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The interplay between host and pathogen is a complex co-evolutionary battle of surveillance and evasion. The pathogen continuously develops mechanisms to subvert the immune response in order to establish infection while the immune system responds with novel mechanisms of detection. Because the majority of Lyme disease pathology is due to an over-exuberant immune response, much research in Borrelia burgdorferi pathogenesis has been devoted to understanding the mammalian host response to the bacterium. Immunological studies continue to be an active area of research employing emerging techniques, such as intra-vital imaging. These studies have furthered our understanding of inflammatory processes during long-term infection and provided some surprising insights, such as the continued presence of bacterial products after clearance. The field of Lyme disease has long debated the etiology of long-term inflammation and recent studies in the murine host have shed light on relevant cell types and inflammatory mediators that participate in the pathology of Lyme arthritis. Live imaging and bioluminescent studies have allowed for a novel view of the bacterial life cycle, including the tick mid-gut, tick-to-mammal transmission and dissemination throughout a mouse. A number of tick and bacterial proteins have been shown to participate in the completion of the enzootic cycle. Novel mechanisms of gene regulation are continuously being identified. However, B. burgdorferi lacks many traditional virulence factors, such as toxins or specialized secretion systems. Many genes in the B. burgdorferi genome have no known homolog in other bacteria. Therefore, studies focusing on host-pathogen interactions have therefore been limited by an incomplete understanding of the repertoire of bacterial virulence factors. Questions such as how the pathogen causes disease, colonizes the tick and evades host immune-surveillance have been difficult to address. Genetic studies involving single gene deletions have identified a number of important bacterial proteins, but a large-scale genomics approach to identify virulence factors has not been attempted until recently. The generation of a site-directed mutagenesis library is an important step towards a detailed analysis of the B. burgdorferi genome and pathogenome. Using this library, high-throughput genomic studies, utilizing techniques such as massively parallel sequencing have been promising and could be used to identify novel virulence determinants of disease in the mammalian host or persistence in the tick vector. Continued research on this unique pathogen and its specific interaction with host and vector may have far reaching consequences and provide insights for diverse disciplines including ecology, infectious disease, and immunology. Here, several reviews will discuss the most recent advances and future studies to be undertaken in the field of B. burgdorferi biology.

Infectious Diseases --- Medicine --- Health & Biological Sciences --- Borrelia burgdorferi --- innate immunity --- adhesins --- Tnseq --- Eicosanoids --- Lyme Disease --- TLR --- c di GMP --- Ixodes scapularis --- Lyme Arthritis

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Dual specificity phosphatases (DUSPs) constitute a heterogeneous group of protein tyrosine phosphatases with the ability to dephosphorylate Ser/Thr and Tyr residues from proteins, as well as from other non-proteinaceous substrates including signaling lipids. DUSPs include, among others, MAP kinase (MAPK) phosphatases (MKPs) and small-size atypical DUSPs. MKPs are enzymes specialized in regulating the activity and subcellular location of MAPKs, whereas the function of small-size atypical DUSPs seems to be more diverse. DUSPs have emerged as key players in the regulation of cell growth, differentiation, stress response, and apoptosis. DUSPs regulate essential physiological processes, including immunity, neurobiology and metabolic homeostasis, and have been implicated in tumorigenesis, pathological inflammation and metabolic disorders. Accordingly, alterations in the expression or function of MKPs and small-size atypical DUSPs have consequences essential to human disease, making these enzymes potential biological markers and therapeutic targets. This Special Issue covers recent advances in the molecular mechanisms and biological functions of MKPs and small-size atypical DUSPs, and their relevance in human disease.

hematopoietic cells --- DEPArray --- n/a --- neuroblastoma --- liver steatosis --- MAPK phosphatase --- DUSP-4 --- granule neurons --- neuronal differentiation --- DUSP10 --- cytokines --- MAPKs --- single cell analysis --- macrophage --- asthma --- E. coli infection --- MAPK --- Cpp1 --- nucleotide receptors --- atypical DUSP --- RSV --- Pmp1 --- cannabinoids --- astrocytes --- sepsis --- influenza --- signaling --- triple-negative breast cancer (TNBC) --- differentiation --- HDAC6 (histone deacetylase isoform 6) --- atypical dual-specificity phosphatases --- microtubules --- respiratory viruses --- MK-STYX (MAPK (mitogen-activated protein kinase) phosphoserine/threonine/tyrosine-binding protein) --- dual-specificity phosphatase --- Msg5 --- TLR signaling --- mitogen-activated protein kinase --- fungal MKPs --- macrophages --- MAP Kinase Phosphatase-2 --- inflammation --- Sdp1 --- circulating tumor cells (CTCs) --- MAP kinases --- MAP kinase phosphatases --- P2X7 --- proliferation --- BDNF --- P2Y13 --- T cell --- hypertriglyceridemia --- integrated omics analysis --- post-translational modification --- rhinovirus --- protein stability --- ubiquitination --- dual-specificity phosphatases --- Mkp-1 --- cancer --- brain metastasis --- HER2 --- COPD --- pseudophosphatase

