Gr\"obner-Shirshov bases for Rota-Baxter algebras

In this paper, we establish the Composition-Diamond lemma for associative nonunitary Rota-Baxter algebras with weight $\lambda$. As applications, we obtain a linear basis of a free commutative Rota-Baxter algebra without unity and show that every countably generated Rota-Baxter algebra with weight 0 can be embedded into a two-generated Rota-Baxter algebra.Comment: 24 page

Cell Contact–Dependent Outer Membrane Exchange in Myxobacteria: Genetic Determinants and Mechanism

Biofilms are dense microbial communities. Although widely distributed and medically important, how biofilm cells interact with one another is poorly understood. Recently, we described a novel process whereby myxobacterial biofilm cells exchange their outer membrane (OM) lipoproteins. For the first time we report here the identification of two host proteins, TraAB, required for transfer. These proteins are predicted to localize in the cell envelope; and TraA encodes a distant PA14 lectin-like domain, a cysteine-rich tandem repeat region, and a putative C-terminal protein sorting tag named MYXO-CTERM, while TraB encodes an OmpA-like domain. Importantly, TraAB are required in donors and recipients, suggesting bidirectional transfer. By use of a lipophilic fluorescent dye, we also discovered that OM lipids are exchanged. Similar to lipoproteins, dye transfer requires TraAB function, gliding motility and a structured biofilm. Importantly, OM exchange was found to regulate swarming and development behaviors, suggesting a new role in cell–cell communication. A working model proposes TraA is a cell surface receptor that mediates cell–cell adhesion for OM fusion, in which lipoproteins/lipids are transferred by lateral diffusion. We further hypothesize that cell contact–dependent exchange helps myxobacteria to coordinate their social behaviors

A systems biology approach to invasive behavior: comparing cancer metastasis and suburban sprawl development

Background Despite constant progress, cancer remains the second leading cause of death in the United States. The ability of tumors to metastasize is central to this dilemma, as many studies demonstrate successful treatment correlating to diagnosis prior to cancer spread. Hence a better understanding of cancer invasiveness and metastasis could provide critical insight. Presentation of the hypothesis We hypothesize that a systems biology-based comparison of cancer invasiveness and suburban sprawl will reveal similarities that are instructive. Testing the hypothesis We compare the structure and behavior of invasive cancer to suburban sprawl development. While these two systems differ vastly in dimension, they appear to adhere to scale-invariant laws consistent with invasive behavior in general. We demonstrate that cancer and sprawl have striking similarities in their natural history, initiating factors, patterns of invasion, vessel distribution and even methods of causing death. Implications of the hypothesis We propose that metastatic cancer and suburban sprawl provide striking analogs in invasive behavior, to the extent that conclusions from one system could be predictive of behavior in the other. We suggest ways in which this model could be used to advance our understanding of cancer biology and treatment

Creating Virtual 3-D Outcrop

Because of the high precision of present-day GPS and reflectorless laser technology, geologic information and remotely sensed data (i.e., seismic and GPR grids, wells) can be positioned accurately in 3-D and reconstructed as a virtual image. Hence, we have developed the “virtual outcrop” for applications that require knowledge about the 3-D spatial arrangements of rock types

Velocity map imaging studies of the ultraviolet photodissociation of methyl chloride

We report a high resolution velocity map imaging study of the ground state and spin–orbit excited Cl atoms and of vibrationally state selected CH3(v) fragments formed in the photodissociation of jet-cooled CH3Cl molecules at three wavelengths in the range 193.3 ≤ λ ≤ 212 nm (in its A band continuum) and when exciting various vibronically resolved absorption features in the ranges 146 ≤ λ ≤ 160 and 138 ≤ λ ≤ 140.6 nm, associated with the first two predissociated Rydberg states of this molecule. Excitation in all cases results in prompt C–Cl bond fission, on timescales shorter than the parent rotational period. Most of the excess energy is partitioned into product kinetic energy, ET, but the deduced Cl/Cl* branching ratios and favored CH3 product vibrational motions are excitation wavelength/excited state dependent. So, too, are the fragment recoil anisotropies which, even within one CH3(v) + Cl/Cl* product channel, are found to be sensitive functions of ET. The trends observed at longer λ reflect the wavelength dependent partial cross sections for excitation to the 3Q1, 3Q0, and 1Q1 components of the A band continuum, but full interpretation of the present data demands a much more detailed, quantum state resolved picture of the non-adiabatic population transfer probabilities between these dissociative parent states and, at higher excitation energies, the Jahn–Teller induced distortions within the photoexcited Rydberg states and their non-adiabatic couplings with the continuum states. Additional CH3+ and Cl+ signals evident in the images at lower ET are attributed to, respectively, two pump photon induced dissociative ionizations and one probe photon induced photodissociation of CH2Cl products formed via a competing primary C–H bond fission process

