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Zeolite chemistry and catalysis are expected to play a decisive role in the next decade(s) to build a more decentralized renewable feedstock-dependent sustainable society owing to the increased scrutiny over carbon emissions. Therefore, the lack of fundamental and mechanistic understanding of these processes is a critical "technical bottleneck" that must be eliminated to maximize economic value and minimize waste. We have identified, considering this objective, that the chemistry related to the first-generation reaction intermediates (i.e., carbocations, radicals, carbenes, ketenes, and carbanions) in zeolite chemistry and catalysis is highly underdeveloped or undervalued compared to other catalysis streams (e.g., homogeneous catalysis). This limitation can often be attributed to the technological restrictions to detect such "short-lived and highly reactive" intermediates at the interface (gas-solid/solid-liquid); however, the recent rise of sophisticated spectroscopic/analytical techniques (including under in situ/operando conditions) and modern data analysis methods collectively compete to unravel the impact of these organic intermediates. This comprehensive review summarizes the state-of-the-art first-generation organic reaction intermediates in zeolite chemistry and catalysis and evaluates their existing challenges and future prospects, to contribute significantly to the "circular carbon economy" initiatives.

Acute respiratory distress syndrome (ARDS), a common respiratory critical illness with multiple causes, is associated with high mortality. The high degree of heterogeneity may be the reason why it is lack of highly specific and sensitive biological biomarkers. Therefore, it is an urgent need to explore biomarkers, perform phenotypic analysis and establish risk stratification model for diagnosis, prognosis, and treatment of ARDS. Endothelial cells specificity molecular-1 (ESM-1, endocan), is a soluble dermatan sulfate proteoglycan, and be involved in regulating biological behaviors such as cell proliferation, differentiation and migration. Numerous studies have confirmed that ESM-1 is closely related to inflammation, endothelial activation and dysfunction. However, the role of ESM-1 in the initiating and developing process of ARDS is still unclear. To provide a scientific basis for its clinical applications in ARDS, such as early prognosis assessment and timely prevent strategies, this paper focuses on the biological properties and the clinical value of ESM-1 as a potential biomarker for ARDS.

There are still many challenges in understanding the absorption and transport mechanism of liposomes in the gastrointestinal tract of infants, especially for liposome-coentrapped two or more substances. In this study, novel docosahexaenoic acid (DHA)-anthocyanidin-codelivery liposomes (DA-LPs) were fabricated and characterized, and their digestive and absorptive behaviors were evaluated using the in vitro infant digestive method combined with the Caco-2 cell model. The liposomal bilayer structure remained intact with the particles aggregated in simulated infant gastric fluid, while their phospholipid membrane underwent enzymatic lipolysis under simulated intestinal conditions. Compared to single substance-loaded liposomes (DHA- or anthocyanidin-loaded liposomes), the digested DA-LPs showed better cell viability, higher cellular uptake and membrane fluidity, and lower reactive oxygen species (ROS). It can be concluded that DA-LPs are promising carriers for simultaneously transporting hydrophobic and hydrophilic molecules and may be beneficial for improving nutrient absorption and alleviating intestinal stress oxidation.

Мы даем обзор ситуации с интегрируемостью геодезических потоков на трехмерных многообразиях $\mathcal M^3$, допускающих одну из трех групповых геометрий в смысле Тeрстона, обращая особое внимание на случай $\operatorname{SL}(2,\mathbb R)$. Основными примерами являются факторы $\mathcal M^3_\Gamma=\Gamma\backslash \operatorname{PSL}(2,\mathbb R)$, где $\Gamma \subset \operatorname{PSL}(2,\mathbb R)$ - кофинитная фуксова группа. Мы показываем, что соответствующее фазовое пространство $T^*\mathcal M_\Gamma^3$ содержит две открытые области с интегрируемым и хаотическим поведением, в которых топологическая энтропия равна нулю и положительна соответственно. В качестве конкретного примера мы рассматриваем модулярное 3-многообразие с модулярной группой $\Gamma=\operatorname{PSL}({2,\mathbb Z})$. Известно, что в этом случае $\mathcal M^3_\Gamma$ оказывается гомеоморфным дополнению к узлу-трилистнику $\mathcal K$ в 3-сфере. Э. Жис доказал замечательный факт: поднятие периодических геодезических с модулярной поверхности на $\mathcal M^3_\Gamma$ приводит к тому же изотопическому классу узлов, который возник в хаотической версии знаменитой системы Лоренца и был подробно изучен Дж. Бирман и Р. Уильямсом. Мы показываем, что в интегрируемом пределе геодезической системы на $\mathcal M^3_\Gamma$ эти узлы переходят в кабельные узлы трилистника. Библиография: 60 названий.

