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Compromised productivity and yield loss due to inadequate nutrient abundance or inefficient mineral absorption from the soil are one of the most prevalent agricultural concerns across the world. Essential minerals, required in trace amounts for optimum plant growth and development, are termed as micronutrients. Due to low abundance of these vital elements (iron, zinc, copper, manganese, boron, nickel, molybdenum and chlorine), significant stretches of agricultural land often have limited supply of these micronutrients. As a result, plants, crops and vegetables grown in such soil exhibit unpredictable anatomical, biochemical and metabolic abnormalities associated with deteriorated physiological alterations. This communication details out the genomic, proteomic and metabolomic dynamism mediated by various plant species exposed to micronutrient starvation or grown under micronutrient-limiting environment. Furthermore, deficiency of vital trace elements inhibits the activity of crucial enzymes associated with detoxification of oxidants and regulation of important physiological processes like photosynthesis, respiration, nitrogen assimilation, sugar metabolism, etc. Thus, these plants experience an inherent oxidative stress and are more susceptible to multiple abiotic stresses due to inefficient defence machinery. The differential physiological adaptations mediated under such variable microelement deficiency have also been critically delineated. Thus, diverse signaling crosstalks, regulated by phytohormonal homeostasis, chiefly synchronize such responses of the physiome during micronutrient deficiency. [ABSTRACT FROM AUTHOR]

Glioblastoma (GB) is the most common and devastating form of brain cancer. Despite conventional treatments, progression or recurrences are systematic. In recent years, immunotherapies have emerged as an effective treatment in a number of cancers, leaving the question of their usefulness also faced with the particular case of brain tumors. The challenge here is major not only because the brain is the seat of our consciousness but also because of its isolation by the blood-brain barrier and the presence of a unique microenvironment that constitutes the central nervous system (CNS) with very specific constituent or patrolling cells. Much of the microenvironment is made up of immune cells or inflammation. Among these, tumor-associated macrophages (TAMs) are of significant interest as they are often involved in facilitating tumor progression as well as the development of resistance to standard therapies. In this review, the ubiquity of TAMs in GB will be discussed while the specific case of microglia resident in the brain will be also emphasized. In addition, the roles of TAMs as accomplices in the progression of GB and resistance to treatment will be presented. Finally, clinical trials targeting TAMs as a means of treating cancer will be discussed.

Glioblastoma (GB) is the most common and devastating form of brain cancer. Despite conventional treatments, progression or recurrences are systematic. In recent years, immunotherapies have emerged as an effective treatment in a number of cancers, leaving the question of their usefulness also faced with the particular case of brain tumors. The challenge here is major not only because the brain is the seat of our consciousness but also because of its isolation by the blood-brain barrier and the presence of a unique microenvironment that constitutes the central nervous system (CNS) with very specific constituent or patrolling cells. Much of the microenvironment is made up of immune cells or inflammation. Among these, tumor-associated macrophages (TAMs) are of significant interest as they are often involved in facilitating tumor progression as well as the development of resistance to standard therapies. In this review, the ubiquity of TAMs in GB will be discussed while the specific case of microglia resident in the brain will be also emphasized. In addition, the roles of TAMs as accomplices in the progression of GB and resistance to treatment will be presented. Finally, clinical trials targeting TAMs as a means of treating cancer will be discussed. [ABSTRACT FROM AUTHOR]

