21 research outputs found
Конверсия попутных нефтяных газов С3-С4 в жидкие углеводороды на модифицированных цеолитных катализаторах
Исследованы влияние модифицирования цеолита типа MFI и активированные плазмой, на кислотные и каталитические свойства в конверсии пропан-бутановой фракции в арены.The effect of modification of MFI zeolite activated by plasma on acid and catalytic properties in the conversion of the propane-butane fraction into arenes was investigated
Resilient cooling strategies – A critical review and qualitative assessment
The global effects of climate change will increase the frequency and intensity of extreme events such as heatwaves and power outages, which have consequences for buildings and their cooling systems. Buildings and their cooling systems should be designed and operated to be resilient under such events to protect occupants from potentially dangerous indoor thermal conditions. This study performed a critical review on the state-of-the-art of cooling strategies, with special attention to their performance under heatwaves and power outages. We proposed a definition of resilient cooling and described four criteria for resilience—absorptive capacity, adaptive capacity, restorative capacity, and recovery speed —and used them to qualitatively evaluate the resilience of each strategy. The literature review and qualitative analyses show that to attain resilient cooling, the four resilience criteria should be considered in the design phase of a building or during the planning of retrofits. The building and relevant cooling system characteristics should be considered simultaneously to withstand extreme events. A combination of strategies with different resilience capacities, such as a passive envelope strategy coupled with a low-energy space-cooling solution, may be needed to obtain resilient cooling. Finally, a further direction for a quantitative assessment approach has been pointed out
Resilient cooling strategies – A critical review and qualitative assessment
The global effects of climate change will increase the frequency and intensity of extreme events such as heatwaves and power outages, which have consequences for buildings and their cooling systems. Buildings and their cooling systems should be designed and operated to be resilient under such events to protect occupants from potentially dangerous indoor thermal conditions. This study performed a critical review on the state-of-the-art of cooling strategies, with special attention to their performance under heatwaves and power outages. We proposed a definition of resilient cooling and described four criteria for resilience—absorptive capacity, adaptive capacity, restorative capacity, and recovery speed —and used them to qualitatively evaluate the resilience of each strategy. The literature review and qualitative analyses show that to attain resilient cooling, the four resilience criteria should be considered in the design phase of a building or during the planning of retrofits. The building and relevant cooling system characteristics should be considered simultaneously to withstand extreme events. A combination of strategies with different resilience capacities, such as a passive envelope strategy coupled with a low-energy space-cooling solution, may be needed to obtain resilient cooling. Finally, a further direction for a quantitative assessment approach has been pointed out
On and Off: Epigenetic Regulation of C. albicans Morphological Switches
The human fungal pathogen Candida albicans is a dimorphic opportunistic pathogen that colonises most of the human population without creating any harm. However, this fungus can also cause life-threatening infections in immunocompromised individuals. The ability to successfully colonise different host niches is critical for establishing infections and pathogenesis. C. albicans can live and divide in various morphological forms critical for its survival in the host. Indeed, C. albicans can grow as both yeast and hyphae and can form biofilms containing hyphae. The transcriptional regulatory network governing the switching between these different forms is complex but well understood. In contrast, non-DNA based epigenetic modulation is emerging as a crucial but still poorly studied regulatory mechanism of morphological transition. This review explores our current understanding of chromatin-mediated epigenetic regulation of the yeast to hyphae switch and biofilm formation. We highlight how modification of chromatin structure and non-coding RNAs contribute to these morphological transitions
Identification of Activating Mutations in the Transmembrane and Extracellular Domains of EGFR
The epidermal growth factor receptor (EGFR) is frequently
mutated
in human cancer, most notably non-small-cell lung cancer and glioblastoma.
While many frequently occurring EGFR mutations are known to confer
constitutive EGFR activation, the situation is less clear for rarely
detected variants. In fact, more than 1000 distinct EGFR mutations
are listed in the Catalogue of Somatic Mutations in Cancer (COSMIC),
but for most of them, the functional consequence is unknown. To identify
additional, previously unknown activating mutations in EGFR, we screened
a randomly mutated EGFR library for constitutive EGFR phosphorylation
using a recently developed high-throughput approach termed PhosphoFlowSeq.
