USP39 regulates pyruvate handling in non-small cell lung cancer.

The ubiquitin-specific peptidase 39 (USP39) belongs to the USP family of cysteine proteases representing the largest group of human deubiquitinases (DUBs). While the oncogenic function of USP39 has been investigated in various cancer types, its roles in non-small cell lung cancer (NSCLC) remain largely unknown. Here, by applying a gene set enrichment analysis (GSEA) on lung adenocarcinoma tissues and metabolite set enrichment analysis (MSEA) on NSCLC cells depleted of USP39, we identified a previously unknown link between USP39 and the metabolism in NSCLC cells.

Deubiquitinase USP9x regulates the proline biosynthesis pathway in non-small cell lung cancer.

Metabolic rewiring has been recognized as a hallmark of malignant transformation, supplying the biosynthetic and energetic demands for rapid cancer cell proliferation and tumor progression. A comprehensive understanding of the regulatory mechanisms governing these metabolic processes is still limited. Here, we identify the deubiquitinase ubiquitin-specific peptidase 9 X-linked (USP9x) as a positive regulator of the proline biosynthesis pathway in non-small cell lung cancer (NSCLC).

Ubiquitous Order-Disorder Transition in the Mn Antisite Sublattice of the (MnBiTe)(BiTe) Magnetic Topological Insulators.

Magnetic topological insulators (TIs) herald a wealth of applications in spin-based technologies, relying on the novel quantum phenomena provided by their topological properties. Particularly promising is the (MnBiTe)(BiTe) layered family of established intrinsic magnetic TIs that can flexibly realize various magnetic orders and topological states. High tunability of this material platform is enabled by manganese-pnictogen intermixing, whose amounts and distribution patterns are controlled by synthetic conditions.

Modeling of Intracellular Taurine Levels Associated with Ovarian Cancer Reveals Activation of p53, ERK, mTOR and DNA-Damage-Sensing-Dependent Cell Protection.

Taurine, a non-proteogenic amino acid and commonly used nutritional supplement, can protect various tissues from degeneration associated with the action of the DNA-damaging chemotherapeutic agent cisplatin. Whether and how taurine protects human ovarian cancer (OC) cells from DNA damage caused by cisplatin is not well understood. We found that OC ascites-derived cells contained significantly more intracellular taurine than cell culture-modeled OC.

Knockout validation of LAMP2A antibodies for immunostaining in human cancer cells.

LAMP2A is the rate-limiting factor of chaperone-mediated autophagy (CMA), a unique selective protein degradative pathway. To date LAMP2A antibodies are not knockout (KO)-validated in human cells. We have recently generated human isoform-specific LAMP2A KO cells, and here we assessed the specificity of select commercial LAMP2A antibodies on wild-type and LAMP2A KO human cancer cells.

Modeling of Intracellular Taurine Levels Associated with Ovarian Cancer Reveals Activation of p53, ERK, mTOR and DNA-damage-sensing-dependent Cell Protection.

Taurine, a non-proteogenic amino acid, and commonly used nutritional supplement can protect various tissues from degeneration associated with the action of the DNA-damaging chemotherapeutic agent cisplatin. Whether and how taurine protects human ovarian cancer (OC) cells from DNA damage caused by cisplatin is not well understood. We have found that OC ascites-derived cells contained significantly more intracellular taurine than cell cultures modeling OC.

Intermixing-Driven Surface and Bulk Ferromagnetism in the Quantum Anomalous Hall Candidate MnBi Te.

The recent realizations of the quantum anomalous Hall effect (QAHE) in MnBi Te and MnBi Te benchmark the (MnBi Te )(Bi Te ) family as a promising hotbed for further QAHE improvements. The family owes its potential to its ferromagnetically (FM) ordered MnBi Te septuple layers (SLs). However, the QAHE realization is complicated in MnBi Te and MnBi Te due to the substantial antiferromagnetic (AFM) coupling between the SLs.

Extraction of Metabolites from Cancer Cells.

Cancer cells possess an elevated demand for nutrients and metabolites due to their uncontrolled proliferation and need to survive in unfavorable conditions. Autophagy is a conservative degradation pathway that counters lack of nutrients and provides organelle and protein quality control, beyond maintenance of cellular metabolism.Mass spectrometry-based metabolomics is a powerful tool to study the metabolome of a cell.