The present study investigated the effects of salt acclimation on the expression of genes, viz., proline dehydrogenase (PDH), Δ1-pyrroline-5-carboxylate-synthetase (P5CS), P5C dehydrogenase (P5CDH), ornithine aminotransferase (OAT), betaine aldehyde dehydrogenase 1 (BADH1), BADH2, triose phosphate isomerase (TPI), ornithine decarboxylase (ODC), arginine decarboxylase (ADC), S-adenosyl-methionine decarboxylase (SAMDC), spermidine synthase (SPDS), spermine synthase (SPMS), diamine oxidase (DAO) and polyamine oxidase (PAO) in four indigenous aromatic varieties, viz., Tulaipanji (TP), Radhunipagal (RP), Kalonunia (KN) and Gobindobhog (GB) along with a non-aromatic cultivar, IR-64. The PDH, P5CS, P5CDH and OAT expression showed the regulation of the P5C pathway of aroma synthesis, with OAT appearing to regulate the crosstalk between the P5C and the polyamine (PA) pathway for the production of aroma. The role of PA pathway was further validated by monitoring the expression of ODC, ADC, SAMDC, SPDS, SPMS, DAO and PAO. The BADH2 expression reflected the fact that the enzyme encoded by the gene was directly and negatively associated with aroma content in rice. The TPI expression established that the enzyme encoded by this gene leading to the synthesis of methylglyoxal (MG) is also a key regulator for aroma synthesis. The current study established the varietal differences in the expression of the aforementioned genes in the selected rice cultivars. The salt-stressed aromatic varieties followed the P5C pathway to synthesize aroma. TP and RP exhibited the capability to generate aroma via PA-dependent pathway. Salt-stressed KN, on the contrary, accumulated higher BADH2 and lower TPI transcripts, which correlated with our previous report of KN accumulating low aroma during salinization due to efficient metabolite channelization towards stress amelioration. [ABSTRACT FROM AUTHOR]

Recent advances in the treatment of various cancers have resulted in the adaptation of several novel immunotherapeutic strategies. Notably, the recent intervention through immune checkpoint inhibitors has resulted in significant clinical responses and prolongation of survival in patients with several therapy-resistant cancers (melanoma, lung, bladder, etc.). This intervention was mediated by various antibodies directed against inhibitory receptors expressed on cytotoxic T-cells or against corresponding ligands expressed on tumor cells and other cells in the tumor microenvironment (TME). However, the clinical responses were only observed in a subset of the treated patients; it was not clear why the remaining patients did not respond to checkpoint inhibitor therapies. One hypothesis stated that the levels of PD-L1 expression correlated with poor clinical responses to cell-mediated anti-tumor immunotherapy. Hence, exploring the underlying mechanisms that regulate PD-L1 expression on tumor cells is one approach to target such mechanisms to reduce PD-L1 expression and, therefore, sensitize the resistant tumor cells to respond to PD-1/PD-L1 antibody treatments. Various investigations revealed that the overexpression of the transcription factor Yin Yang 1 (YY1) in most cancers is involved in the regulation of tumor cells' resistance to cell-mediated immunotherapies. We, therefore, hypothesized that the role of YY1 in cancer immune resistance may be correlated with PD-L1 overexpression on cancer cells. This hypothesis was investigated and analysis of the reported literature revealed that several signaling crosstalk pathways exist between the regulations of both YY1 and PD-L1 expressions. Such pathways include p53, miR34a, STAT3, NF-kB, PI3K/AKT/mTOR, c-Myc, and COX-2. Noteworthy, many clinical and pre-clinical drugs have been utilized to target these above pathways in various cancers independent of their roles in the regulation of PD-L1 expression. Therefore, the direct inhibition of YY1 and/or the use of the above targeted drugs in combination with checkpoint inhibitors should result in enhancing the cell-mediated anti-tumor cell response and also reverse the resistance observed with the use of checkpoint inhibitors alone. [ABSTRACT FROM AUTHOR]

Biocompatible and plastic neural interface devices allow for minimally invasive recording of brain activity. Increasing electrode density in such devices is essential for high-resolution neural recordings. Superimposing conductive leads in devices can help multiply the number of recording sites while keeping probes width small and suitable for implantation. However, because of leads' vertical proximity, this can create capacitive coupling (CC) between overlapping channels, which leads to crosstalk. Here, we present a thorough investigation of CC phenomenon in multi-gold layer thin-film multi-electrode arrays with a parylene C (PaC) insulation layer between superimposed leads. We also propose a guideline on the design, fabrication, and characterization of such type of neural interface devices for high spatial resolution recording. Our results demonstrate that the capacitance created through CC between superimposed tracks decreases non-linearly and then linearly with the increase of insulation thickness. We identify an optimal PaC insulation thickness that leads to a drastic reduction of CC between superimposed gold channels while not significantly increasing the overall device thickness. Finally, we show that double gold layer electrocorticography probes with the optimal insulation thickness exhibit similar performances in vivo when compared to single-layer devices. This confirms that these probes are adequate for high-quality neural recordings.

