177 research outputs found
Tuning Metal-Organic Frameworks and Porous Polymers for Gas Storage and Separations
The focus of this research is to investigate how the exact shape, functionalization, and pore structure, specifically the distribution and filling of meso- and micropores, affects the chemical environment within the pores, especially when it comes to the adsorption and condensation of gas molecules. This is accomplished through pore engineering, tuning the nanostructures of the material for a particular application. However, the true rational design of MOFs and other porous materials is still a goal we have taken only a few small steps towards. Thus, considerable effort has also been devoted to the development of synthetic techniques necessary to grow new kinds of MOFs and PPNs in a planned manner.
The development of an extensive library of synthetic and post-synthetic modification techniques for MOFs and porous polymers is how researchers will be able to eventually achieve âtotal synthesisâ of desired porous materials, rather than relying on trial and error and serendipitously discovered existing materials. Organic chemists were able to achieve the total synthesis of complex natural products only after centuries of synthetic and theoretical study. Porous materials chemists will eventually be able to design or mimic complex pore environments such as enzyme active sites or catalysts for complex tandem and multistep reactions. However, this will only occur if we can develop a similarly massive library of complicated synthetic techniques and improved theoretical understanding of crystallization processes.
Our work towards this goal begins with a comprehensive review of recent developments in MOF synthesis, especially the development of new synthetic methods to impart intricate functionality into ultrastable MOFs. Our groupâs development of Kinetically Tuned Dimensional Augmentation, Post-synthetic Metathesis and Oxidation, and Sequential Linker Installation and Cluster Metalation have contributed to the grand challenge of the rational design and total synthesis of MOF structures and greater control of pore environments. As a related subject, we also cover recent development in the design of various types of porous carbons for hydrogen storage.
We then cover the development of pre-synthetic modulation methods to alter MOF properties and produce new MOFs. Using lithium salts as a modulator, the porosity and hydrogen uptake of anionic MOFs can be improved. We can also use Mn sources in different oxidation states to produce Mn(II) MOFs with different structures and porosities with the same linker.
Post-synthetic modification techniques are explored through the loading of sorbents for CO2 and methane uptake with liquid alkylamines and alkanes, respectively, in order to combine adsorption and absorption in a single material and efficiently use an available volume. Both techniques demonstrate improvements in uptake over the unmodified materials, with a focus on their exceptional stability, cyclability, and cost-effectiveness, as they are targeted for widespread application
The Tully-Fisher relation for S0 galaxies
We present a study of the local B and K-band Tully-Fisher Relation (TFR)
between absolute magnitude and maximum circular speed in S0 galaxies. To make
this study, we have combined kinematic data, including a new high-quality
spectral data set from the Fornax Cluster, with homogeneous photometry from the
RC3 and 2MASS catalogues, to construct the largest sample of S0 galaxies ever
used in a study of the TFR. Independent of environment, S0 galaxies are found
to lie systematically below the TFR for nearby spirals in both optical and
infrared bands. This offset can be crudely interpreted as arising from the
luminosity evolution of spiral galaxies that have faded since ceasing star
formation. However, we also find a large scatter in the TFR. We show that most
of this scatter is intrinsic, not due to the observational uncertainties. The
presence of such a large scatter means that the population of S0 galaxies
cannot have formed exclusively by the above simple fading mechanism after all
transforming at a single epoch. To better understand the complexity of the
transformation mechanism, we have searched for correlations between the offset
from the TFR and other properties of the galaxies such as their structural
properties, central velocity dispersions and ages (as estimated from line
indices). For the Fornax Cluster data, the offset from the TFR relates with the
estimated age of the stars in the individual galaxies, in the sense and of the
magnitude expected if S0 galaxies had passively faded since being converted
from spirals. This correlation implies that a significant part of the scatter
in the TFR arises from the different times at which galaxies began their
transformation.Comment: 17 pages, 11 figures, 3 tables, accepted for publication in MNRA
Structural properties of disk galaxies. II. Intrinsic shape of bulges
(Abridged) The structural parameters of a magnitude-limited sample of 148
unbarred S0-Sb galaxies were analyzed to derive the intrinsic shape of their
bulges. We developed a new method to derive the intrinsic shape of bulges based
on the geometrical relationships between the apparent and intrinsic shapes of
bulges and disks. The equatorial ellipticity and intrinsic flattening of bulges
were obtained from the length of the apparent major and minor semi-axes of the
bulge, twist angle between the apparent major axis of the bulge and the galaxy
line of nodes, and galaxy inclination. We found that the intrinsic shape is
well constrained for a subsample of 115 bulges with favorable viewing angles. A
large fraction of them is characterized by an elliptical section (B/A<0.9).