Enrichment of the well-known activating mutations S768I, T790M, and
L858R validated the experimental approach. Importantly, we also identified
the activating mutations S442I and L658Q located in the extracellular
and transmembrane domains of EGFR, respectively. To the best of our
knowledge, neither S442I nor L658Q has been associated with an activating
phenotype before. However, both have been detected in cancer samples.
Interestingly, molecular dynamics (MD) simulations suggest that the
L658Q mutation located in the hydrophobic transmembrane region forms
intermolecular hydrogen bonds, thereby promoting EGFR dimerization
and activation. Based on these findings, we screened the COSMIC database
for additional hydrophilic mutations in the EGFR transmembrane region
and indeed detected moderate constitutive activation of EGFR-G652R.
Together, this study demonstrates that unbiased screening for activating
mutations in EGFR not only yields well-established substitutions located
in the kinase domain but also activating mutations in other regions
of EGFR, including the extracellular and transmembrane domains
Identification of Activating Mutations in the Transmembrane and Extracellular Domains of EGFR
The epidermal growth factor receptor (EGFR) is frequently
mutated
in human cancer, most notably non-small-cell lung cancer and glioblastoma.
While many frequently occurring EGFR mutations are known to confer
constitutive EGFR activation, the situation is less clear for rarely
detected variants. In fact, more than 1000 distinct EGFR mutations
are listed in the Catalogue of Somatic Mutations in Cancer (COSMIC),
but for most of them, the functional consequence is unknown. To identify
additional, previously unknown activating mutations in EGFR, we screened
a randomly mutated EGFR library for constitutive EGFR phosphorylation
using a recently developed high-throughput approach termed PhosphoFlowSeq.
Enrichment of the well-known activating mutations S768I, T790M, and
L858R validated the experimental approach. Importantly, we also identified
the activating mutations S442I and L658Q located in the extracellular
and transmembrane domains of EGFR, respectively. To the best of our
knowledge, neither S442I nor L658Q has been associated with an activating
phenotype before. However, both have been detected in cancer samples.
Interestingly, molecular dynamics (MD) simulations suggest that the
L658Q mutation located in the hydrophobic transmembrane region forms
intermolecular hydrogen bonds, thereby promoting EGFR dimerization
and activation. Based on these findings, we screened the COSMIC database
for additional hydrophilic mutations in the EGFR transmembrane region
and indeed detected moderate constitutive activation of EGFR-G652R.
Together, this study demonstrates that unbiased screening for activating
mutations in EGFR not only yields well-established substitutions located
in the kinase domain but also activating mutations in other regions
of EGFR, including the extracellular and transmembrane domains
Identification of Activating Mutations in the Transmembrane and Extracellular Domains of EGFR
The epidermal growth factor receptor (EGFR) is frequently
mutated
in human cancer, most notably non-small-cell lung cancer and glioblastoma.
While many frequently occurring EGFR mutations are known to confer
constitutive EGFR activation, the situation is less clear for rarely
detected variants. In fact, more than 1000 distinct EGFR mutations
are listed in the Catalogue of Somatic Mutations in Cancer (COSMIC),
but for most of them, the functional consequence is unknown. To identify
additional, previously unknown activating mutations in EGFR, we screened
a randomly mutated EGFR library for constitutive EGFR phosphorylation
using a recently developed high-throughput approach termed PhosphoFlowSeq.
Enrichment of the well-known activating mutations S768I, T790M, and
L858R validated the experimental approach. Importantly, we also identified
the activating mutations S442I and L658Q located in the extracellular
and transmembrane domains of EGFR, respectively. To the best of our
knowledge, neither S442I nor L658Q has been associated with an activating
phenotype before. However, both have been detected in cancer samples.
Interestingly, molecular dynamics (MD) simulations suggest that the
L658Q mutation located in the hydrophobic transmembrane region forms
intermolecular hydrogen bonds, thereby promoting EGFR dimerization
and activation. Based on these findings, we screened the COSMIC database
for additional hydrophilic mutations in the EGFR transmembrane region
and indeed detected moderate constitutive activation of EGFR-G652R.
Together, this study demonstrates that unbiased screening for activating
mutations in EGFR not only yields well-established substitutions located
in the kinase domain but also activating mutations in other regions
of EGFR, including the extracellular and transmembrane domains