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Trichomes are specialized epidermal cells that play multiple roles in plant development. However, knowledge about the molecular mechanism of trichome development in rice is limited. In this study, a hairy leaf locus HL6 SWWR of rice variety Suwangwanger (SWWR) was identified by map-based cloning. Transgenic complementation and knock-out mutation demonstrated that HL6 SWWR regulated trichomes on leaves and expression levels of HL6 SWWR affected trichome elongation. Transgenic experiments of PRO SWWR :HL6 NIP and PRO NIP :HL6 SWWR indicated that the promoter and coding sequences of HL6 SWWR were indispensable for trichome regulation. Sequencing alignment of the promoter and coding regions of HL6 in 22 varieties showed that some cis -binding elements in the promoter region may be related to trichome development, while no decisive variation was found in the coding sequence. Furthermore, RNA-sequencing analysis revealed that 1 415 differential expression genes (DEGs) were detected in hl6 SWWR mutant vs wild type and that 1 010 DEGs were found in HL6 SWWR complementary transgenic line vs wild type. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that most of the DEGs were involved in metabolite pathway, secondary metabolite biosynthesis, plant pathogen interaction and phytohormone signal transduction in both the two groups. The results indicated that these enhanced pathways are critical during trichome development in rice. Taken together, our results provided new views into the regulatory mechanism of trichome formation in rice. [ABSTRACT FROM AUTHOR]

The mechanisms modulated by periodontal pathogens in atherosclerosis are not fully understood. Aim: to perform an integrative analysis of gene and protein expression modulated by periodontal pathogens in cells and animal models for atherosclerosis. Cochrane, PRISMA and AMSTAR2 guidelines for systematic reviews were followed. Data search was conducted in Pub-med, LILACS and Science Direct databases. Gene and protein expression data were collected from the included papers to perform an overrepresentation analysis using the Reactome Pathway Analysis tool and the KEGG database. Thirty-two papers were included in the review, they analyzed the effect of Fusobacterium nucleatum , Porphyromonas gingivalis , Streptococcus anginosus , Streptococcus sanguinis , Tannerella forsythia , and Treponema denticola or/and their virulent factors on gene and protein expression in human cells and animal models of atherosclerosis. Some of the modulated pathways include the immune system, programmed cell death, cellular responses to external stimuli, transport of small molecules, and signal transduction (p < 0.05). Those pathways are known to be involved in different stages of atherosclerosis progression. Based on the performed analysis, it is possible to state that periodontal pathogens have the potential to be a contributing factor for atherosclerosis even in absence of a high-fat diet or high shear stress. [ABSTRACT FROM AUTHOR]

Immunotherapy has become the cornerstone of current malignant tumor treatment. However, the response of different patients to immunotherapy is highly heterogeneous, and not all patients can benefit from it. There is an urgent need to find biomarkers that can effectively predict the efficacy of immunotherapy. C-C chemokine ligand 4 (CCL4) is a cytokine, belonging to the inflammatory CCL subfamily. It is mainly secreted by immune cells and tumor cells and shows low or no expression in normal tissues but abnormally high expression in various malignant tumor tissues. After binding to CCL4 and its receptor C-C chemokine receptor type 5 (CCR5), it can recruit and mediate immune cell migration, destroy the stability of the tumor microenvironment (TME), participate in carcinogenesis and promote the development of tumors. In the tumor immune microenvironment, CCL4 can mediate and recruit the directed migration of key immune cells such as monocytes, macrophages, natural killer (NK) cells, and T cells, which makes it a potentially important element affecting the efficacy of immunotherapy and has specific value. This paper reviews the research progresses of CCL4's effects on immune escape in TME, in order to provide clues and references for basic research and clinical diagnosis and treatment. [ABSTRACT FROM AUTHOR]

CGK733 was reported as a compound that inhibited ATM/ATR kinase activities and blocked their checkpoint signaling pathways with great selectivity. However, this paper was subsequently retracted, and the truth about the activity of CGK733 remains unclear. We synthesized various analogs of CGK733 with a modification of the carboxylic acid moiety and/or the aniline derivative moiety to accumulate knowledge of the structure-activity relationship of this compound. Growth inhibitory activity of CGK733 and novel 35 analogs against HeLa S3 cells was evaluated, and the structure-activity relationship revealed that analogs with the 2-naphthyl or 4-fluorophenyl group instead of the benzhydryl group have activity comparable to CGK733 and that the 3-nitro group on the aniline moiety significantly affects the activity. [ABSTRACT FROM AUTHOR]

The regulation of the cell cycle is essential for maintaining normal cellular function, especially in the development of diseases such as lung cancer. The cell cycle consists of four major phases (G1, S, G2 and M phases), which are characterized by a series of precise molecular events to ensure proper cell proliferation and division. In lung cancer cells, cell cycle dysregulation can lead to disordered proliferation and increased invasiveness of cancer cells. G2 and S-phase expressed 1 (GTSE1) is a regulatory protein found in the cytoplasm of the cell, which plays a key role in the cell cycle distribution of a wide range of cancer cells and is involved in life processes such as cell proliferation and apoptosis. GTSE1 affects cell cycle progression by interacting with cyclin-dependent kinase inhibitor 1A (p21) and maintaining the stability of p21, which in turn inhibits the activity of cyclin-dependent kinase 1/2 (CDK1/2). In addition, GTSE1 is also involved in the regulation of tumor protein 53 (p53) signaling pathway. With the assistance of mouse double minute 2 homolog (MDM2), GTSE1 is able to transport p53 from the nucleus to the cytoplasm and promote its ubiquitination and degradation, thus affecting cell cycle and cell deathrelated signaling pathways. This paper reviews the expression of GTSE1 in lung cancer cells and its effects on lung cancer, as well as its potential mechanisms involved in cell cycle regulation. [ABSTRACT FROM AUTHOR]

