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We consider a reconfigurable intelligent surface (RIS) assisted multiple-input multiple-output (MIMO) system in the presence of scattering objects. The MIMO transmitter and receiver, the RIS, and the scattering objects are modeled as mutually coupled thin wires connected to load impedances. We introduce a novel numerical algorithm for optimizing the tunable loads connected to the RIS, which does not utilize the Neumann series approximation. The algorithm is provably convergent, has polynomial complexity with the number of RIS elements, and outperforms the most relevant benchmark algorithms while requiring fewer iterations and converging in a shorter time.

We consider a fading channel in which a multi-antenna transmitter communicates with a multi-antenna receiver through a reconfigurable intelligent surface (RIS) that is made of ${N}$ reconfigurable passive scatterers impaired by phase noise. The beamforming vector at the transmitter, the combining vector at the receiver, and the phase shifts of the ${N}$ scatterers are optimized in order to maximize the signal-to-noise-ratio (SNR) at the receiver. By assuming Rayleigh fading (or line-of-sight propagation) on the transmitter-RIS link and Rayleigh fading on the RIS-receiver link, we prove that the SNR is a random variable that is equivalent in distribution to the product of three (or two) independent random variables whose distributions are approximated by two (or one) gamma random variables and the sum of two scaled non-central chi-square random variables. The proposed analytical framework allows us to quantify the robustness of RIS-aided transmission to fading channels. For example, we prove that the amount of fading experienced on the transmitter-RIS-receiver channel linearly decreases with ${N}~\gg ~1.$ This proves that RISs of large size can be effectively employed to make fading less severe and wireless channels more reliable.

We consider a multiuser multirelay network where each source communicates with its destination via an assigned relay. To ensure fairness among the users, the minimum of the users’ energy efficiencies (in bit-per-Joule) is jointly maximized with respect to the relay assignment and transmit power of both source and relay nodes. The resulting algorithm is provably convergent, requires limited complexity, and significantly outperforms the baseline scenario in which no joint optimization of transmit powers and relay assignment is performed.

Combustion stabilization and enhancement of the flammability limits are mandatory objectives to improve nowadays combustion chambers. At this purpose, the use of an electric field in the flame region provides a solution which is, at the same time, easy to implement and effective to modify the flame structure. The present work describes an efficient flamelet progress-variable approach developed to model the fluid dynamics of flames immersed in an electric field. The main feature of this model is that it can use complex ionization mechanisms without increasing the computational cost of the simulation. The model is based on the assumption that the combustion process is not directly influenced by the electric field and has been tested using two chemi-ionization mechanisms of different complexity in order to examine its behavior with and without the presence of heavy anions in the mixture. Using a one- and a two-dimensional numerical test cases, the present approach has been able to reproduce all the major aspects encountered when a flame is subject to an imposed electric field and the main effects of the different chemical mechanisms. Moreover, the proposed model is shown to produce a large reduction in the computational cost, being able to shorten the time needed to perform a simulation up to 40 times. [ABSTRACT FROM AUTHOR]

Mycobacterium avium complex is a facultative intracellular pathogen that can cause pulmonary disease in immunocompromised individuals. Dendritic cells (DCs) play a central role in protective immunity against mycobacteria. Mycobacterium avium complex infects DCs but does not impair in vitroinfected monocytes' differentiation into DCs. A 54-year old woman affected by chronic graft-versus-host-disease (cGVHD) was referred to our Division of Dermatology. Immature DCs were generated from her monocytes. One week later she was hospitalized due to a lung infection with Mycobacterium avium complex. Monocyte-derived DCs during Mycobacterium avium infection expressed low levels of CD1a and CD80 as determined by flow cytometry. They also expressed high levels of CD83 and CD86, and when stimulated with LPS for 24 hrs they slightly up-regulated CD83 and did not produce IL12. When monocyte-derived DCs were obtained from the patient after having recovered from the Mycobacterium avium complex infection, they expressed normal levels of CD1a and CD80 and were negative both for CD83 and for CD86. IL12 production in response to LPS was restored. Inhibition of DC maturation by the in vivoinfection with Mycobacterium avium may be an immune-evasion mechanism used by the pathogen because incompletely matured DCs may not activate effector T cells efficiently in vivo.

Summary: Plants were regenerated by shoot multiplication from four clones of Melia azedarach L. during 12 mo. of subculturing. One hundred and one of these plants were examined by randomly amplified polymorphic DNA analysis. All regenerated plants showed at least one polymorphism. However, no chromosome number alterations were observed. The pattern of variation obtained by principal coordinated analysis showed a random distribution of variation among regenerated plants and their controls, indicating that genetic alterations were not cumulative during in vitro culture. Similar results were found using Shannon's index, which revealed that 50% of the observed diversity resided among plants coming from the same subculture generation. This high intraclonal variation does not provide a clear scenario for predicting the amount of culture time required to preserve genetic fidelity in commercially micropropagated M. azedarach plants. Our work suggests that other mechanisms, such as chimerism, contribute to intraclonal heterogeneity in vitro.

