Non-Invasive Assessment of Skin Surface Proteins of Psoriasis Vulgaris Patients in Response to Biological Therapy.

Measurements of skin surface biomarkers have enormous value for the detailed assessment of skin conditions, both for clinical application and in skin care. The main goals of the current study were to assess whether expression patterns of skin surface hBD-1, hBD-2, IL-1α, CXCL-1, and CXCL-8, examples of proteins known to be involved in psoriasis pathology, are associated with disease severity and whether expression patterns of these proteins on the skin surface can be used to measure pharmacodynamic effects of biological therapy. In this observational study using transdermal analysis patch (TAP), levels of skin surface IL-1α, hBD-1, hBD-2, CXCL-1/2, and CXCL-8 of psoriasis vulgaris (PV) patients over biological therapy were assessed.

Protection of β2GPI Deficient Mice from Thrombosis Reflects a Defect in PAR3-facilitated Platelet Activation.

Background: Antibodies to β2-glycoprotein I (β2GPI) cause thrombosis in antiphospholipid syndrome, however the role of β2GPI itself in regulation of coagulation pathways is not well understood.

Methods: We developed β2GPI-deficient mice by deleting exon 2 and 3 of using CRISPR/Cas9 and compared the propensity of wild-type (WT) and mice to develop thrombosis using rose bengal and FeCl -induced carotid thrombosis, laser-induced cremaster arteriolar injury, and inferior vena cava (IVC) stasis models. We also compared tail bleeding times and assessed platelet activation in WT and mice in the absence and presence of exogenous β2GPI.

C1 inhibitor and prolylcarboxypeptidase modulate prekallikrein activation on endothelial cells.

Background: We examined how prekallikrein (PK) activation on human microvascular endothelial cells (HMVECs) is regulated by the ambient concentration of C1 inhibitor (C1INH) and prolylcarboxypeptidase (PRCP).

Objective: We sought to examine the specificity of PK activation on HMVECs by PRCP and the role of C1INH to regulate it, high-molecular-weight kininogen (HK) cleavage, and bradykinin (BK) liberation.

Methods: Investigations were performed on cultured HMVECs.

Vascular surgery patients with elevated neutrophil-to-lymphocyte ratios have downregulated neutrophil complement RNA expression.

Elevated neutrophil-to-lymphocyte ratio (NLR) in patients who undergo elective vascular surgery (EVS) have increased mortality independent of perioperative surgical outcome. To understand why high NLR is associated with higher mortality, we investigated neutrophil and lymphocyte transcriptome expression in patients undergoing EVS. Blood samples were collected from patients undergoing EVS and healthy donors for NLR calculation.

Polyphosphate expression by cancer cell extracellular vesicles mediates binding of factor XII and contact activation.

Extracellular vesicles (EV) have been implicated in diverse biological processes, including intracellular communication, transport of nucleic acids, and regulation of vascular function. Levels of EVs are elevated in cancer, and studies suggest that EV may stimulate thrombosis in patients with cancer through expression of tissue factor. However, limited data also implicate EV in the activation of the contact pathway of coagulation through activation of factor XII (FXII) to FXIIa.

Tunable Band-Edge Potentials and Charge Storage in Colloidal Tin-Doped Indium Oxide (ITO) Nanocrystals.

Degenerately doped metal-oxide nanocrystals (NCs) show localized surface plasmon resonances (LSPRs) that are tunable via their tunable excess charge-carrier densities. Modulation of excess charge carriers has also been used to control magnetism in colloidal doped metal-oxide NCs. The addition of excess delocalized conduction-band (CB) electrons can be achieved through aliovalent doping or by postsynthetic techniques such as electrochemistry or photodoping.

Case Report: Unmasked Inherited Dysfibrinogenemia After Everolimus Therapy.

A previously hemostatically asymptomatic patient with common variable hypogammaglobulinemia was given everolimus to prevent growth of her liver. Within several months, the patient developed a severe bleeding disorder. The bleeding was due to fibrin polymerization defect that upon sequencing was shown to be dysfibrinogenemia Krakow III.

Ponatinib treatment promotes arterial thrombosis and hyperactive platelets.