Brain-derived neurotrophic factor (BDNF) is a crucial neurotrophic factor adding to neurons' development and endurance. The amount of BDNF present in the brain determines susceptibility to various neurodegenerative diseases. In Alzheimer's disease (AD), often it is seen that low levels of BDNF are present, which primarily contributes to cognition deficit by regulating long-term potentiation (LTP) and synaptic plasticity. Molecular mechanisms underlying the synthesis, storage and release of BDNF are widely studied. New molecules are found, which contribute to the signal transduction pathway. Two important receptors of BDNF are TrkB and p75NTR. When BDNF binds to the TrkB receptor, it activates three main signalling pathways-phospholipase C, MAPK/ERK, PI3/AKT. BDNF holds an imperative part in LTP and dendritic development, which are essential for memory formation. BDNF supports synaptic integrity by influencing LTP and LTD. This action is conducted by modulating the glutamate receptors; AMPA and NMDA. This review paper discusses the aforesaid points along with inducers of BDNF. Drugs and herbals promote neuroprotection by increasing the hippocampus' BDNF level in various disease-induced animal models for neurodegeneration. Advancement in finding pertinent molecules contributing to the BDNF signalling pathway has been discussed, along with the areas that require further research and study. [ABSTRACT FROM AUTHOR]

Copyright of Revista Brasileira de Medicina do Esporte is the property of Redprint Editora Ltda. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

As an indispensable component of the extracellular matrix, perlecan (Pln) plays an essential role in cartilaginous tissue function. Although there exist studies suggesting that Pln expressed by cartilaginous tissues is critical for chondrogenesis, few papers have discussed the potential impact Pln may have on cartilage regeneration. In this review, we delineate Pln structure, biomechanical properties, and interactive ligands—which together contribute to the effect Pln has on cartilaginous tissue development. We also review how the signaling pathways of Pln affect cartilage development and scrutinize the potential application of Pln to divisions of cartilage regeneration, spanning vascularization, stem cell differentiation, and biomaterial improvement. The aim of this review is to deepen our understanding of the spatial and temporal interactions that occur between Pln and cartilaginous tissue and ultimately apply Pln in scaffold design to improve cell-based cartilage engineering and regeneration. As a key component of the basement membrane, Pln plays a critical role in tissue development and repair. Recent findings suggest that Pln existing in the pericellular matrix surrounding mature chondrocytes is actively involved in cartilage regeneration and functionality. We propose that Pln is essential to developing an in vitro matrix niche within biological scaffolds for cartilage tissue engineering. Perlecan's potential application in cartilage regeneration. [Display omitted] [ABSTRACT FROM AUTHOR]

Eccentric exercise training is effective for increasing muscle mass and strength, and improving insulin sensitivity and blood lipid profiles. However, potential muscle damage symptoms such as prolonged loss of muscle function and delayed onset of muscle soreness may restrict the use of eccentric exercise, especially in clinical populations. Therefore, strategies to reduce eccentric exercise-induced muscle damage (EIMD) are necessary, and an extensive number of scientific studies have tried to identify potential intervention modalities to perform eccentric exercises without adverse effects. The present paper is based on a narrative review of current literature, and provides a novel hypothesis by which an ischemic preconditioning (IPC) of the extremities may reduce EIMD. IPC consists of an intermittent application of short-time non-lethal ischemia to an extremity (e.g. using a tourniquet) followed by reperfusion and was discovered in clinical settings in an attempt to minimize inflammatory responses induced by ischemia and ischemia-reperfusion-injury (I/R-Injury) during surgery. The present hypothesis is based on morphological and biochemical similarities in the pathophysiology of skeletal muscle damage during clinical surgery and EIMD. Even though the primary origin of stress differs between I/R-Injury and EIMD, subsequent cellular alterations characterized by an intracellular accumulation of Ca2+, an increased production of reactive oxygen species or increased apoptotic signaling are essential elements for both. Moreover, the incipient immune response appears to be similar in I/R-Injury and EIMD, which is indicated by an infiltration of leukocytes into the damaged soft-tissue. Thus far, IPC is considered as a potential intervention strategy in the area of cardiovascular or orthopedic surgery and provides significant impact on soft-tissue protection and downregulation of undesired excessive inflammation induced by I/R-Injury. Based on the known major impact of IPC on skeletal muscle physiology and immunology, the present paper aims to illustrate the potential protective effects of IPC on EIMD by discussing possible underlying mechanisms. [ABSTRACT FROM AUTHOR]

Surgery is currently the most appropriate treatment for early-stage non-small cell lung cancer (NSCLC). Increasing unilateral or bilateral multiple primary lung cancer being found, segmentectomy has attracted wide attention for its unique advantages in the treatment for such tumors. Ground glass opacity dominant early-stage NSCLC is associated with a good prognosis and can be cured by segmentectomy, however, the treatment of solid-dominant NSCLC remains controversial owing to the invasive nature. With the in-depth study on the lymph node metastasis pathway, radiological characteristics and molecular biology of NSCLC, a large part of solid nodules with certain characteristics can also be cured by segmentectomy. This paper reviews the research status and progress about the indication of segmentectomy. [ABSTRACT FROM AUTHOR]

The biological effects of low frequency magnetic fields (LF MF) at high flux densities are well known and the underlying mechanism is established. In contrast, health associated effects at lower flux densities, which can be found in the human environment, are controversial, and no accepted interaction mechanism has been presented. Here we present a hypothesis regarding the biological aspect of interaction between LF MF and cells. We suggest that the endoplasmic reticulum (ER) membrane protein STIM1, which functions as a sensor for several cellular conditions (low Ca2+ levels, temperature increase, increased levels of oxygen radicals, hypoxia), is a candidate LF MF sensor. Such a sensor function can be either direct (via local temperature increase caused by intracellularly induced electric fields), or indirect due to responses to increased reactive oxygen species (ROS) levels. Activated STIM1 leads to downstream effects by activation of signal transduction processes and changes in gene expression leading to secondary events. The nature of these changes would be dependent on both cell type and the particular physiological state the cell displays at the time of STIM1 activation. Results from testing of this hypothesis, as suggested in this paper, would greatly assist in understanding of the possible health-related effects of low-level LF MF. This would benefit both safety assessments regarding MF exposure as well as possible use of MF in medicine. A better understanding of the biological mechanisms underpinning MF exposure effects of living matter allows the targeted use of the fields in medical applications. There are several examples already in use based on empiric and not on mechanistic knowledge. Knowledge generated from our hypothesis testing makes it possible for MF based medical applications to be optimized. [ABSTRACT FROM AUTHOR]

The epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) and programmed death receptor 1 (PD-1)/programmed death ligand 1 (PD-L1) immune checkpoint inhibitors were landmarks in the treatment of non-small cell lung cancer (NSCLC). However, the regulation mechanisms of PD-L1 expression were not fully clear in NSCLC patients with EGFR mutations. Multiple signaling pathways may be involved in the tumorigenesis regulation. This paper summarized and reviewed the potential EGFR mutations impacting on PD-L1 expression with aims to the development of strategies on immunochemical therapy for NSCLC. [ABSTRACT FROM AUTHOR]

Experiments have demonstrated that signals in nerve fibers are composed by electrical and mechanical components. In this paper a coupled mathematical model is described which unites the governing equations for the action potential, the pressure wave in the axoplasm and the longitudinal and the transverse waves in the surrounding biomembrane into one system of equations. As a solution of this system, an ensemble of waves is generated. The main hypotheses of such a model are related to the nature of coupling forces between the single waves in the ensemble. These coupling forces are assumed to have bi-polar shapes leading to energetically stable solutions. The in silico modeling demonstrates the qualitative resemblance of computed wave profiles to experimental ones. The ideas of possible experimental validation of the model are briefly described. [ABSTRACT FROM AUTHOR]

The article focuses on the topic of contemporary commercial music (CCM), discussing its comparison with music theater. It reports that music theaterpedagogy is considered synonymous with the CCM pedagogy. It informs on the origin of CCM as research paper by Edrie Means and Jeanette LoVetri. CCM hods the controversy of surrounding the word 'commercial', its need of individualized attention and technique considerations.

Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The third-generation EGFR-TKIs has been approved to overcome the EGFR T790M mutation in patients resistant to the first-or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. Unfortunately, acquired resistance inevitably develops after application of approximately 10 months. Heterogeneities of the tumor determines the diversity of resistance. Mechanisms of resistance to the third-generation TKIs includs EGFR-dependent pathway (such as new EGFR mutations, T790M reduction/disappearance and EGFR amplification, etc.) and EGFR-independent pathway (such as bypass pathway activation and histological transformation, etc.). In this paper, we reviewed principle mechanisms of acquired resistance to third-generation EGFR-TKIs. [ABSTRACT FROM AUTHOR]

Professional organizations for academics such as the Academy of Management and Association for Information Systems (AIS) create best publications awards to honour and promote exemplary contributions that align with the core values and priorities of their distinct fields. Despite the strategic importance of awards, researchers rarely investigate meaningful patterns implicit in the contribution characteristics of award-winning articles. We conduct a reconstructive study of the 10-year history of the AIS Best Publications Awards by outlining a framework that reveals contribution characteristics, demographic patterns, and citation histories of the award-winning articles. Comparing the AIS results to a complete sample of MIS Quarterly paper-of-the-year articles (1993–2015) demonstrates consistent patterns implicit in IS articles that win best publications awards. We develop a model that explains both how these awards shape patterns and discusses what changes might be needed as the field confronts new realities. Our analyses reinforce the importance of taking strategic actions to support the continuous development of the field and advance literature on change and evolving trends in academic fields. [ABSTRACT FROM AUTHOR]

The crystalline lens appears to be a simple organ with the sole role of focusing light upon the retina. However, numerous studies have underscored its dynamic nature with a host of compartmentalized physiological processes. As the individual ages, the normal lens develops two inescapable processes, presbyopia and cataracts. Yet, to date, there is no uniform explanation for presbyopia and many factors have been proposed as contributors including continuous enlargement of the lens, loss of power of the ciliary muscle and hardening of the lens fibers. Proposed explanations are incomplete and need experimental confirmation. This paper analyzes the possible causes for presbyopia and proposes a new one for it: a decrease in the permeability of aquaporin zero (AQP-0) also known as major intrinsic protein (MIP). Based on original findings of our laboratory, this paper proposes that a fluid flow exists inside the avascular lens. This fluid enters and leaves the lens during the accommodation process. We believe that for this to occur the lens utilizes the permeability of aquaporin zero which is abundant in the membrane of the fiber cells. Volume change due to fluid traversing the surface of the lens occurs during accommodation. We present the hypothesis that increasing the permeability of AQP-0 would facilitate accommodation. Therefore, defects in AQP-0 permeability may be a cause for presbyopia. We would also like to propose that it is possible to visualize and measure the fluid volume lost during un-accommodation and determine if the fluid is lost across the anterior, posterior or both surfaces. An age-related loss in lens water permeability could reduce fluid fluxes during the shape changes of accommodation potentially contributing to presbyopia. [ABSTRACT FROM AUTHOR]

Rapid re-endothelialization following balloon angioplasty can reduce restenosis by inhibiting smooth muscle cell migration and proliferation. However, formation of a neointima layer following angioplasty can be inhibited due to endothelial cell dysfunction and denudation. In a companion paper, it has been illustrated that mechanical loading causes a decrease in DNA synthesis in bovine aortic endothelial cells (BAECs) thus rendering them dysfunctional. The purpose of this study was to overcome BAEC dysfunction by incubation with pharmacological agents to increase DNA synthesis. Previous studies demonstrated that the adenosine dinucleotides Ap4A and Ap2A induced nitric oxide (NO) production from BAEC while Ap3A, Ap5A and Ap6A did not. This paper demonstrates that Ap4A and Ap2A induce a 1.46- and 1.16-fold increase in DNA synthesis in mechanically stressed BAECs respectively, while Ap3A, Ap5A and Ap6A do not. Additionally, NOC-18, a slow NO release NO donor, significantly increases DNA synthesis in mechanically stressed BAECs without affecting unloaded cells. These results are consistent with NO inducing DNA synthesis in mechanically stressed BAECs. [ABSTRACT FROM AUTHOR]