This fraction is 33%, 55%, and 43% if using their maximum, mean, or median
equatorial ellipticity, respectively. Most are flattened along their polar axis
(C<(A+B)/2). The distribution of triaxiality is strongly bimodal. This
bimodality is driven by bulges with Sersic index n>2, or equivalently, by the
bulges of galaxies with a bulge-to-total ratio B/T>0.3. In particular, bulges
with n\leq2 and with B/T\leq0.3 show a larger fraction of oblate axisymmetric
(or nearly axisymmetric) bulges, a smaller fraction of triaxial bulges, and
fewer prolate axisymmetric (or nearly axisymmetric) bulges with respect to
bulges with n>2 and with B/T>0.3, respectively. According to predictions of the
numerical simulations of bulge formation, bulges with n\leq2, which show a high
fraction of oblate axisymmetric (or nearly axisymmetric) shapes and have
B/T\leq0.3, could be the result of dissipational minor mergers. Both major
dissipational and dissipationless mergers seem to be required to explain the
variety of shapes found for bulges with n>2 and B/T>0.3.Comment: 16 pages, 12 figures; accepted for publication in A&
Thickening of galactic disks through clustered star formation
(Abridged) The building blocks of galaxies are star clusters. These form with
low-star formation efficiencies and, consequently, loose a large part of their
stars that expand outwards once the residual gas is expelled by the action of
the massive stars. Massive star clusters may thus add kinematically hot
components to galactic field populations. This kinematical imprint on the
stellar distribution function is estimated here by calculating the velocity
distribution function for ensembles of star-clusters distributed as power-law
or log-normal initial cluster mass functions (ICMFs). The resulting stellar
velocity distribution function is non-Gaussian and may be interpreted as being
composed of multiple kinematical sub-populations. The notion that the formation
of star-clusters may add hot kinematical components to a galaxy is applied to
the age--velocity-dispersion relation of the Milky Way disk to study the
implied history of clustered star formation, with an emphasis on the possible
origin of the thick disk.Comment: MNRAS, accepted, 27 pages, 9 figure
Inhibition of histone deacetylase 6 (HDAC6) protects against vincristine-induced peripheral neuropathies and inhibits tumor growth
As cancer is becoming more and more a chronic disease, a large proportion of patients is confronted with devastating side effects of certain anti-cancer drugs. The most common neurological complications are painful peripheral neuropathies. Chemotherapeutics that interfere with microtubules, including plant-derived vinca-alkaloids such as vincristine, can cause these chemotherapy-induced peripheral neuropathies (CIPN). Available treatments focus on symptom alleviation and pain reduction rather than prevention of the neuropathy. The aim of this study was to investigate the potential of specific histone deacetylase 6 (HDAC6) inhibitors as a preventive therapy for CIPN using multiple rodent models for vincristine-induced peripheral neuropathies (VIPN). HDAC6 inhibition increased the level of acetylated α-tubulin in tissues of rodents undergoing vincristine-based chemotherapy, which correlates to a reduced severity of the neurological symptoms, both at the electrophysiological and the behavioral level. Mechanistically, disturbances in axonal transport of mitochondria is considered as an important contributing factor in the pathophysiology of VIPN. As vincristine interferes with the polymerization of microtubules, we investigated whether disturbances in axonal transport could contribute to VIPN. We observed that increasing α-tubulin acetylation through HDAC6 inhibition restores vincristine-induced defects of axonal transport in cultured dorsal root ganglion neurons. Finally, we assured that HDAC6-inhibition offers neuroprotection without interfering with the anti-cancer efficacy of vincristine using a mouse model for acute lymphoblastic leukemia. Taken together, our results emphasize the therapeutic potential of HDAC6 inhibitors with beneficial effects both on vincristine-induced neurotoxicity, as well as on tumor proliferation. ispartof: Neurobiology of Disease vol:111 pages:59-69 ispartof: location:United States status: publishe
