Singlet fission is a process whereby two triplet excitons can be produced from one photon, potentially increasing the efficiency of photovoltaic devices. Endothermic singlet fission is desired for a ...maximum energy-conversion efficiency, and such systems have been considered to form an excimer-like state with multiexcitonic character prior to the appearance of triplets. However, the role of the excimer as an intermediate has, until now, been unclear. Here we show, using 5,12-bis((triisopropylsilyl)ethynyl)tetracene in solution as a prototypical example, that, rather than acting as an intermediate, the excimer serves to trap excited states to the detriment of singlet-fission yield. We clearly demonstrate that singlet fission and its conjugate process, triplet-triplet annihilation, occur at a longer intermolecular distance than an excimer intermediate would impute. These results establish that an endothermic singlet-fission material must be designed to avoid excimer formation, thus allowing singlet fission to reach its full potential in enhancing photovoltaic energy conversion.
Patients with proximal deep-vein thrombosis were assigned to undergo anticoagulation either alone or combined with pharmacomechanical thrombolysis. After 6 to 24 months, there was no significant ...between-group difference in the incidence of the post-thrombotic syndrome.
Actin filament functional diversity is paralleled by variation in the composition of isoforms of tropomyosin in these filaments. Although the role of tropomyosin is well understood in skeletal ...muscle, where it regulates the actin–myosin interaction, its role in the cytoskeleton has been obscure. The intracellular sorting of tropomyosin isoforms indicated a role in spatial specialization of actin filament function. Genetic manipulation and protein chemistry studies have confirmed that these isoforms are functionally distinct. Tropomyosins differ in their recruitment of myosin motors and their interaction with actin filament regulators such as ADF-cofilin. Tropomyosin isoforms have therefore provided a powerful mechanism to diversify actin filament function in different intracellular compartments.
Abstract Background context Intraoperative imaging is essential in spinal surgery to both determine the correct level and place implants safely. Surgeons have a variety of options: C-arm fluoroscopy ...(C-arm), portable X-ray (XR) radiography, and portable cone-beam computed tomography (O-arm). Although these modalities have their respective advantages and disadvantages, direct comparison of radiation exposure to either the patient or the operating room (OR) staff has not been made. Purpose To determine the amount of radiation exposure to patients and OR staff during spine surgery with C-arm, XR, and O-arm. Study design An experimental model to assess radiation exposure to OR staff and phantom patient during spine surgery. Methods A plastic phantom was created to emulate patient volume and absorption scattering characteristics of a typical sized adult abdominal volume. Radiation exposure was measured with ion chamber dosimeters to determine entrance phantom and scatter exposures at common positions occupied by OR staff for C-arm, XR, and O-arm in typical image acquisition during spinal surgery. Results Single lateral (LAT)/posterior-anterior entrance patient radiation exposure for C-arm was on average 116/102 mR, single-exposure XR for LAT/anterior-posterior (AP) was 3,435/2,160 mR, and single-exposure O-arm for LAT/AP was 4,360/5,220 mR. O-arm surface exposure LAT/AP was equivalent to 38/41 C-arm and 1.5/2.4 XR exposures. The surgeon and surgeon assistant had higher levels of scatter radiation for C-arm, followed by O-arm and XR. For the LAT C-arm acquisition, a 7.7-fold increase in radiation exposure was measured on the X-ray tube side compared with the detector side. The anesthesiologist scatter radiation level for a single acquisition was highest for O-arm, followed by XR and C-arm. The radiologic technologist scatter radiation level was highest for XR, followed by O-arm and fluoroscopy. Overall radiation exposure to OR staff was less than 4.4 mR for a single acquisition in all modalities. Conclusions Assessment of radiation risk to the patient and OR staff should be part of the decision for utilization of any specific imaging modality during spinal surgery. This study provides the surgeon with information to better weigh the risks and benefits of each imaging modality.
Recent studies demonstrated that lignite application in feedlot can mitigate ammonia (NH3) emission from intensive livestock production, which is an important source of environmental pollution. ...However, the use of lignite on feedlot requires mining and transport of lignite, which are themselves sources of greenhouse gas and other gaseous pollutants. There is a need for an integrated assessment on the gas emissions to determine the potential impact of those additions to the production chain. Using a case study in Victoria, Australia, carbon dioxide (CO2) and NH3 were identified as key emission changes compared to business as usual (BAU). Social costs and benefits analysis indicated that these changes in emissions translate to social benefits of AUD$11 − $151 and $18 − $256 per cattle per year at lignite application rate of 3 and 6 kg m−2 respectively, while the corresponding social costs of the additional gaseous emissions are AUD$2 − $19 and $3 − $28 per cattle per year per 200 km. Our results indicate that the use of lignite in feedlot to mitigate NH3 can be targeted at feedlots located in proximity to lignite source, population centre and/or vulnerable ecosystems to maximise social benefits and minimise social costs. More broadly, estimating the social costs and benefits of changing manure management practice to mitigate NH3 emission generates information that can be used to evaluate alternative policies for N management.
•Lignite application in feedlot is effective at mitigating NH3 emission.•The trade-off from emissions from mining and transport of lignite is evaluated.•Social benefits are derived mainly from mitigated NH3 and indirect N2O.•Social costs mainly arise from CO2 and NOx emissions from transport.
More than a billion humans worldwide are predicted to be completely deficient in the fast skeletal muscle fiber protein α-actinin-3 owing to homozygosity for a premature stop codon polymorphism, ...R577X, in the ACTN3 gene. The R577X polymorphism is associated with elite athlete status and human muscle performance, suggesting that α-actinin-3 deficiency influences the function of fast muscle fibers. Here we show that loss of α-actinin-3 expression in a knockout mouse model results in a shift in muscle metabolism toward the more efficient aerobic pathway and an increase in intrinsic endurance performance. In addition, we demonstrate that the genomic region surrounding the 577X null allele shows low levels of genetic variation and recombination in individuals of European and East Asian descent, consistent with strong, recent positive selection. We propose that the 577X allele has been positively selected in some human populations owing to its effect on skeletal muscle metabolism.