Rapid re-endothelialization following balloon angioplasty can reduce restenosis by inhibiting smooth muscle cell migration and proliferation. However, formation of a neointima following angioplasty can be inhibited due to endothelial cell dysfunction and denudation. The purpose of this study was to evaluate mechanical tensile stress as a cause of endothelial cell dysfunction. The Flexercell strain unit was utilized to generate both short-term cyclic and static tensile strain on cultured bovine aortic endothelial cells (BAECs). Before analysis of this loading on BAECs, strain behaviour of the Flexercell system and DNA assay conditions were optimized. This paper demonstrates that, when compared with unloaded controls, 4-h cyclic loading at 4 per cent elongation and 0.1 Hz, and static loading at 4 per cent elongation cause a 44 and 70 per cent decrease in DNA synthesis respectively. In a companion paper, it is demonstrated that low DNA synthesis levels in mechanically loaded cells can be increased by incubation with Ap4A and/or NO donors. [ABSTRACT FROM AUTHOR]

Recently, accidental spills of heavy oil have caused adverse effects in marine organisms. Oil pollution can induce damages on development and reproduction, linking with detrimental effects on diverse molecular levels of genes and proteins in plankton and fish. However, most information was mainly focused on marine vertebrates and consequently, limited information was available in marine invertebrates. Furthermore, there is still a lack of knowledge bridging in vivo endpoints with the functional regulation of cytochrome P450 ( CYP ) genes in response to oil spill pollution in marine invertebrates. In this paper, adverse effects of oil spill pollution in marine invertebrates are summarized with the importance of CYP genes as a potential biomarker, applying for environmental monitoring to detect oil spill using marine copepods. [ABSTRACT FROM AUTHOR]

Due to the advantages of low transmit power consumption, high spectral efficiency and extended system coverage, Device-to-Device (D2D) communication has drawn explosive attention in wireless communication field. Considering that intra-cell interference caused between cellular signals and D2D signals, in this paper, a network coding-based D2D relay cooperative transmission algorithm is proposed. Under D2D single-hop relay transmission mode, cellular interfering signals can be regarded as useful signals to code with D2D signals at D2D relay node. Using cellular interfering signals and network coded signals, D2D receiver restores the D2D signals to achieve the effect of interference suppression. Theoretical analysis shows that, compared with Amplify-and-forward (AF) mode and Decode-and-forward (DF) mode, the proposed algorithm can dramatically increase the link achievable rate. Furthermore, simulation experiment verifies that by employing the proposed algorithm, the interference signals in D2D communication can be eliminated effectively, and meanwhile the symbol error rate (SER) performance can be improved. [ABSTRACT FROM AUTHOR]

During the past decade, neural interfaces have attracted great interest due to their potential of body-machine communication for disease diagnosis and therapy. Considering the significant material mismatch between the electrode implants and the native tissue, a thin coating is employed on the electrode sites as an intermediate layer to bridge the material differences and has been proved to play an important role in the promotion of neural cell attachment and signal transmission. Micro- and nanostructured coating materials, together with surface functionalization such as biological cues, provide not only high surface areas for signal transduction but also a biomimetic platform for the cells. In this paper, we review the performance of different kinds of micro- and nanostructured coating materials including metallic materials, carbon materials, conducting polymeric materials and composite materials and then complement the discussion with the influence of the fabrication process on the performance of the coatings. The coating could be functionalized by various advanced techniques, which are also reviewed. The existing challenge and future research directions of electrode coatings are briefly discussed at the end of the review. [ABSTRACT FROM AUTHOR]

Nanomedicine is revolutionizing current methods for diagnosing, treatment and prevention of diseases with the integration of molecular biology, biotechnology as well as nanotechnology for sensing and actuation capabilities at the molecular scale using nanoscale devices, namely nanomachines. While numerous examples of these applications have been tested in vivo , the real deployments are far from reality. Limitations in controlling, monitoring, miniaturization, and computing inhibit access and manipulation of information at the nano-scale. Integrating communication and networking functionalities provide new opportunities for such challenges with the newly introduced Molecular Communications. These natural communication systems are found with plurality inside the human body. The current challenge is to utilize these natural systems to create artificial biocompatible communication networks that can interconnect multiple nanomachines in multiple parts of the body and connected to the cloud, is defined as the Internet of Bio-Nano Things ( IoBNT ). Nanonetworks inside cellular tissues perform communication using a signaling process such as Ca 2+ . This specifically signaling process is very important for many regulatory functions in tissues and its control and communication is crucial to allow nanomedicine capabilities towards diagnosis and treatments of diseases at the nano-scale. This paper presents a review of techniques that enable the design of the Ca 2+ -signaling-based molecular communication system for cellular tissues, essential tools for its deployment, application and, lastly, the research future direction in this field. In the end, one must acquire the sufficient knowledge to understand both biological and telecommunication concepts that encompass this technology to bring it further. [ABSTRACT FROM AUTHOR]

Hair follicle stem cells play important roles in maintaining homeostasis and skin tissue self-renewal. Transit-amplifying cells represent the transition of cells from hair follicle stem cells into differentiated epidermal cells. Thus far, the signaling pathway and the molecular biological mechanism that regulate the proliferation and differentiation of hair follicle stem cells remain unclear. In this paper, we studied the relationship between β-catenin and c-myc during the process of the differentiation of hair follicle stem cells into transit-amplifying cells. Based on our results, the expression of β-catenin can activate the nuclear gene c-myc and regulate the expression of transit-amplifying cell markers K15, K19, a6-integrin and β1-integrin, indicating that β-catenin is involved in the transformation process from hair follicle stem cells to transit-amplifying cells and suggesting that β-catenin plays an important biological role in the induction of this differentiation process. [ABSTRACT FROM AUTHOR]

Use of an ion-sensitive field-effect transistor (ISFET) as a signal transducer in a chemical analytical system is of great scientific and application interest. Modification of the gate dielectric surface with biomolecules makes ISFET a universal platform for different applications. In this paper horseradish peroxidase (HRP, EC 1.11.1.7) was used as a label for determination of interaction between thrombin and its aptamer on the ISFET surface. The approach for thrombin detection was based on the replacement of complementary sDNA-probe containing HRP from immobilized aptamer (sDNA) with thrombin, and monitoring residual HRP activity. The biosensor was shown to detect thrombin at the level of 7·10 -7 M. [ABSTRACT FROM AUTHOR]