A Method to Identify Potential Prognostic Markers Across Distinct Tumor Types.

The identification of novel biomarkers in cancer patients often requires both survival and gene expression analyses. The Kaplan-Meier survival analysis is one of the most common methods to assess the fraction of subjects living for a certain amount of time.Here, we describe a method for researchers to identify potential prognostic markers across distinct tumor types.

Approaches and Protocols to Analyze Autophagy and Its Role in Death of Apoptosis-Resistant Senescent Tumor Cells.

Anticancer therapy is complicated by the ability of malignant cells to activate cytoprotective autophagy that rescues treated cells. This protocol describes methods for analysis of autophagic process in apoptosis-resistant tumor cells treated with damaging agents. Induction of autophagy in these cells can activate apoptotic death.

Accumulation of storage proteins in plant seeds is mediated by amyloid formation.

Amyloids are protein aggregates with a highly ordered spatial structure giving them unique physicochemical properties. Different amyloids not only participate in the development of numerous incurable diseases but control vital functions in archaea, bacteria and eukarya. Plants are a poorly studied systematic group in the field of amyloid biology.

Challenging Europe: Technology, Environment, and the Quest for Resource Security.

Since the nineteenth century, access to and the development of natural resources became an important element of national and international politics. Resource security emerged as an issue vital to national security; and resource competition and crises gave rise to international tensions as well as to technological innovation and new modes of transnational cooperation.

Suppression of mTORC1 activity in senescent Ras-transformed cells neither restores autophagy nor abrogates apoptotic death caused by inhibition of MEK/ERK kinases.

Autophagy is conservative catabolic process that degrades organelles, in particular, mitochondria, and misfolded proteins within the lysosomes, thus maintaining cellular viability. Despite the close relationship between mitochondrial dysfunction and cellular senescence, it is unclear how mitochondria damage can induce autophagy in senescent cells. We show that MEK/ERK suppression induces mitochondria damage followed by apoptosis of senescent Ras-expressing cells.

A first Mn member in the struvite morphotropic series, CsMn(HO)(PO): hydrothermal synthesis, crystal structure and interconnections within the family of related phosphates.

Caesium manganese hexahydrate phosphate, CsMn(HO)(PO), was synthesized under hydrothermal conditions. Its crystal structure was determined from single-crystal X-ray diffraction data. The novel phase crystallizes in the hexagonal space group P6mc and represents the first manganese member in the struvite morphotropic series, AM(HO)(TO).

[Issues of Adipokine Regulation in Idiopathic Pulmonary Arterial Hypertension and Systemic Osteopenia].

Purpose: to determine the role of adipokines and vascular remodeling in formation of osteoporosis in idiopathic pulmonary arterial hypertension (IPAH).

Materials And Methods: Functional and hemodynamic parameters, bone mineral density (BMD) T-score in lumbar spine (LS) and femoral neck (FN), blood serum levels of leptin, adiponectin, visfatin and endothelin-1 were measured in 27 patients with severe IPAH and 30 healthy volunteers.

Results: Half of IPAH patients had osteoporosis.

Targeted elimination of senescent Ras-transformed cells by suppression of MEK/ERK pathway.

The Ras-Raf-MEK-ERK pathway plays a central role in tumorigenesis and is a target for anticancer therapy. The successful strategy based on the activation of cell death in Ras-expressing cells is associated with the suppression of kinases involved in Ras pathway. However, activation of cytoprotective autophagy overcomes antiproliferative effect of the inhibitors and develops drug resistance.

ROLE OF Wip1-p53 AXIS IN RESPONSE OF MURINE CELLS TO TREATMENT WITH SODIUM BUTYRATE AND MEK/ERK SIGNALLING PATHWAY INHIBITOR.

The use of histone deacetylase inhibitors and inhibitors of MEK/ERK-pathway is proposed as a novel potential approach in cancer treatment. Here we studied the effects of histone deacetylase inhibitor, sodium butyrate, and MEK/ERK-pathway inhibitor, PD0325901, on cells with modifications in genes involved in anti-cancer therapy response, Wip1 phosphatase and p53. We have investigated the effect of these agents on cell cycle of wild-type cells, Wip1 knockout cells and cells with double deletion of Wip1 and p53.