Background: Acute respiratory distress syndrome (ARDS) is a challenging clinical problem. To date, no standardized diagnostic biomarker has been validated for community-acquired pneumonia (CAP)-induced ARDS. An integrated analysis of changes in the metabolic profile could help detect biomarkers for early prediction of ARDS development and evaluation of treatment efficacy.Methods: A total of 88 patients were enrolled for the final analysis and divided into two groups: the ARDS group (n = 43) and the no-ARDS group (n = 45). We examined differences in serum and urine metabolites and explored dynamic changes with nuclear magnetic resonance (NMR) spectroscopy.Results: A total of 20 serum and 42 urine metabolites were identified using NMR spectroscopy. Serum metabolites, including leucine, 3-hydroxybutyrate, lactate, acetone, citrate, and choline, and urine metabolites, including creatine and creatinine, could distinguish patients with CAP with and without ARDS, with areas under the receiver operating characteristic curve (AUC) values of 0.790 and 0.747, respectively. The treatment efficacy of patients with ARDS was achieved at an AUC of 0.862 with serum metabolites 3-hydroxybutyrate, lactate, acetone, acetoacetate, citrate, and choline, and of 0.691 with urine metabolites taurine and glucose. The treatment efficacy of patients without ARDS was achieved at an AUC of 0.845 with serum metabolites alanine, acetate, acetoacetate, glutamine, creatine, and glucose and 0.891 with urine metabolites choline, tryptamine, and 3-indoxyl sulfate. We also proposed a combined biomarker of associated serum and urine metabolites to predict ARDS in patients with CAP (AUC = 0.865) and evaluate treatment efficacy for patients with and without ARDS (AUC = 0.921 and 0.893, respectively).Conclusions: Serum and urine analyses showed that metabolomics provides potential circulatory markers for early prediction and evaluation of treatment efficacy in patients with CAP with and without ARDS.

There are still many challenges in understanding the absorption and transport mechanism of liposomes in the gastrointestinal tract of infants, especially for liposome-coentrapped two or more substances. In this study, novel docosahexaenoic acid (DHA)-anthocyanidin-codelivery liposomes (DA-LPs) were fabricated and characterized, and their digestive and absorptive behaviors were evaluated using the

Minimal hepatic encephalopathy (MHE) is implicated in the impairment of memory function. Fibroblast growth factor-2 (FGF2) is involved in modulating synaptic and neuronal formation. The aim of this study is to examined the impacts of FGF2 on MHE pathology. Our study addressed whether FGF2 could trigger neuregulin1 (NRG1) release to ameliorate synaptic impairment in MHE rats and in primary cultured neurons. The results showed the decreased FGF2 expression in MHE brains. After treatment with FGF2, secreted neuregulin1 (NRG1) and ErbB4 were increased, and the interaction of the 2 proteins was enhanced. Additionally, treatment with FGF2 or NRG1 induced synaptic formation, with increase in the activity of synapse and the density of dendritic spine, through Sirt1.NRG1 signaling was prevented by administration of FGF2, which acts through the FGFR1 in MHE rats. Intracerebroventricular injection with FGF2 or NRG1 mitigated the impairment of synaptogenesis. The data suggest that FGF2 may be a promising latent therapeutic reagent for MHE pathogenesis.

The thesis consists of two parts. In the first part, we study the integrability of geodesic flows on 3-manifolds that admit $\widetilde{SL(2,\mathbb R)}$ geometry in Thurston's sense. The main examples are the quotients $\mathcal M^3_\Gamma=\Gamma\backslash PSL(2,\mathbb R)$, where $\Gamma \subset PSL(2,\mathbb R)$ is a cofinite Fuchsian group. We show that the corresponding phase space $T^*\mathcal M_\Gamma^3$ contains two open regions with integrable and chaotic behaviour. In the integrable region we have Liouville integrability with analytic integrals, while in the chaotic region the system is not Liouville integrable even in smooth category and has positive topological entropy.In the concrete example of the modular group $\Gamma=PSL({2,\mathbb Z})$ we extend the link of periodic geodesics with knot theory, discovered by Ghys, to the integrable region. In the second part, we consider the integrable generalisations of the Dirac magnetic monopole on sphere $\mathbb S^2$ with general metric and constant non-zero density of magnetic field. We complete the local classification results of such systems by Ferapontov, Sayles and Veselov, extending them to the analytic integrable systems on the topological sphere. In the limiting even case we have the new integrable two-centre problem on the usual round sphere in the external field of Dirac magnetic monopole.