Phosphate and sulfate are essential macro-elements for plant growth and development, and deficiencies in these mineral elements alter many metabolic functions. Nutritional constraints are not restricted to macro-elements. Essential metals such as zinc and iron have their homeostasis strictly genetically controlled, and deficiency or excess of these micro-elements can generate major physiological disorders, also impacting plant growth and development. Phosphate and sulfate on one hand, and zinc and iron on the other hand, are known to interact. These interactions have been partly described at the molecular and physiological levels, and are reviewed here. Furthermore the two macro-elements phosphate and sulfate not only interact between themselves but also influence zinc and iron nutrition. These intricated nutritional cross-talks are presented. The responses of plants to phosphorus, sulfur, zinc, or iron deficiencies have been widely studied considering each element separately, and some molecular actors of these regulations have been characterized in detail. Although some scarce reports have started to examine the interaction of these mineral elements two by two, a more complex analysis of the interactions and cross-talks between the signaling pathways integrating the homeostasis of these various elements is still lacking. However, a MYB-like transcription factor, PHOSPHATE STARVATION RESPONSE 1, emerges as a common regulator of phosphate, sulfate, zinc, and iron homeostasis, and its role as a potential general integrator for the control of mineral nutrition is discussed. [ABSTRACT FROM AUTHOR]

Abstract: Shigella flexneri type III secreted effector OspF harbors a phosphothreonine lyase activity that irreversibly dephosphorylates MAP kinases (MAPKs) p38 and ERK in infected epithelial cells and thereby, dampens innate immunity. Whereas this activity has been well characterized, the impact of OspF on other host signaling pathways that control inflammation was unknown. Here we report that OspF potentiates the activation of the MAPK JNK and the transcription factor NF-κB during S. flexneri infection. This unexpected effect of OspF was dependent on the phosphothreonine lyase activity of OspF on p38, and resulted from the disruption of a negative feedback loop regulation between p38 and TGF-beta activated kinase 1 (TAK1), mediated via the phosphorylation of TAK1-binding protein 1. Interestingly, potentiated JNK activation was not associated with enhanced c-Jun signaling as OspF also inhibits c-Jun expression at the transcriptional level. Altogether, our data reveal the impact of OspF on the activation of NF-κB, JNK and c-Jun, and demonstrate the existence of a negative feedback loop regulation between p38 and TAK1 during S. flexneri infection. Furthermore, this study validates the use of bacterial effectors as molecular tools to identify the crosstalks that connect important host signaling pathways induced upon bacterial infection. [Copyright &y& Elsevier]

All cells receive and respond to signals from their environment, whether they live freely or are part of a tissue. Feedback loops are one among the interactions in signal-transduction cascades, in which the information from the downstream components is sent back to the upstream components of the system. Crosstalks between signal-transduction cascades are able to combine the information's received and processed to trigger the appropriate response. To understand how signaling networks make decisions, the dynamic interactions of proteins in the signal-transduction cascades are important rather than just creating static maps of pathways. Based on reaction kinetics, we have developed mathematical models to predict and analyze the impacts of the feedback loops in JNK cascades and the crosstalks between JNK and P38 kinase cascades. Feedback loops in JNK cascades and crosstalks between JNK and P38 kinase cascades plays the complementary roles in making the impacts on the activation of JNK and P38 kinases. JNK and P38 kinase cascades with feedbacks and crosstalks is a robust system. [ABSTRACT FROM PUBLISHER]