Adipokines: A Possible Contribution to Vascular and Bone Remodeling in Idiopathic Pulmonary Arterial Hypertension.

Osteoporosis is a major comorbidity of cardio-respiratory diseases, but the mechanistic links between pulmonary arterial hypertension and bone remain elusive. The purpose of the stud was to evaluate serum adipokines and endothelin-1 (ET-1) levels in the patients with idiopathic pulmonary arterial hypertension (IPAH) NYHA class III-IV and to determine its associations with bone mineral density (BMD). Pulmonary and hemodynamic parameters, BMD Z-scores at the lumbar spine (LS) and femoral neck (FN), serum leptin, adiponectin, visfatin and endothelin-1 (ET-1), were evaluated in 32 patients with IPAH NYHA class III-IV and 30 healthy volunteers.

Seeing the Forest and the Trees: Western Forestry Systems and Soviet Engineers, 1955-1964.

This article examines the transfer of technology from Finnish enterprises to Soviet industry during the USSR's period of technological modernization between 1955 and 1964. It centers on the forestry sector, which was a particular focus of modernization programs and a key area for the transfer of foreign techniques and expertise. The aim of the article is to investigate the role of trips made by Soviet specialists to foreign (primarily Finnish) enterprises in order to illustrate the nontechnological influences that occurred during the transfer of technologies across the cold war border.

[Role of vascular remodeling markers in the development of osteoporosis in idiopathic pulmonary arterial hypertension].

Aim: To define the role of circulating biomarkers for the metabolism of collagen and intercellular substance and vascular remodeling in the development of osteoporosis (OP) in idiopathic pulmonary arterial hypertension (IPAH).

Material And Methods: Functional hemodynamic parameters, bone mineral density (BMD) in the lumbar spine and femoral neck and the serum levels of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), MMP-9/TIMP-1 complex, C-terminal telopeptide of collagen type 1 (CITP), and endothelin-1 (ET-1) were determined in 27 high-risk IPAH patients and 30 healthy volunteers.

Results: OP in IPAH was detected in 50% of the examinees.

The Role of Tumor Necrosis Factor Alpha and TNF Superfamily Members in Bone Damage in Patients with End-Stage Chronic Obstructive Lung Disease Prior to Lung Transplantation.

A disequilibrium of tumor necrosis superfamily (TNF) members, including the serum osteoprotegerin, soluble receptor activator of nuclear factor-κB ligand, soluble TNF-related apoptosis-inducing ligand and TNF-α, was associated with the occurrence of a reduced skeletal mass and osteoporosis in male patients with end-stage chronic obstructive pulmonary disease (COPD). The purpose of this study was to explore the associations between serum biomarkers of tumor necrosis factor (TNF) superfamily and body and bone compositions in end-stage COPD males. Pulmonary function, T-score at the lumbar spine and femoral neck, lean mass, serum osteoprotegerin (OPG), soluble receptor activator of nuclear factor-κB ligand (sRANKL), TNF-α and its receptors (sTNFR-I, sTNFR-II) and soluble TNF-related apoptosis-inducing ligand (sTRAIL) levels were evaluated in 48 male patients with end-stage COPD and 36 healthy male volunteers.

Role of Osteoprotegerin and Receptor Activator of Nuclear Factor-κB Ligand in Bone Loss Related to Advanced Chronic Obstructive Pulmonary Disease.

Background: Osteoporosis is a common complication of chronic obstructive pulmonary disease (COPD). Recent clinical and biological researches have increasingly delineated the biomolecular pathways of bone metabolism regulation in COPD. We extended this work by examining the specific association and potential contribution of the osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL) axis to the pathogenesis of osteoporosis in advanced COPD.

[Therapy and Rehabilitation of Patients with Pulmonary Tuberculosis and Different Treatment Adherence].

The pulmonary tuberculosis process as dependent on the disease form and the therapy efficacy with the use of Cycloferon in the treatment scheme were investigated. The study had two stages. At the first stage the data concerning 358 patients with primary pulmonary tuberculosis and infiltration (93 patients) or degradation (89 patients) and 176 patients with pulmonary fibrocavernous tuberculosis were analysed.