Photo-plethysmography (PPG) is a non-contact non-invasive optical imaging technique which uses intensity and colour based information of transmitted or reflected light for bio-signal analysis. The major application areas are blood pulsation and blood oxygen saturation measurement. One of the major concerns of conventional PPG for blood pulsation measurement is its accuracy. Reflection based PPG contains a useful backscattered light component from the superficial and deep layer tissues of the skin and non-informative direct reflection from the skin surface. The direct reflection component reduces accuracy of blood pulsation measurement. This paper presents a technique, termed as Polarization Sensitive PPG (PSPPG), which removes the direct reflection component using polarizing filters. Experimental results show 30% improvement in the accuracy of blood pulsation measurement over conventional PPG. Further, statistical analysis of the measured results shows that the PSPPG is more accurate and reliable in comparison to conventional PPG for better bio-signal analysis. [ABSTRACT FROM AUTHOR]

Highly purified calf hemodialysate (HPCH) known as Actovegin® or Solcoseryl® is one of the most controversial drugs currently marketed worldwide. It is not registered as drug in some countries and therefore its medical use there is illegal, while in others it is often among the top 10 of the best-selling medications. It could be also found in the list of the "most useless drugs" and was banned for short time by World Anti-Doping Agency as performance enhancer. However, the degree of its usefulness or uselessness remains unclear and there is not enough convincing data to make reliable conclusions. HPCH is claimed to have wound/muscular injuries healing, neuroprotective and antioxidant properties, to enhance glucose uptake and oxygen consumption, and possibly to improve performance of athletes. Since HPCH consists of over 200 naturally occurring substances which potentially may exert some pharmacological effects, it is extremely difficult to perform pharmacokinetic and pharmacodynamical studies. In this paper we have analyzed the available literature concerning clinical evidence, in vitro, ex vivo and in vivo effects of HPCH. Based on these data we suggest that the main target of the drug may be endothelium and improvement of endothelial function may be responsible for numerous largely nonspecific effects. We also propose the improvement of protein quality control by the means of activation of ubiquitin-proteasomal system as the most important biochemical mechanism responsible for its effects. The role of sphingolipids as potential proteasome-activators is extensively discussed. The effects of HPCH may also include direct or indirect ones on NF-kB-, Nrf2- and FOXO-mediated regulation of metabolic processes in the cells, which result in improved protein quality control, enhanced energy metabolism and increased resistance to oxidative stress. [ABSTRACT FROM AUTHOR]

The present paper presents a mechanistic model of cerebral autoregulation, in which the dual effects of the arachidonic acid metabolites 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) on vascular smooth muscle mediate the cerebrovascular adjustments to a change in cerebral perfusion pressure (CPP). 20-HETE signalling in vascular smooth muscle mediates myogenic feedback to changes in vessel wall stretch, which may be modulated by metabolic feedback through EETs released from astrocytes and endothelial cells in response to changes in brain tissue oxygen tension. The metabolic feedback pathway is much faster than 20-HETE-dependent myogenic feedback, and the former thus initiates the cerebral autoregulatory response, while myogenic feedback comprises a relatively slower mechanism that functions to set the basal cerebrovascular tone. Therefore, assessments of dynamic cerebral autoregulation, which may provide information on the response time of the cerebrovasculature, may specifically be used to yield information on metabolic feedback mechanisms, while data based on assessments of static cerebral autoregulation represent the integrated functionality of myogenic and metabolic feedback. [ABSTRACT FROM AUTHOR]

Long term infection of Helicobacter pylori (Hp) virulent strains is a key factor in the genesis of human gastric cancer, and so are certain dietary proinflammatory and genotoxic compounds. Carcinogenic bracken fern (Pteridium spp.) is one of these. Toxins from this plant are consumed as bracken culinary preparations, through milk and meat of bracken-exposed livestock, and drain waters from bracken swards. Bracken toxin ptaquiloside (PtQ), a suspected human carcinogen, elicits complex responses in animals leading to death. PtQ and Hp might cooperate in gastric pathologies. This paper presents an hypothesis on PtQ-Hp association leading to the enhancement of carcinogenesis in the human gastric environment that might explain the high gastric cancer incidence and death rates among Hp-infected people living in bracken zones at two levels: (1) The macroscopic scale comprising the flow of PtQ in the human diet. (2) the microscopic scale encompassing (A) gastric luminal medium; (B) gastric mucus structure and mucin degradation elicited by Hp; (C) bacterial pH gradient modification of the gastric mucosa that favors PtQ survival and its penetration into epithelial tissue; (D) combined PtQ/Hp effects on gastric immune and inflammatory responses; (E) PtQ-Hp complementary activity at selected cell signaling cascades and genome disturbance. [ABSTRACT FROM AUTHOR]

Recent evidence shows that mitochondria regulate nuclear transcriptional activity both in normal and cell stress conditions, known as retrograde signaling. Under normal mitochondrial function, retrograde signaling is associated with mitochondrial biogenesis, normal cell phenotype and metabolic profile. In contrast, mitochondrial dysfunction leads to abnormal (oncogenic) cell phenotype and altered bio-energetic profile (nucleus reprogramming). Despite intense research efforts, a concrete mechanism through which mitochondria determine the group of genes expressed by the nucleus is still missing. The present paper proposes a novel hypothesis regarding retrograde signaling. More specifically, it reveals the mitochondrial membrane potential (MMP) and the accompanied strong electromagnetic field (EF) as key regulatory factors of nuclear activity. Mitochondrial emitted EFs extend in long distance and affect the function of nuclear membrane receptors. Depending on their frequencies, EFs can directly activate or deactivate different groups of nuclear receptors and so determine nuclear gene expression. One of the key features of the above hypothesis is that nuclear membrane receptors, besides their own endogenous or chemical ligands (hormones, lipids, etc.), can also be activated by electromagnetic signals. Moreover, normal MMP values (about -140 mV) are associated with the production of high ATP quantities and small levels of reactive oxygen species (ROS) while the hyperpolarization observed in all cancer cell types leads to a dramatic fall in ATP production and an analogous increase in ROS. The diminished ATP and increased ROS production negatively affect the function of all cellular systems including nucleus. Restoration of mitochondrial function, which is characterized by the fluctuation of MMP and EF values within a certain (normal) range, is proposed as a necessary condition for normal nuclear function and cancer therapy. [ABSTRACT FROM AUTHOR]