Abstract: Inflammatory and lipid factors share an important role in atherosclerosis. Recent studies showed the concomitant presence and increase of complement components and lipid both in the atherosclerotic plaque and the circulating blood. The aim of this study was to examine the relationship between the complement system and lipid disorders. We evaluated the circulating complement terminal complex C5b-9, a clear sign of complement activation, in three groups of 30 patients the first with hypercholesterolemia, the second with hypertriglyceridemia (associated with low values of HDL-cholesterol), the third with low levels of HDL-cholesterol compared with an equivalent group of matched normolipemic subjects. We found a significant increase of sC5b-9 in each group of patients compared with controls. The mean sC5b-9 level in the hypercholesterolemic population was 366.2±141.2 ng/ml (P<0.01), 395.4±118.2 ng/ml in the hypertrygliceridemic group (P<0.01), 414.8±126.4 ng/ml in the low HDL-chol subjects (P<0.01), and 182.0±40.8. ng/ml in the control group. Regression analysis showed a significant direct correlation between sC5b-9 and triglycerides (r=0.64), and a significant inverse correlation between sC5b-9, HDL-chol (r=0.74), and apo-A1 (r=0.68); no significant relationship was found between sC5b-9 and cholesterol. We suggest that complement activation is associated with the various lipid disorders and is more important in those dyslipidemic conditions in which other factors may be involved. In particular, hypertriglyceridemia may be associated with endothelial and fibrinolytic disturbances, and the decrease of HDL may induce the failure of the regulatory proteins transported by the same HDL.

A protein with an Mr of 145,000 (p145) was detected by antibodies to phosphotyrosine by Western blot (immunoblot) analysis. This protein was phosphorylated on tyrosine in a gastric carcinoma cell line. In cells that were metabolically labeled with 32Pi, this protein was phosphorylated on tyrosine and serine. p145 is a cysteine-rich transmembrane glycoprotein. The extracellular domain could be labeled by 125I under nonpermeating conditions and was cleaved by mild trypsin treatment of intact cells. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions revealed a shift of p145 mobility to an apparent Mr of 190,000. After immunoprecipitation with phosphotyrosine antibodies, p145 displayed a strong associated protein kinase activity in vitro, becoming phosphorylated on tyrosine. There was no immunological cross-reaction between p145 and known tyrosine kinases. Both in vivo and in vitro tyrosine phosphorylations were unaffected by the addition of known growth factors. However, p145 was rapidly dephosphorylated in vivo when cells were exposed to low pH, a condition that is known to dissociate ligands from their receptors. These data suggest that p145 is associated with a protein tyrosine kinase activity which, in the tumor cell line studied, is activated by an as yet unidentified factor.

Abstract: The c-MET oncogene encodes the receptor for hepatocyte growth factor/scatter factor (HGF/SF), which is known to stimulate the invasive growth of epithelial cells cultured in vitro. TheMet/HGF receptor is a heterodimeric transmembrane tyrosine kinase, which is a prototype for a new family of growth factor receptors. The c-MET oncogene is expressed in several types of epithelial tissue including keratinocytes and is over-expressed in a number of human carcinomas. Studies on various carcinoma cell lines have shown that over-expression and structural alteration of the receptor result in its activation and confer tumorigenesis. We have studiedMet/HGF receptor expression in tissue specimens from 34 patients with head and neck squamous cell carcinomas (HNSCC) and in 17 regional lymph node metastases. Western blot analysis was employed, using monoclonal antibodies directed against either the intracellular or extracellular domain of the receptor. Each sample was compared to its normal counterpart. The receptor did not show any major structural alterations in HNSCC tissues, but its expression was increased from 2- to 50-fold in about 70% of tumors. Immunohistochemistry then showed that the same antibodies stained only a few cells in the basal layer of normal squamous epithelium but intensely marked tumor cells. In the lymph node metastases of Met-positive tumors, receptor expression was maintained and sometimes increased with respect to primary tumors. Immunohistochemical analysis of the metastatic lymph nodes showed that cells were negative in the normal lymphatic tissue and strongly stained in tumor cells. Over-expression of theMet/HGF receptor was found at all tumor stages but was more significant in those associated with enlarged or multiple (N2–N3) lymph node metastases. These data show that expression of theMet/HGF receptor may be involved in the progression of HNSCC towards a metastatic phenotype and may be a useful marker of head and neck tumor cell spread to regional lymph nodes.

Hepatocyte Growth Factor (HGF, also known as Scatter Factor) is a powerful mitogen or motility factor in different cells, acting through the tyrosine kinase receptor encoded by the MET protooncogene. Endothelial cells express the MET gene and expose at the cell surface the mature protein (p190MET) made of a 50 kD (alpha) subunit disulfide linked to a 145-kD (beta) subunit. HGF binding to endothelial cells identifies two sites with different affinities. The higher affinity binding site (Kd = 0.35 nM) corresponds to the p190MET receptor. Sub-nanomolar concentrations of HGF, but not of a recombinant inactive precursor, stimulate the receptor kinase activity, cell proliferation and motility. HGF induces repairs of a wound in endothelial cell monolayer. HGF stimulates the scatter of endothelial cells grown on three-dimensional collagen gels, inducing an elongated phenotype. In the rabbit cornea, highly purified HGF promotes neovascularization at sub-nanomolar concentrations. HGF lacks activities related to hemostasis-thrombosis, inflammation and endothelial cells accessory functions. These data show that HGF is an in vivo potent angiogenic factor and in vitro induces endothelial cells to proliferate and migrate.