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Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of chronic kidney disease in the sequel. Whereas the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function—in both the short- and long-term—is urgently needed. This Special Issue includes papers investigating the pathological mechanisms of renal inflammation and AKI and diagnostics using new biomarkers. Furthermore, experimental in vitro and in vivo studies examining potential new approaches to attenuate kidney dysfunction are included, as well as review articles.

inflammation --- chronic kidney disease --- anemia --- anemia of inflammation --- ESA hyporesponsiveness --- renal tubular epithelial cells --- macrophages --- lipocalin-2 --- iron --- cilastatin --- hypoxia inducible factor-1-α --- ischemia-reperfusion injury --- acute kidney injury --- cyclophilin A --- fibrosis --- renal fibrosis --- tubular necrosis --- preeclampsia --- podocytes --- VEGF --- FSGS --- proteinuria --- endocan --- ESM-1 --- renal replacement therapy --- kidney transplantation --- biomarker --- diabetic nephropathy --- focal segmental glomerulosclerosis --- innate immunity --- membranous nephropathy --- minimal change diseases --- TLR --- NOX1 --- ML171 --- reactive oxygen species --- ERK --- T cells --- glomerulonephritis --- chemokines --- renal disease --- DJ-1 --- ND-13 --- renal inflammation --- oxidative stress --- UUO --- autophagy --- apoptosis --- trehalose --- simvastatin --- endotoxin --- tubular apoptosis --- cytochrome C --- Bcl-XL --- survivin --- hypercholesterolemia --- xanthine oxidase --- NF-κB pathway --- tertiary lymphoid organs --- B cells --- BAFF --- kidney fibrosis --- myofibroblast activation --- extracellular matrix --- Hippo pathway --- verteporfin --- IgAN --- CKD --- progression --- ACEI --- corticosteroids --- costimulation --- coinhibition --- kidney transplant --- SPR --- protein binding affinity --- adaptive immunity --- epithelial-to-mesenchymal transition --- E. cava extracts --- dieckol --- spontaneously hypertensive rats --- angiotensin II --- n/a

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Adipose tissue is a rich, ubiquitous, and easily accessible source for multipotent mesenchymal stromal/stem cells (MSCs), so-called adipose-derived stromal/stem cells (ASCs). Primary isolated ASCs are a heterogeneous preparation consisting of several subpopulations of stromal/stem and precursor cells. Donor-specific differences in ASC isolations and the lack of culture standardization hinder the comparison of results from different studies. Nevertheless, ASCs are already being used in different in vivo models and clinical trials to investigate their ability to improve tissue and organ regeneration. Many questions concerning their counterparts and biology in situ, their differentiation potential in vitro and in vivo, and the mechanisms of regeneration (paracrine effects, including regeneration-promoting factors and extracellular vesicles, differentiation, and immunomodulation) are not completely understood or remain unanswered. This Special Issue covers research articles investigating various adipose tissues as a source for ASC isolation, specific cultures methods to enhance proliferation or viability, and the differentiation capacity. Furthermore, other studies highlight aspects of various diseases, the immunosuppressive potential of ASCs and their derivates, or the in vivo tracking of transplanted ASCs. This edition is complemented by a review that summarizes the current knowledge of spheroid culture system methods and applications for mesenchymal stem cells.

lipomas --- adipose tissue --- stem cells --- adipogenesis --- osteogenesis --- mesenchymal stem cells --- T-cells --- conditioned medium --- extracellular vesicles --- TLR --- INF-γ --- adipose-derived stromal cells --- equine metabolic syndrome --- metformin --- adipose-derived stem cells --- adipocytes --- differentiation --- collagen I --- adiponectin --- integrins --- discoidin domain-containing receptor --- ageing --- subcutaneous fat --- adipose tissue-derived mesenchymal stromal/stem cells (ASCs) --- cell differentiation --- volatile organic compounds --- metabolic monitoring --- adipose-derived stromal/stem cells --- chondrogenesis --- colony forming unit-fibroblast --- fetal bovine serum --- human platelet lysate --- mesenchymal stem cell --- regenerative medicine --- human adipose-derived stem cells --- stem cell proliferation --- signaling pathway --- adipose-derived mesenchymal stem cells --- migration --- secretion --- primary cilium --- sonic hedgehog signaling --- mesenchymal stromal/stem cells --- perirenal --- fat --- characterization --- stimulation --- lipopolysaccharide --- cytokines --- cytomegalovirus --- angiogenesis --- adipose derived mesenchymal cells --- Histogel --- 3D cell culture --- spheroid culture --- biomaterials --- phenotype --- secretory potential --- ankylosing spondylitis --- systemic lupus erythematosus --- systemic sclerosis --- mesenchymal stromal cells --- breast cancer --- tumor microenvironment --- perineural invasion --- adipose derived stem cells --- valproic acid --- protein interactions --- MAPK pathway --- JAK/STAT pathway --- mesenchymal stromal cell --- tissue of origin --- prolonged culture --- epigenetic memory --- tracking --- bio imaging --- bioluminescence --- qRT-PCR --- Ataxia telangiectasia --- Atm --- n/a