Serious infection elicits inflammatory processes that act through a range of molecular pathways, including cytokine signaling. It is not established however that noradrenaline (NA), a widely distributed neurotransmitter in the brain that is also a principal output molecule of the sympathetic nervous system, can produce psychological effects associated with infection. This paper puts forth the hypothesis that through neural-immune crosstalk, serious infection increases noradrenergic signaling, both in the central nervous system and in peripheral organs. In this manner, elevated noradrenergic transmission may help produce basic symptoms of infection such as fever, fatigue, aches and pains (including headache), nausea, and loss of appetite. NA may also promote cognitive impairment, major depression, unipolar mania, and even epileptic seizures in some cases. The paper focuses on three major types of infection: influenza (viral), tuberculosis (bacterial), malaria (parasitic), while also summarizing the potential relationship between NA and human immunodeficiency virus (HIV) infection. Four lines of evidence are used to test association between NA and influenza, tuberculosis, and malaria: direct measures of NA and its metabolites; and incidence of hypertension, bipolar mania, and epileptic seizures, since the latter three conditions may be associated with elevated NA. In addition, heart rate variability data are examined with respect to a number of infectious diseases, since those data provide information on sympathetic nervous system activity. While the data do not unequivocally support elevated noradrenergic signaling promoting psychological symptomatology with infection, many studies are consistent with this view. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: This study investigated the bacterial community involved in primary endodontic diseases, evaluated its ability to activate the macrophage Toll-like receptor 4 receptor through p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways, and determined the levels of endotoxins and interleukins (interleukin [IL]-6 and -10) produced by endodontic content-stimulated macrophages. Methods: Samples were taken from 21 root canals by using sterile/apyrogenic paper points. Raw 264.7 macrophages were stimulated with root canal contents. Checkerboard DNA-DNA hybridization was used for bacterial analysis and the limulus amebocyte lysate assay for endotoxin measurement; p38 MAPK and NF-κB activation was determined by Western blot analysis. IL-6 and IL-10 were measured using the enzyme-linked immunosorbent assay. Results: Bacteria and endotoxins were detected in 100% of the samples (21/21). The most frequently observed species were Parvimonas micra (16/21, 76%), Fusobacterium nucleatum ssp. nucleatum (15/21, 71%), and Porphyromonas endodontalis (14/21, 66%). Correlations were found between endotoxins and IL-6 and IL-10 (P < .05); p38 phosphorylation had a peak at 60 minutes, and NF-κB was quickly activated after 10 minutes of stimulation. Conclusions: It was concluded that the complex bacterial community was shown to be a potent activator of TLR-4 determined by the p38 MAPK and NF-κB signaling pathways, culminating in a high antigenicity against macrophages through the levels of IL-6 and IL-10, all significantly affected by endotoxin levels. [Copyright &y& Elsevier]

Copyright of Polimery is the property of Industrial Chemistry Research Institute and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: In this paper, we discuss data and methodological challenges for building bacterial communication networks using two examples: E. coli as a flagellate bacterium and G. sulfurreducens as a biofilm forming bacterium. We first highlight the link between the bacterial network communication design with respect to metabolic information processing design. The potentialities of designing routing network schemes described previously in the literature and based on bacteria motility and genetic message exchanges will depend on the genes coding for the intracellular and intercellular signalling pathways. In bacteria, the “mobilome” is related to horizontal gene transfer. Bacteria trade-off the acquisition of new genes which could improve their survival (and often their communication bandwidth), keeping their genome small enough to ensure quick DNA replication and fast increase of the biomass to speed up cell division. First, by using a multi-objective optimisation procedure, we search for the optimal trade-off between energy production, which is a requirement for the motility, and biomass growth, which is related to the overall survival and fitness of the bacterium. We use flux balance analysis of the genome-scale biochemical network of E. coli k-13 MG1655. Then, as a second case study, we analyse the electric properties and biomass trade-off of the bacterium G. sulfurreducens, which constructs an electric biofilm where electrons move across the nanowires. Here we discuss the potentialities of optimisation methodologies to design and select bacterial strains with desiderata properties. The optimisation methodologies establish also a relation between metabolism, network communication and computing. Moreover, we point to genetic design and synthetic biology as key areas to develop bacterial nano communication networks. [Copyright &y& Elsevier]

Abstract: Peritoneal fibrosis is a chronic, progressive progress, which is associated with ultrafiltration failure. In the development of peritoneal fibrosis, Epithelial to mesenchymal transition is an important cellular process whereby epithelial cells transform into mesenchymal cells under physiology and pathology conditions, along with change of cell morphology and expression of related genes. It plays an important role in embryogenesis and development of tissues and organs, as well as organ fibrosis and tumorigenesis. Several intracellular signal transduction pathways induce the process of Epithelial to mesenchymal transition. In recent researches, Wnt/β-catenin induced epithelial to mesenchymal transition was suggested to be an important reason for tissues and organs fibrosis. The following paper reviews the potential role of Wnt/β-catenin induced epithelial to mesenchymal transition in peritoneal fibrosis. New potential therapeutic interventions of peritoneal fibrosis are discussed. [Copyright &y& Elsevier]