Dietary Long-Chain n-3 Polyunsaturated Fatty Acid Supplementation Alters Electrophysiological Properties in the Nucleus Accumbens and Emotional Behavior in NaĂŻve and Chronically Stressed Mice
Long-chain (LC) n-3 polyunsaturated fatty acids (PUFAs) have drawn attention in the field of neuropsychiatric disorders, in particular depression. However, whether dietary supplementation with LC n-3 PUFA protects from the development of mood disorders is still a matter of debate. In the present study, we studied the effect of a two-month exposure to isocaloric diets containing n-3 PUFAs in the form of relatively short-chain (SC) (6% of rapeseed oil, enriched in α-linolenic acid (ALA)) or LC (6% of tuna oil, enriched in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) PUFAs on behavior and synaptic plasticity of mice submitted or not to a chronic social defeat stress (CSDS), previously reported to alter emotional and social behavior, as well as synaptic plasticity in the nucleus accumbens (NAc). First, fatty acid content and lipid metabolism gene expression were measured in the NAc of mice fed a SC (control) or LC n-3 (supplemented) PUFA diet. Our results indicate that LC n-3 supplementation significantly increased some n-3 PUFAs, while decreasing some n-6 PUFAs. Then, in another cohort, control and n-3 PUFA-supplemented mice were subjected to CSDS, and social and emotional behaviors were assessed, together with long-term depression plasticity in accumbal medium spiny neurons. Overall, mice fed with n-3 PUFA supplementation displayed an emotional behavior profile and electrophysiological properties of medium spiny neurons which was distinct from the ones displayed by mice fed with the control diet, and this, independently of CSDS. Using the social interaction index to discriminate resilient and susceptible mice in the CSDS groups, n-3 supplementation promoted resiliency. Altogether, our results pinpoint that exposure to a diet rich in LC n-3 PUFA, as compared to a diet rich in SC n-3 PUFA, influences the NAc fatty acid profile. In addition, electrophysiological properties and emotional behavior were altered in LC n-3 PUFA mice, independently of CSDS. Our results bring new insights about the effect of LC n-3 PUFA on emotional behavior and synaptic plasticity
Estrogen regulation of TRPM8 expression in breast cancer cells
<p>Abstract</p> <p>Background</p> <p>The calcium-permeable cation channel TRPM8 (melastatin-related transient receptor potential member 8) is over-expressed in several cancers. The present study aimed at investigating the expression, function and potential regulation of TRPM8 channels by ER alpha (estrogen receptor alpha) in breast cancer.</p> <p>Methods</p> <p>RT-PCR, Western blot, immuno-histochemical, and siRNA techniques were used to investigate TRPM8 expression, its regulation by estrogen receptors, and its expression in breast tissue. To investigate the channel activity in MCF-7 cells, we used the whole cell patch clamp and the calcium imaging techniques.</p> <p>Results</p> <p>TRPM8 channels are expressed at both mRNA and protein levels in the breast cancer cell line MCF-7. Bath application of the potent TRPM8 agonist Icilin (20 ΌM) induced a strong outwardly rectifying current at depolarizing potentials, which is associated with an elevation of cytosolic calcium concentration, consistent with established TRPM8 channel properties. RT-PCR experiments revealed a decrease in TRPM8 mRNA expression following steroid deprivation for 48 and 72 hours. In steroid deprived medium, addition of 17-beta-estradiol (E<sub>2</sub>, 10 nM) increased both TRPM8 mRNA expression and the number of cells which respond to Icilin, but failed to affect the Ca<sup>2+ </sup>entry amplitude. Moreover, silencing ERα mRNA expression with small interfering RNA reduced the expression of TRPM8. Immuno-histochemical examination of the expression of TRPM8 channels in human breast tissues revealed an over-expression of TRPM8 in breast adenocarcinomas, which is correlated with estrogen receptor positive (ER<sup>+</sup>) status of the tumours.</p> <p>Conclusion</p> <p>Taken together, these results show that TRPM8 channels are expressed and functional in breast cancer and that their expression is regulated by ER alpha.</p
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