Publications by authors named "Paszkiewicz G"

The formation of a flat and thin leaf presents a developmentally challenging problem, requiring intricate regulation of adaxial-abaxial (top-bottom) polarity. The patterning principles controlling the spatial arrangement of these domains during organ growth have remained unclear. Here we show that this regulation in Arabidopsis thaliana is achieved by an organ-autonomous Turing reaction-diffusion system centred on mobile small RNAs.

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Known concentrations of and were applied on gloves and gowns then sampled with E-swabs and BBL liquid Amies swabs. The mean numbers of colony-forming units per milliliter (CFU/mL) obtained from culture of the 2 swab types were not different, suggesting that either can be used for recovery of these two pathogens from personal protective equipment.

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Background: Clostridioides difficile is the most common cause of healthcare-associated infections in the United States. It is unknown whether universal gown and glove use in intensive care units (ICUs) decreases acquisition of C. difficile.

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Developmental boundaries play an important role in coordinating the growth and patterning of lateral organs. In plants, specification of dorsiventrality is critical to leaf morphogenesis. Despite its central importance, the mechanism by which leaf primordia acquire adaxial versus abaxial cell fates to establish dorsiventrality remains a topic of much debate.

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Article Synopsis
  • * The study explores the use of entolimod, a TLR5 agonist, and demonstrates that it protects liver and lung tissues from TNF and LPS-induced toxicity in mouse models, reducing indicators of tissue damage.
  • * Entolimod's protective effects rely on TLR5 expression in non-hematopoietic cells and do not interfere with TNF's anticancer effectiveness, suggesting TLR5 agonists could enhance cancer treatment safety by minimizing toxicity risks.
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FUSCA3 (FUS3) is a master regulator of seed development important in establishing and maintaining embryonic identity whose expression is tightly regulated at genetic and epigenetic levels. Despite this prominent role, the control of FUS3 expression remains poorly understood. Promoter and functional complementation analyses provided insight into the regulation of FUS3.

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Understanding the underlying reasons for tumor aggressiveness, such as why some tumors grow slowly and locally, while others rapidly progress to a lethal metastatic disease, is still limited. This is especially critical in breast cancer (BrCa) due to its high prevalence and also due to the possibility that it can be detected early. Several oncogenes and tumor suppressors have been identified and are used in the prognosis and treatment of BrCa.

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Although breast cancer (BrCa) may be detected at an early stage, there is a shortage of markers that predict tumor aggressiveness and a lack of targeted therapies. Histone chaperone FACT, expressed in a limited number of normal cells, is overexpressed in different types of cancer, including BrCa. Recently, we found that FACT expression in BrCa correlates with markers of aggressive BrCa, which prompted us to explore the consequences of FACT inhibition in BrCa cells with varying levels of FACT.

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Seed germination is a vital developmental transition for production of progeny by sexual reproduction in spermatophytes. Quiescent cells in nondormant dry embryos are reawakened first by imbibition and then by perception of germination triggers. Reanimated tissues enter into a germination program requiring energy for expansion growth.

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One of the most striking features of plant mitochondria when visualized in living tissue is their dynamism. The beauty of cytoplasmic streaming, driving, and being driven by the motility of mitochondria and other small organelles belies the complexity of the process. Equally, capturing that dynamism and investigating the genes, proteins, and mechanisms underpinning the processes using molecular cell biology and bioimaging is a complex process.

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TOR is involved in aging in a wide range of species from yeast to mammals. Here we show that, after overnight fasting, mTOR activity is higher in the livers of 28 months old female mice compared with middle-aged mice. Taken together with previous reports, our data predict that the life-extending effect of calorie restriction (CR) may be diminished, if CR is started in very old age.

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At a wide range of doses, rapamycin extends life span in mice. It was shown that intraperitoneal injections (i.p.

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Late embryogenesis abundant (LEA) proteins are hydrophilic, mostly intrinsically disordered proteins, which play major roles in desiccation tolerance. In Arabidopsis thaliana, 51 genes encoding LEA proteins clustered into nine families have been inventoried. To increase our understanding of the yet enigmatic functions of these gene families, we report the subcellular location of each protein.