Multilayer thin-film waveguides (MTFWs) are analyzed using the beam-propagation method based on Yee's mesh. The birefringence properties of the MTFW are demonstrated by the eigenmode analysis based on the imaginary-distance procedure. Taking advantage of the birefringence, a polarization splitter composed of two parallel MTFWs is proposed. Calculation shows that a short device length of 270 mum is obtainable with crosstalks of -33.5 dB for the quasi-transverse-electric mode and -20.7 dB for the quasi-transverse-magnetic mode. A crossing-type polarization splitter is also developed, and the device length is further reduced to 120 mum. [ABSTRACT FROM PUBLISHER]

A novel polarization-independent splitter based on index-guiding all-solid silica-based photonic-crystal fibers is proposed. The polarization-independent feature of the splitter is realized by reducing the difference in coupling lengths between the two polarization states to lower than 1%, which is due to the low index contrast in the splitter. Numerical results obtained for a device length of 10.69 mm show crosstalks of as low as -20 dB with bandwidths as great as 25.4 and 42.2 nm around the wavelengths of 1.55 and 1.31 mum, respectively [ABSTRACT FROM PUBLISHER]

A polymeric 1 × 6 thermooptic switch is fabricated and demonstrated. The device utilizes an elliptic total internal reflection waveguide mirror imaging the input channel waveguide onto the first output channel waveguide and a prism-array heating electrode steering the beam to corresponding output channel waveguides. At 1310 nm, 1 × 6 switching was demonstrated; the extinction ratios and crosstalks were found to be >20 and -20 dB, respectively. Switching time as low as 4 ms was observed. The device offers the advantage of a single-electrode driving scheme for 1×N(N>2) switching. [ABSTRACT FROM PUBLISHER]

Based on the total internal reflection and the plasma dispersion effect of SiGe alloy, an intersectional rib optical waveguide switch with bow-tie electrode has been proposed and fabricated for operating wavelengths of 1.3 and 1.55 μm. The thickness of the SiGe layer is 2.6 μm and the width is 9 μm. The branch angle of the switch is 2° and the bow-tie angle is 1.5°. The crosstalks are -19.6 dB for 1.3 μm and -21.8 dB for 1.55 μm. At both wavelengths, the extinction ratio is larger than 38.5 dB and the insertion loss is less than 1.70 dB. The switching time is about 180 ns [ABSTRACT FROM PUBLISHER]

High-speed optical switches are essential devices to construct next-generation optical networks. We have studied 22 InAlGaAs/InAlAs hybrid-waveguide-type Mach-Zehnder interferometer-type optical switches and demonstrated low-polarization-dependent switching operation with crosstalks of less than , injection currents of about 5 mA, and response times of about 3 ns. In this letter, our conventional 22 optical switch was extended to a 44 optical-switch fabric by a cascading approach. As a result, fundamental switching operation was confirmed with low power consumption and low polarization dependence. [ABSTRACT FROM PUBLISHER]

Thermooptic 2×2 switches with zero-voltage operation state are demonstrated. The devices made of ultraviolet curable fluorinated polymer are composed of four asymmetric digital optical switches and designed for bar-state operation with initial zero-voltage state. This zero-voltage operation is essential for protection switching in optical networks. The crosstalks of initial bar and cross states are more than 40 dB. The insertion loss and the polarization-dependent loss of the device are less than 1.8 and 0.1 dB for both states, respectively. The power consumption is about 350 mW. The wavelength and temperature dependences of the insertion loss are less than 0.3 dB. [ABSTRACT FROM PUBLISHER]

Orthogonally pumped four-wave mixing is known as an effective technique for polarization-insensitive optical phase conjugation in optical fibers. However, for phase conjugation of broad-band optical signals, a wide pump wavelength separation is a necessity in order to avoid crosstalks. This can result in an increase in polarization sensitivity of the scheme. As a solution to this problem, we propose a filter-free scheme that automatically rejects unwanted four-wave mixing products, such that broad-band optical phase conjugation can be achieved with a narrow pump wavelength separation for improved polarization insensitivity [ABSTRACT FROM PUBLISHER]