Ponatinib therapy heightens arterial thrombosis and platelet reactivity. Concurrent pioglitazone treatment reverses heightened thrombosis risk and platelet reactivity induced by ponatinib.

Factor XII Activation Promotes Platelet Consumption in the Presence of Bacterial-Type Long-Chain Polyphosphate In Vitro and In Vivo.

Objective- Terminal complications of bacterial sepsis include development of disseminated intravascular consumptive coagulopathy. Bacterial constituents, including long-chain polyphosphates (polyP), have been shown to activate the contact pathway of coagulation in plasma. Recent work shows that activation of the contact pathway in flowing whole blood promotes thrombin generation and platelet activation and consumption distal to thrombus formation ex vivo and in vivo.

Lithium and Sodium Ion Distributions in A[WI] Structures.

Ag[WI] and A[WI] compounds with A = Na, Li were prepared from binary tungsten iodides (WI) and corresponding metal iodides. Their crystal structures are analyzed on the basis of X-ray diffraction data. Li and Na solid-state NMR measurements reveal that Li and Na ions are distributed over two sites in the respective structures.

Factor XII and uPAR upregulate neutrophil functions to influence wound healing.

Coagulation factor XII (FXII) deficiency is associated with decreased neutrophil migration, but the mechanisms remain uncharacterized. Here, we examine how FXII contributes to the inflammatory response. In 2 models of sterile inflammation, FXII-deficient mice (F12-/-) had fewer neutrophils recruited than WT mice.

A Cross-sectional Study of KLKB1 and PRCP Polymorphisms in Patient Samples with Cardiovascular Disease.

Plasma kallikrein formed from prekallikrein (PK) produces bradykinin from kininogens and activates factor XII. Plasma PK is activated by factors αXIIa, βXIIa, or prolylcarboxypeptidase (PRCP). A cross-sectional investigation determined if there is an association of PRCP and KLKB1 polymorphisms with cardiovascular disease (CVD).

[The study of functional status in the perception of visual information depending on the method of technical color mixing on LCD and DLP projectors technology].

The case of compare two ways of projection color visual images, characterized by different spatial-temporal characteristics of visual stimuli, presents the methodology and the set of techniques. Received comparative data, identifying risks of regulation disorder of the functional state and development general, mental and visual fatigue during prolonged strenuous visual activity, according to two types of test tasks, which are the most typical for the use of modern projectors to work with the audience, both inthe process of implementation of learning technologies and the collective take responsible decisions by expert groups that control of complex technological processes.

Reduced thrombosis in Klkb1-/- mice is mediated by increased Mas receptor, prostacyclin, Sirt1, and KLF4 and decreased tissue factor.

The precise mechanism for reduced thrombosis in prekallikrein null mice (Klkb1(-/-)) is unknown. Klkb1(-/-) mice have delayed carotid artery occlusion times on the rose bengal and ferric chloride thrombosis models. Klkb1(-/-) plasmas have long-activated partial thromboplastin times and defective contact activation-induced thrombin generation that partially corrects upon prolonged incubation.

[Study of speech characteristics in hearing-impaired pilots for creation of voice-activated system operating airborne equipment].

Comparative experimental study covered speech characteristics in speakers with normal hearing and pilot speakers with neurosensory deafness. Evaluation criteria were duration, speech volume, spectral characteristics of words. Main difference of speach in pilot speakers with hearing disorders was higher variability of its characteristics.

[Labor physiology role in workers of different type labor activity workability and health. Progress and prospects].

There are presented the data of workers overstrain and fatigue conditions mechanisms based on physiological, psychological and ergonomic aspects of work processes in different types of activities (mental, visual-strained, physical). 15-year historical analysis, current state and prospects of labor physiology methods development are shown. Complex physiological and ergonomic investigations have allowed developing the measures of work ability raise and diseases prevention for workers various professions.

Prolylcarboxypeptidase promotes angiogenesis and vascular repair.