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Dostopno za:
DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Actin has an ill‐defined role in the trafficking of GLUT4 glucose transporter vesicles to the plasma membrane (PM). We have identified novel actin filaments defined by the tropomyosin Tpm3.1 at ...glucose uptake sites in white adipose tissue (WAT) and skeletal muscle. In Tpm 3.1‐overexpressing mice, insulin‐stimulated glucose uptake was increased; while Tpm3.1‐null mice they were more sensitive to the impact of high‐fat diet on glucose uptake. Inhibition of Tpm3.1 function in 3T3‐L1 adipocytes abrogates insulin‐stimulated GLUT4 translocation and glucose uptake. In WAT, the amount of filamentous actin is determined by Tpm3.1 levels and is paralleled by changes in exocyst component (sec8) and Myo1c levels. In adipocytes, Tpm3.1 localizes with MyoIIA, but not Myo1c, and it inhibits Myo1c binding to actin. We propose that Tpm3.1 determines the amount of cortical actin that can engage MyoIIA and generate contractile force, and in parallel limits the interaction of Myo1c with actin filaments. The balance between these actin filament populations may determine the efficiency of movement and/or fusion of GLUT4 vesicles with the PM.
Actin's role in GLUT4 glucose transporter trafficking is unclear. We have identified novel actin filaments defined by the tropomyosin Tpm3.1 that regulates GLUT4 trafficking and glucose uptake. MyoIIA and Myo1c are known regulators of GLUT4 trafficking. Tpm3.1 has been shown to recruit MyoIIA to actin filaments and here we show that it inhibits Myo1c binding. The balance between Tpm3.1/MyoIIA and Tpm3.1‐free/Myo1c actin filament populations may determine the efficiency of movement and/or fusion of GLUT4 vesicles with the plasma membrane.
Sexual reproduction in animals requires close interactions with the opposite sex. These interactions may generate costs of reproduction, because mates can induce detrimental physiological or physical ...effects on one another, due to their interest in maximising their own fitness. To understand how a male's presence influences aspects of female physiology implicated in reproductive costs in mice, independent of offspring production, we paired females with vasectomised, castrated or intact males, or other females. Being paired with a male, irrespective of his gonadal status, increased female weight. This effect was transient in females paired with castrated males but more persistent in those with vasectomised males. Those paired with males also showed an increase in corticosterone, suggesting an increased stress response. However, this was dependent on the gonadal status of the male housing partner, since those housed with vasectomised males had lower corticosterone than those with castrated males. Altered energy metabolism was only detectable in pregnant females, and oxidative stress was not consistently affected by a female's housing partner. These results suggest that a male's presence alters female weight, and stresses associated with reproduction could be induced by simply the presence of a male, but reduced by mating and/or being solicited to mate.
Regulators of skeletal muscle mass are of interest, given the morbidity and mortality of muscle atrophy and myopathy. Four-and-a-half LIM protein 1 (FHL1) is mutated in several human myopathies, ...including reducing-body myopathy (RBM). The normal function of FHL1 in muscle and how it causes myopathy remains unknown. We find that FHL1 transgenic expression in mouse skeletal muscle promotes hypertrophy and an oxidative fiber-type switch, leading to increased whole-body strength and fatigue resistance. Additionally, FHL1 overexpression enhances myoblast fusion, resulting in hypertrophic myotubes in C2C12 cells, (a phenotype rescued by calcineurin inhibition). In FHL1-RBM C2C12 cells, there are no hypertrophic myotubes. FHL1 binds with the calcineurin-regulated transcription factor NFATc1 (nuclear factor of activated T cells, cytoplasmic, calcineurin-dependent 1), enhancing NFATc1 transcriptional activity. Mutant RBM-FHL1 forms aggregate bodies in C2C12 cells, sequestering NFATc1 and resulting in reduced NFAT nuclear translocation and transcriptional activity. NFATc1 also colocalizes with mutant FHL1 to reducing bodies in RBM-afflicted skeletal muscle. Therefore, via NFATc1 signaling regulation, FHL1 appears to modulate muscle mass and strength enhancement.
ERK-regulated cell proliferation requires multiple phosphorylation events catalyzed first by MEK and then by casein kinase 2 (CK2), followed by interaction with importin7 and subsequent nuclear ...translocation of pERK. We report that genetic manipulation of a core component of the actin filaments of cancer cells, the tropomyosin Tm5NM1, regulates the proliferation of normal cells both in vitro and in vivo. Mouse embryo fibroblasts (MEFs) lacking Tm5NM1, which have reduced proliferative capacity, are insensitive to inhibition of ERK by peptide and small-molecule inhibitors, indicating that ERK is unable to regulate proliferation of these knockout (KO) cells. Treatment of wild-type MEFs with a CK2 inhibitor to block phosphorylation of the nuclear translocation signal in pERK resulted in greatly decreased cell proliferation and a significant reduction in the nuclear translocation of pERK. In contrast, Tm5NM1 KO MEFs, which show reduced nuclear translocation of pERK, were unaffected by inhibition of CK2. This suggested that it is nuclear translocation of CK2-phosphorylated pERK that regulates cell proliferation and this capacity is absent in Tm5NM1 KO cells. Proximity ligation assays confirmed a growth factor-stimulated interaction of pERK with Tm5NM1 and that the interaction of pERK with importin7 is greatly reduced in the Tm5NM1 KO cells.
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