Abstract: Surface topography affects cell function and differentiation. It has been previously shown that rough surfaces can enhance the activation of canonical Wnt signaling, an important pathway for osteoblast differentiation and bone maintenance, but the underlying mechanisms are still poorly understood. The present paper investigates whether cytoskeletal organization contributes to regulating this pathway. Rho-associated protein kinase (ROCK), an important controller of actin microfilaments, was inhibited with 2mM specific antagonist Y-27632 in mesenchymal and osteoblastic cells growing on titanium discs with a polished or acid-etched, sand-blasted (SLA) surface. Y-27632 subverted the morphology of the cytoskeleton on polished and, to a lesser extent, on SLA surfaces, as evidenced by fluorescence microscopy. Although ROCK inhibition did not affect cell viability, it increased activation of Wnt signaling in uncommitted C2C12 mesenchymal cells on polished surfaces but not on SLA discs upon reporter assay. Consistently with this, real-time polymerase chain reaction analysis showed that MC3T3 cells on polished surfaces expressed higher mRNA levels for β-catenin and alkaline phosphatase, a known Wnt target gene, and for the osteoblastic differentiation marker osteocalcin after ROCK inhibition. Taken together, these data demonstrate that cytoskeletal organization mediates activation of Wnt canonical signaling in cells on titanium surfaces with different topographies. [Copyright &y& Elsevier]

Abstract: The spatiotemporal dynamics of elementary Ca2+ release events, such as “blips” and “puffs” shapes the hierarchal Ca2+ signaling in many cell types. Despite being the building blocks of Ca2+ patterning, the mechanism responsible for the observed properties of puffs, especially their termination is incompletely understood. In this paper, we employ a data-driven approach to gain insights into the complex dynamics of blips and puffs. We use a model of inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) derived directly from single channel patch clamp data taken at 10μM concentration of IP3 to simulate calcium puffs. We first reproduce recent observations regarding puffs and blips and then investigate the mechanism of puff termination. Our model suggests that during a puff, IP3R s proceed around a loop through kinetic states from “rest” to “open” to “inhibited” and back to “rest”. A puff terminates because of self-inhibition. Based on our simulations, we rule out the endoplasmic reticulum (ER) Ca2+ depletion as a possible cause for puff termination. The data-driven approach also enables us to estimate the current through a single IP3R and the peak Ca2+ concentration near the channel pore. [Copyright &y& Elsevier]

Abstract: Extracellular matrix contains an abundant variety of signals that are received by cell surface receptors contributing to cell fate, via regulation of cellular activities such as proliferation, migration and differentiation. Cues from extracellular matrix can be used for the development of materials to direct cells into their desired fate. Neural extracellular matrix (ECM) is rich in axonal growth inducer proteins, and by mimicking these permissive elements in the cellular environment, neural differentiation as well as neurite outgrowth can be induced. In this paper, we used a synthetic peptide nanofiber system that can mimic not only the activity of laminin, an axonal growth-promoting constituent of the neural ECM, but also the activity of heparan sulfate proteoglycans in order to induce neuritogenesis. Heparan sulfate mimetic groups that were utilized in our system have an affinity to growth factors and induce the neuroregenerative effect of laminin mimetic peptide nanofibers. The self-assembled peptide nanofibers with heparan sulfate mimetic and laminin-derived epitopes significantly promoted neurite outgrowth by PC-12 cells. In addition, these scaffolds were even effective in the presence of chondroitin sulfate proteoglycans (CSPGs), which are the major inhibitory components of the central nervous system. In the presence of these nanofibers, cells could overcome CSPG inhibitory effect and extend neurites on peptide nanofiber scaffolds. [Copyright &y& Elsevier]

Abstract: Calcium ions and cyclic adenosine monophosphate (cAMP) are virtually ubiquitous intracellular signaling molecules in mammalian cells. This paper will focus on the cross-talk between Ca2+ and cAMP mobilizing signaling pathways and summarize the underlying molecular mechanisms. Subsequently, workings of adenohypophyseal corticotrope cells will be reviewed to highlight the physiological relevance of a Ca2+ cAMP interactions in neuroendocrinology. [Copyright &y& Elsevier]

Abstract: All cells have to adapt to changing chemical environments. The signaling system reacts to external molecular ‘inputs’ arriving at the receptors by activating cellular responses via transcription factors generating proper proteins as ‘outputs’. The signal transduction network connecting inputs and outputs acts as a molecular computer mimicking a neural network, a ‘chemical brain’ of the cell. The dynamics of concentrations of various signal proteins in the cell are described by continuous kinetic models proposed recently. In this paper we introduce a special neural network model based on the ordinary differential equations of the kinetic processes. We show that supervised learning can be implemented using the delta rule for updating the weights of the molecular neurons. We demonstrate the concept by realizing some of the basic logic gates in the model. [Copyright &y& Elsevier]

Bone mesenchymal stem cells(BMSCs), which are force-sensitive cells, have potentials for differentiation into cells of various types. Their biological characteristics can change functionally according to the appropriate stimulation in vitro, in order to reach the optimal demand of the stimulation. Many signal pathways are involved in osteogenesis. However, how BMSCs transform mechanical stimulation into biological signals and then instruct the bone formation and remodeling is still unclear. The exact mechanism remains to be studied further. This paper summarizes the recent research of effect and possible mechanism that mechanical stimulation acts on bone differentiation of BMSCs in vitro. Supported by National Natural Science Foundation of China (30901698,10972142) and Research Fund of Science and Technology Commission of Shanghai Municipality(08411961600). [ABSTRACT FROM AUTHOR]

Abstract: The Golgi apparatus plays a central role in lipid and protein post-translational modification and sorting. Morphologically the organelle is heterogeneous and it is possible to distinguish stacks of flat cysternae (cis- and medial Golgi), tubular–reticular networks and vesicles (trans-Golgi). These morphological differences parallel a distinct functionality with a selective distribution and complementary roles of the enzymes found in the different compartments. The Golgi apparatus has been also shown to be involved in Ca2+ signalling: it is indeed endowed with Ca2+ pumps, Ca2+ release channels and Ca2+ binding proteins and is thought to participate in determining the spatio-temporal complexity of the Ca2+ signal within the cell, though this role is still poorly understood. Recently, it has been demonstrated that the organelle is heterogeneous in terms of Ca2+ handling and selective reduction of Ca2+ concentration, both in vitro and in a genetic human disease, within one of its sub-compartment results in alterations of protein trafficking within the secretory pathway and of the entire Golgi morphology. In this paper we review the available information on the Ca2+ toolkit within the Golgi, its heterogeneous distribution in the organelle sub-compartments and discuss the implications of these characteristics for the physiopathology of the Golgi apparatus. [Copyright &y& Elsevier]