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Recent discoveries have revealed the key role of mTOR (target of rapamycin) in aging. Furthermore, rapamycin extends lifespan in mice, especially in female mice. Here, we treated obese male mice on high-fat diet with rapamycin given intermittently: either weekly (once a week) or alternating bi-weekly (three injections every other week).

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Mammalian or mechanistic target of rapamycin (mTOR) is involved in growth, aging, and age-related diseases including cancer. There is an extensive cross talk between p53 and mTOR. In cell culture, p53 inhibits the mTOR pathway in a cell type-dependent manner.

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Males, who are bigger and stronger than females, live shorter in most species from flies to mammals including humans. Cellular mass growth is driven in part by mTOR (Target of Rapamycin). When developmental growth is completed, then, instead of growth, mTOR drives aging, manifested by increased cellular functions, such as hyper-secretion by fibroblasts, thus altering homeostasis, leading to age-related diseases and death.

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High doses of rapamycin, an antiaging agent, can prevent obesity in mice on high fat diet (HFD). Obesity is usually associated with hyperinsulinemia. Here, we showed that rapamycin given orally, at doses that did not affect weight gain in male mice on HFD, tended to decrease fasting insulin levels.

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TOR (Target of Rapamycin) pathway accelerates cellular and organismal aging. Similar to rapamycin, p53 can inhibit the mTOR pathway in some mammalian cells. Mice lacking one copy of p53 (p53+/- mice) have an increased cancer incidence and a shorter lifespan.

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Development of safe and effective tumor-preventive treatments for high-risk patient populations and therapies for early-stage cancer remains a critical need in oncology. We have recently discovered compound with anticancer activity, Curaxin-137, which modulates several important signaling pathways involved in even the very early stages of cancer. In tumor cells, Curaxin-137 inhibits NF-κB- and HSF1-dependent transcription (prosurvival pathways) and activates p53 (a proapoptotic pathway) without inducing DNA damage.

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The Facilitates Chromatin Transcription (FACT) chromatin remodeling complex, comprised of two subunits, SSRP1 and SPT16, is involved in transcription, replication and DNA repair. We recently showed that curaxins, small molecules with anti-cancer activity, target FACT and kill tumor cells in a FACT-dependent manner. We also found that FACT is overexpressed in human and mouse tumors and that tumor cells are sensitive to FACT downregulation.

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Chronic inflammation associated with cigarette smoke fosters malignant transformation and tumor cell proliferation and promotes certain nonneoplastic pulmonary diseases. The question arises as to whether chronic inflammation and/or colonization of the airway can be attributed, at least in part, to tobacco-associated microbes (bacteria, fungi, and spores) and/or microbial toxins (endotoxins and mycotoxins) in tobacco. To address this question, a literature search of documents in various databases was performed.

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Chronic inflammation contributes to the initiation and progression of tumors and tobacco smoke-associated inflammation is associated with malignant and certain non-neoplastic lung diseases. Reported herein are the results of an interpretative synthesis review of the literature assessing the inflammatory response of lung macrophages (MPhi) and epithelial cells to tobacco smoke as measured ex vivo. Papers were retrieved using Boolean operations from PubMed and Scopus.

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Background: Cigarettes are being marketed with filters that differ in composition and design. The filters have different toxicant trapping efficiencies, and smoking stains reflect variations in smoking behavior. Presented herein are the results of a structured literature review that was done to identify cigarette filter-based assays that may serve as proxies for mouth-level exposure and assessing smoking methods.

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Chronic inflammation that has been observed for malignant and non-neoplastic lung diseases of smokers has been attributed to the numerous and diverse particulate ('tar')-phase and gas-phase chemicals in mainstream smoke, most of which arise from the burning of tobacco. The primary cell-mediator of lung inflammation is the macrophage. Most probably, inflammation is promoted also from some of the more than 50 other cell types of the lung.

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Almost all cigarettes sold have a filter (United States, >98%; worldwide, >95%). In the last 25 years cigarette manufacturers have introduced diverse filters designed to reduce components in tobacco smoke. Today, there exists a need to establish assays to assess the efficacy of cigarette filters to retain total particulate matter (TPM), particularly unique filters of cigarettes that are being marketed as potential reduced exposure products (PREPs).

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