene products. Our search for potential GRIM-19-binding proteins, using mass spectrometry, that permit its antitumor actions led to the inhibitor of cyclin-dependent kinase 4, CDKN2A.

Cytokine-induced tumor suppressors: a GRIM story.

Cytokines belonging to the IFN family are potent growth suppressors. In a number of clinical and preclinical studies, vitamin A and its derivatives like retinoic acid (RA) have been shown to exert synergistic growth-suppressive effects on several tumor cells. We have employed a genome-wide expression-knockout approach to identify the genes critical for IFN/RA-induced growth suppression.

Down-regulation of GRIM-19 expression is associated with hyperactivation of STAT3-induced gene expression and tumor growth in human cervical cancers.

Cervical cancer is the most common malignant disease responsible for the deaths of a large number of women in the developing world. Although certain strains of human papillomavirus (HPV) have been identified as the cause of this disease, events that lead to formation of malignant tumors are not fully clear. STAT3 is a major oncogenic transcription factor involved in the development and progression of a number of human tumors.

GRIM-19 inhibits v-Src-induced cell motility by interfering with cytoskeletal restructuring.

GRIM-19 (Gene associated with Retinoid-Interferon-induced Mortality 19) is a novel tumor suppressor regulated by interferon/retinoid combination. We have recently shown that GRIM-19 inhibits v-Src-induced oncogenic transformation and metastatic behavior of cells. Oncogenic v-Src induces cell motility by cytoskeletal remodeling, especially the formation of podosomes and.

GRIM-19: A Double-edged Sword that Regulates Anti-Tumor and Innate Immune Responses.

Gene associated with retinoid-interferon-β-induced mortality (GRIM)-19, was originally identified as a critical regulatory protein necessary for Interferon-β-Retinoic acid-induced cell death. Overexpression of GRIM-19 activates cell death and its suppression or inactivation promotes cell growth. GRIM-19 targets multiple proteins/pathways for exerting growth control and cell death.

Tumor suppressive protein gene associated with retinoid-interferon-induced mortality (GRIM)-19 inhibits src-induced oncogenic transformation at multiple levels.

Interferons (IFNs) inhibit the growth of infectious pathogens and tumor development. Although IFNs are potent tumor suppressors, they modestly inhibit the growth of some human solid tumors. Their weak activity against such tumors is augmented by co-treatment with differentiation-inducing agents such as retinoids.

Tumor-suppressive activity of the cell death activator GRIM-19 on a constitutively active signal transducer and activator of transcription 3.

Signal transducers and activators of transcription 3 (STAT3) was originally identified as a transcription factor that mediates cytokine-induced responses. In these pathways, Janus-activated kinase (JAK)-induced transient tyrosine phosphorylation of STAT3 promotes gene expression in response to a number of cytokines, which is inhibited by feedback mechanisms. A number of studies have shown that STAT3 is constitutively activated in human cancer cells, leading to cell proliferation.

The IFN-beta and retinoic acid-induced cell death regulator GRIM-19 is upregulated during focal cerebral ischemia.

The induction of GRIM-19 has been shown to be essential for interferon-beta (IFN-beta)-induced and retinoic acid (RA)-induced tumor cell death. We have studied the localization and levels of GRIM-19 in IFN/RA-induced cell death in neural cells and in focal cerebral ischemia. Exposure to IFN/RA caused a approximately 15-fold increase in GRIM-19 protein levels and induced >50% cell death in human neuroblastoma SH-SY5Y cells.

GRIM-19 associates with the serine protease HtrA2 for promoting cell death.

We have isolated a novel interferon (IFN)-retinoid regulated cell death regulatory protein genes associated with retinoid-IFN-induced mortality (GRIM)-19 earlier. To understand its mechanism of action, we have employed a yeast-two-hybrid screen and identified serine protease HtrA2 as its binding partner. GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner.

Ophthalmoscopic and morphogenetic changes in rat lens induced by galactose: attenuation by pyruvate.

Background: Investigations have been conducted on the potential of pyruvate, a normal tissue metabolite, in the prevention of cataract formation.

Methods: Cataract was induced by maintaining young rats on a diet containing 30% galactose. The progress of cataract was monitored by visual inspection and ophthalmoscopic and slit-lamp examinations.