Abstract: Changes in cytosolic free Ca2+ concentration play a pivotal role in the regulation of platelet functions, from secretion of autocrine and procoagulant factors to reversible or irreversible aggregation. It has long been recognized that platelet agonists release Ca2+ accumulated into the dense tubular system, the analogue of the endoplasmic reticulum. However, current evidence indicates that Ca2+ can also be stored and released from a number of acidic organelles, including lysosomes and lysosome-related organelles. Ca2+ release from the dense tubular system is mediated through phospholipase C-dependent synthesis of inositol 1,4,5-trisphosphate, whereas Ca2+ efflux from the acidic stores seems to be associated to the second messenger nicotinic acid adenine dinucleotide phosphate. The biochemical and biophysical properties of both Ca2+ stores in platelets have been reported to show significant differences. Selective discharge of one or both stores depends on the platelet agonist and the concentration used, which further supports the complexity of the Ca2+ signals that regulate platelet function. In this paper, we summarize the current knowledge on the role of acidic organelles in agonist-evoked Ca2+ mobilization and highlight recent progress in understanding the functional aspects of the acidic Ca2+ stores in Ca2+ signalling and platelet physiology. [Copyright &y& Elsevier]

The dynamic, innovative temperament of Christian Gespach is ideally suited to unraveling some aspects of the complex molecular networks connected with signal transduction, cancer progression and treatment. He is one of the pioneers who opened, in the early 1980s, new insights into the signaling mechanisms of G-protein coupled receptor (GPCR) activation, desensitization, internalisation and crosstalks. Twenty five years later and in collaboration with Gespach, IPSEN pharmaceuticals designed pan-inhibitors of GPCR signaling, targeting Gα subunits in breast cancer progression and other epithelial cancers. Creativity is of vital importance to understand signal transduction pathways engaged in cancer cell motility, invasion and drug resistance. Christian Gespach has published more than 200 papers in cancer research, a true signal transduction tale. [ABSTRACT FROM AUTHOR]

Copyright of Psychiatria Polska is the property of Editorial Committee of Polish Psychiatric Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: It has long been speculated that cellular microdomains are important for many cellular processes, especially those involving Ca2+ signalling. Measurements of cytosolic Ca2+ report maximum concentrations of less than few micromolar, yet several cytosolic enzymes require concentrations of more than 20μM Ca2+ to be activated. In this paper, we have resolved this apparent paradox by showing that the surface topology of cells represents an important and hitherto unrecognized feature for generating microdomains of high Ca2+ in cells. We show that whereas the standard modeling assumption of a smooth cell surface predicts only moderate localized effects, the more realistic “wrinkled” surface topology predicts that Ca2+ concentrations up to 80μM can persist within the folds of membranes for significant times. This intra-wrinkle location may account for 5% of the total cell volume. Using different geometries of wrinkles, our simulations show that high Ca2+ microdomains will be generated most effectively by long narrow membrane wrinkles of similar dimensions to those found experimentally. This is a new concept which has not previously been considered, but which has ramifications as the intra-wrinkle location is also a strategic location at which Ca2+ acts as a regulator of the cortical cytoskeleton and plasma membrane expansion. [Copyright &y& Elsevier]

Abstract: Although there is evidence that caveolae and cholesterol play an important role in myocyte signalling processes, details of the mechanisms involved remain sparse. In this paper we have studied for the first time the clinically relevant intact coronary artery and measured in situ Ca2+ signals in individual myocytes using confocal microscopy. We have examined the effect of the cholesterol-depleting agents, methyl-cyclodextrin (MCD) and cholesterol oxidase, on high K+, caffeine and agonist-induced Ca2+ signals. We find that cholesterol depletion produces a stimulus-specific alteration in Ca2+ responses; with 5-HT (10μM) and endothelin-1 (10nM) responses being selectively decreased, the phenylephrine response (100μM) increased and the responses to high K+ (60mM) and caffeine (10mM) unaffected. Agonist-induced Ca2+ signals were restored when cholesterol was replenished using cholesterol-saturated MCD. In additional experiments, enzymatically isolated myocytes were patch clamped. We found that cholesterol depletion caused a selective modification of ion channel function, with whole cell inward Ca2+ current being unaltered, whereas outward K+ current was increased, due to BKCa channel activation. There was also a significant decrease in cell capacitance. These data are discussed in terms of the involvement of caveolae in receptor localisation, Ca2+ entry pathways and SR Ca2+ release, and the role of these in agonist signalling. [Copyright &y& Elsevier]

Abstract: Diverse Gram-negative bacteria communicate with each other by using diffusible N-acyl-homoserine lactone (AHL) signaling molecules to coordinate gene expression with cell population density. This mechanism termed ‘quorum sensing’ is involved in the regulation of physiological functions as well as multiple virulence determinants. It becomes more and more evident, that bacteria communicate not only with each other but also with their host. Up to now, little is known about this interkingdom communication. The AHL quorum sensing molecule N-3-(oxododecanoyl)-l-homoserine lactone (OdDHL) from Pseudomonas aeruginosa has been shown to influence the immune system of the host. The role and potential influence of other AHL molecules from other bacteria have so far not been determined. In this paper, we investigated the role of 7 different AHLs on apoptosis of human Jurkat T lymphocytes. We found, that among all homoserine lactones tested, only OdDHL rapidly induced apoptosis which was accompanied by the breakdown of the mitochondrial transmembrane potential (ΔΨ m). Since overexpression of anti-apoptotic Bcl-2 completely abrogated the apoptotic effect, we presume that OdDHL induces apoptosis by activation of the intrinsic mitochondrial apoptosis pathway. The reason that bacteria induce apoptosis is largely unknown. We suspect that through apoptosis an anti-inflammatory response is triggered. [Copyright &y& Elsevier]