Consumer Connectivity in a Complex, Technology-Enabled, and Mobile-Oriented World with Smart Products

Today’s consumers are immersed in a vast and complex array of networks. Each network features an interconnected mesh of people and firms, and now, with the rise of the Internet of Things (IoT), also objects. Technology (particularly mobile devices) enables such connections, and facilitates many kinds of interactions in these networks - from transactions, to social information sharing, to people interfacing with connected devices (e.g., wearable technology). We introduce the POP-framework, discuss how People, Objects and the Physical world interconnect with each other and how it results in an increasing amount of connected data, and briefly summarize existing knowledge on these inter-connections. We also provide an agenda for future research focused on examining potential impact of IoT and smart products on consumer behavior and firm strategies

Comparison of DNA adducts from exposure to complex mixtures in various human tissues and experimental systems

DNA adducts derived from complex mixtures of polycyclic aromatic compounds emitted from tobacco smoke are compared to industrial pollution sources (e.g., coke ovens and aluminum smelters), smoky coal burning, and urban air pollution. Exposures to coke oven emissions and smoky coal, both potent rodent skin tumor initiators and lung carcinogens in humans, result in high levels of DNA adducts compared to tobacco smoke in the in vitro calf thymus DNA model system, in cultured lymphocytes, and in the mouse skin assay. Using tobacco smoke as a model in human studies, we have compared relative DNA adduct levels detected in blood lymphocytes, placental tissue, bronchoalveolar lung lavage cells, sperm, and autopsy tissues of smokers and nonsmokers. Adduct levels in DNA isolated from smokers were highest in human heart and lung tissue with smaller but detectable differences in placental tissue and lung lavage cells. Comparison of the DNA adduct levels resulting from human exposure to different complex mixtures shows that emissions from coke ovens, aluminum smelters, and smoky coal result in higher DNA adduct levels than tobacco smoke exposure. These studies suggest that humans exposed to complex combustion mixtures will have higher DNA adduct levels in target cells (e.g., lung) as compared to nontarget cells (e.g., lymphocytes) and that the adduct levels will be dependent on the genotoxic and DNA adduct-forming potency of the mixture

A TRPV4-dependent neuroimmune axis in the spinal cord promotes neuropathic pain

Microglia, resident macrophages of the CNS, are essential to brain development, homeostasis, and disease. Microglial activation and proliferation are hallmarks of many CNS diseases, including neuropathic pain. However, molecular mechanisms that govern the spinal neuroimmune axis in the setting of neuropathic pain remain incompletely understood. Here, we show that genetic ablation or pharmacological blockade of transient receptor potential vanilloid type 4 (TRPV4) markedly attenuated neuropathic pain-like behaviors in a mouse model of spared nerve injury. Mechanistically, microglia-expressed TRPV4 mediated microglial activation and proliferation and promoted functional and structural plasticity of excitatory spinal neurons through release of lipocalin-2. Our results suggest that microglial TRPV4 channels reside at the center of the neuroimmune axis in the spinal cord, which transforms peripheral nerve injury into central sensitization and neuropathic pain, thereby identifying TRPV4 as a potential new target for the treatment of chronic pain

MMP28 (epilysin) as a novel promoter of invasion and metastasis in gastric cancer

Background\ud The purpose of this study was to investigate invasion and metastasis related genes in gastric cancer.\ud \ud Methods\ud The transwell migration assay was used to select a highly invasive sub-line from minimally invasive parent gastric cancer cells, and gene expression was compared using a microarray. MMP28 upregulation was confirmed using qRT-PCR. MMP28 immunohistochemistry was performed in normal and gastric cancer specimens. Invasiveness and tumor formation of stable cells overexpressing MMP28 were tested in vitro and in vivo.\ud \ud Results\ud MMP28 was overexpressed in the highly invasive sub-cell line. Immunohistochemistry revealed MMP28 expression was markedly increased in gastric carcinoma relative to normal epithelia, and was significantly associated with depth of tumor invasion, lymph node metastasis and poorer overall survival. Ectopic expression of MMP28 indicated MMP28 promoted tumor cell invasion in vitro and increased gastric carcinoma metastasis in vivo.\ud \ud Conclusions\ud This study indicates MMP28 is frequently overexpressed during progression of gastric carcinoma, and contributes to tumor cell invasion and metastasis. MMP28 may be a novel therapeutic target for prevention and treatment of metastases in gastric cancer