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This book is a printed edition of the Special Issue entitled “Anticancer Agents: Design, Synthesis and Evaluation” that was published in Molecules. Two review articles and thirty research papers are included in the Special Issue. Three second-generation androgen receptor antagonists that have been approved by the U.S. FDA for the treatment of prostate cancer have been reviewed. Identification of mimics of protein partners as protein-protein interaction inhibitors via virtual screening has been summarized and discussed. Anticancer agents targeting various protein targets, including IGF-1R, Src, protein kinase, aromatase, HDAC, PARP, Toll-Like receptor, c-Met, PI3Kdelta, topoisomerase II, p53, and indoleamine 2,3-dioxygenase, have been explored. The analogs of three well-known tubulin-interacting natural products, paclitaxel, zampanolide, and colchicine, have been designed, synthesized, and evaluated. Several anticancer agents representing diverse chemical scaffolds were assessed in different kinds of cancer cell models. The capability of some anticancer agents to overcome the resistance to currently available drugs was also studied. In addition to looking into the in vitro ability of the anticancer agents to inhibit cancer cell proliferation, apoptosis, and cell cycle, in vivo antitumor efficacy in animal models and DFT were also investigated in some papers.

benzofurans --- chemical synthesis --- cytotoxic properties --- HeLa --- MOLT-4 --- K562 --- anticancer --- anti-neuroinflammation --- coumarin --- dihydroartemisinin --- flavonoids --- allene --- E-stereoselective --- regioselective --- anti-cancer activity --- cyanopyridone --- substituted pyridine --- pyridotriazine --- pyrazolopyridine --- thioxotriazopyridine --- anticancer activity --- HepG2 --- antitumor activity --- computational docking --- MDM2-p53 interaction --- xanthones --- yeast-based assays --- estrone derivatives --- hydrazine --- N-substituted pyrazoline --- anti-ovarian cancer --- topoisomerase II inhibitor --- kinase inhibitor --- antiproliferative agent --- urea --- synthesis --- antiproliferative activity --- apoptosis --- indoleamine 2,3-dioxygenase --- inhibitor --- anti-tumor --- immune modulation --- tryptophan metabolism --- taxoids --- βIII-tubulin --- P-glycoprotein --- drug resistance --- thiopene --- thienopyrimidinone --- thiazolidinone --- breast cancer --- benzofuran–pyrazole --- nanoparticles --- cytotoxic activity --- PARP-1 inhibition --- 3,6-dibromocarbazole --- 5-bromoindole --- carbazole --- actin --- migration --- Thienopyrimidine --- Pyrazole --- PI3Kα inhibitor --- quinazolin-4(3H)-one --- quinazolin-4(3H)-thione --- Schiff base --- antioxidant activity --- DFT study --- ortho-quinones --- beta-lapachone --- tanshione IIA --- PI3Ks --- PI3Kδ inhibitors --- 2H-benzo[e][1,2,4]thiadiazine 1,1-dioxide --- anticancer agents --- protein–protein interactions --- virtual screening --- mimetics --- drug discovery --- bivalency --- polyvalency --- antitumor --- cell cycle --- ovarian cancer --- P-MAPA --- IL-12 --- TLR signaling --- inflammation --- chemoresistance --- 4-(pyridin-4-yloxy)benzamide --- 1,2,3-triazole --- c-Met --- natural product --- anticancer agent --- zampanolide --- Talazoparib --- PARP inhibitor --- prodrug --- o-nitro-benzyl --- photoactivatable protecting groups --- salinomycin --- overcoming drug resistance --- tumor specificity --- synergy --- 5-fluorouracil --- gemcitabine --- amides/esters --- colchicine analogs --- thiocolchicine --- colchiceine --- antimitotic agents --- hydrates --- dihydropyranoindole --- HDAC inhibitors --- neuroblastoma --- aromatase --- MCF-7 --- NIH3T3 --- benzimidazole --- triazolothiadiazine --- docking --- ADME --- organosilicon compounds --- SILA-409 (Alis-409) --- SILA-421 (Alis-421) --- multidrug resistance (MDR) reversal --- ABCB1 (P-glycoprotein) --- colon cancer --- colchicine amide --- colchicine sulfonamide --- tubulin inhibitors --- docking studies --- crystal structure --- PROTACs --- protein degradation --- IGF-1R --- Src --- protein kinase --- phenylpyrazolopyrimidine --- enzyme inhibition --- molecular simulation --- androgen receptor --- prostate cancer --- enzalutamide --- apalutamide --- darolutamide --- triple-negative breast cancer --- cytotoxicity --- chrysin analogues --- flavonoid --- anticancer compounds