Prolylcarboxypeptidase (PRCP) is associated with leanness, hypertension, and thrombosis. PRCP-depleted mice have injured vessels with reduced Kruppel-like factor (KLF)2, KLF4, endothelial nitric oxide synthase (eNOS), and thrombomodulin. Does PRCP influence vessel growth, angiogenesis, and injury repair? PRCP depletion reduced endothelial cell growth, whereas transfection of hPRCP cDNA enhanced cell proliferation.

Domain 2 of uPAR regulates single-chain urokinase-mediated angiogenesis through β1-integrin and VEGFR2.

How single-chain urokinase (ScuPA) mediates angiogenesis is incompletely understood. ScuPA (≥4 nM) induces phosphorylated (p)ERK1/2 (MAPK44 and MAPK42) and pAkt (Ser(473)) in umbilical vein and dermal microvascular endothelial cells. Activation of pERK1/2 by ScuPA is blocked by PD-98059 or U-0126, and pAkt (Ser(473)) activation is inhibited by wortmannin or LY-294002.

Notch promotes vascular maturation by inducing integrin-mediated smooth muscle cell adhesion to the endothelial basement membrane.

Vascular development and angiogenesis initially depend on endothelial tip cell invasion, which is followed by a series of maturation steps, including lumen formation and recruitment of perivascular cells. Notch ligands expressed on the endothelium and their cognate receptors expressed on perivascular cells are involved in blood vessel maturation, though little is known regarding the Notch-dependent effectors that facilitate perivascular coverage of nascent vessels. Here, we report that vascular smooth muscle cell (VSMC) recognition of the Notch ligand Jagged1 on endothelial cells leads to expression of integrin αvβ3 on VSMCs.

Oxidative stress induces angiogenesis by activating TLR2 with novel endogenous ligands.

Reciprocity of inflammation, oxidative stress and neovascularization is emerging as an important mechanism underlying numerous processes from tissue healing and remodelling to cancer progression. Whereas the mechanism of hypoxia-driven angiogenesis is well understood, the link between inflammation-induced oxidation and de novo blood vessel growth remains obscure. Here we show that the end products of lipid oxidation, ω-(2-carboxyethyl)pyrrole (CEP) and other related pyrroles, are generated during inflammation and wound healing and accumulate at high levels in ageing tissues in mice and in highly vascularized tumours in both murine and human melanoma.

Genetic and epigenetic classifications define clinical phenotypes and determine patient outcomes in colorectal cancer.

Background: A molecular classification of colorectal cancer has been proposed based on microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and mutations in the KRAS and BRAF oncogenes. This study examined the prevalence of these molecular classes, and differences in clinical presentation and outcome.

Methods: Demographics, tumour characteristics and survival were recorded for 391 subjects with colorectal cancer.

No association between phosphatase and tensin homolog genetic polymorphisms and colon cancer.

Aim: To investigate the association between single nucleotide polymorphisms (SNPs) in the phosphatase and tensin homolog (PTEN) tumor suppressor gene and risk of colon cancer.

Methods: We utilized a population-based case-control study of incident colon cancer individuals (n = 421) and controls (n = 483) aged > or = 30 years to conduct a comprehensive tagSNP association analysis of the PTEN gene.

Results: None of the PTEN SNPs were statistically significantly associated with colon cancer when controlled for age, gender, and race, or when additionally adjusted for other known risk factors (P > 0.

No association between cyclooxygenase-2 and uridine diphosphate glucuronosyltransferase 1A6 genetic polymorphisms and colon cancer risk.

Aim: To investigate the association of variations in the cyclooxygenase-2 (COX2) and uridine diphosphate glucuronosyltransferase 1A6 (UGT1A6) genes and non-steroidal anti-inflammatory drugs (NSAIDs) use with risk of colon cancer.

Methods: NSAIDs, which are known to reduce the risk of colon cancer, act directly on COX2 and reduce its activity. Epidemiological studies have associated variations in the COX2 gene with colon cancer risk, but others were unable to replicate this finding.

A common 8q24 variant and the risk of colon cancer: a population-based case-control study.

Three recent studies identified common variants on 8q24 that confer modestly increased susceptibility to colorectal cancer. Here, we replicate the association in a population-based case-control study of colon cancer, including 561 cases and 721 unrelated controls. The rs6983267 marker was significantly associated with colon cancer risk.