BackgroundMinimal hepatic encephalopathy (MHE) is implicated in the impairment of memory function. Fibroblast growth factor-2 (FGF2) is involved in modulating synaptic and neuronal formation.MethodsThe aim of this study is to examined the impacts of FGF2 on MHE pathology. Our study addressed whether FGF2 could trigger neuregulin-1 (NRG1) release to ameliorate synaptic impairment in MHE rats and in primary cultured neurons.ResultsThe results showed the decreased FGF2 expression in MHE brains. After treatment with FGF2, secreted neuregulin-1 (NRG1) and ErbB4 were increased, and the interaction of the 2 proteins was enhanced. Additionally, treatment with FGF2 or NRG1 induced synaptic formation, with increase in the activity of synapse and the density of dendritic spine, through Sirt1. NRG1 signaling was prevented by administration of FGF2, which acts through the FGFR1 in MHE rats. Finally, intracerebroventricular injection with FGF2 or NRG1 mitigated the impairment of synaptogenesis.ConclusionThe data suggest that FGF2 may be a promising latent therapeutic reagent for MHE pathogenesis.

Background: We previously reported that elevation of intracranial dopamine (DA) levels from cirrhotic livers is implicated in the pathogenesis of minimal hepatic encephalopathy (MHE). Intracellular events in neurons, which lead to memory loss in MHE by elevated DA, however, remain elusive. Methods: In our present study, an MHE rat model, a DA - intracerebroventricularly (i.c.v.) injected rat model and DA-treated primary cortical neurons (PCNs) were used to study this issue using behavioral tests, double-labeled fluorescent staining, immunoblotting, and semi-quantitative RT-PCR. Results: Cognitive impairment was observed in MHE rats and DA (10 µg, i.c.v.)-treated rats. The levels of DA in the cerebral cortex of both MHE and DA (10 µg)-treated rats were increased. DA conversely modulated the p-JAK2/p-STAT3 levels in PCNs. In accordance, DA downregulated an anacetylcholine-producing enzyme, choline acetyltransferase (ChAT), and desensitized the M1-type muscarinic acetylcholine receptor (M1 mAChR). Furthermore, naringin completely restored cognitive function in MHE/DA (10 µg)-treated models by activating the JAK2/STAT3 axis, paralleling the upregulation of ChAT and sensitization of M1 mAChR. Conclusions: We propose a hypothesis accounting for memory impairment related to MHE: DA-dependent inactivation of the JAK2/STAT3 axis causes memory loss through cholinergic dysfunction. Our findings provide not only a novel pathological hallmark in MHE but also a novel target in MHE therapy.

In a previous study by our group memory impairment in rats with minimal hepatic encephalopathy (MHE) was associated with the inhibition of the glutamate-nitric oxide-cyclic guanosine monophosphate (Glu-NO-cGMP) pathway due to elevated dopamine (DA). However, the effects of DA on the Glu-NO-cGMP pathway localized in primary cortical astrocytes (PCAs) had not been elucidated in rats with MHE. In the present study, it was identified that when the levels of DA in the cerebral cortex of rats with MHE and high-dose DA (3 mg/kg)-treated rats were increased, the co-localization of N-methyl-d-aspartate receptors subunit 1 (NMDAR1), calmodulin (CaM), nitric oxide synthase (nNOS), soluble guanylyl cyclase (sGC) and cyclic guanine monophosphate (cGMP) with the glial fibrillary acidic protein (GFAP), a marker protein of astrocytes, all significantly decreased, in both the MHE and high-dose DA-treated rats (P

Dopamine (DA)-induced learning and memory impairment is well documented in minimal hepatic encephalopathy (MHE), but the contribution of DA to neurodegeneration and the involved underlying mechanisms are not fully understood. In this study, the effect of DA on neuronal apoptosis was initially detected. The results showed that MHE/DA (10 μg)-treated rats displayed neuronal apoptosis. However, we found that DA (10 μM) treatment did not induce evident apoptosis in primary cultured neurons (PCNs) but did produce TNF-α in primary cultured astrocytes (PCAs). Furthermore, co-cultures between PCAs and PCNs exposed to DA exhibited increased astrocytic TNF-α levels and neuronal apoptosis compared with co-cultures exposed to the vehicle, indicating the attribution of the neuronal apoptosis to astrocytic TNF-α. We also demonstrated that DA enhanced TNF-α production from astrocytes by activation of the TLR4/MyD88/NF-κB pathway, and secreted astrocytic TNF-α-potentiated neuronal apoptosis through inactivation of the PI3K/Akt/mTOR pathway. Overall, the findings from this study suggest that DA stimulates substantial production and secretion of astrocytic TNF-α, consequently and indirectly triggering progressive neurodegeneration, resulting in cognitive decline and memory loss in MHE.

Background We previously demonstrated that dopamine (DA) overload may be a key mechanism behind development of minimal hepatic encephalopathy (MHE) in rats. It has been shown that low-grade cerebral oedema and oxidative stress play important roles in the pathogenesis of MHE. In the current study, DA-triggered oxidative injury in cerebral cortex was studied. Methods An MHE rat model was used. DA was injected intracerebroventricularly (i.c.v.) into rats and added to primary cortical astrocytes (PCAs). Immunoblotting, immunoprecipitation and immunostaining were conducted after DA injection. Results Cognitive impairment and cerebral edema were observed in MHE rats and rats injected with 10 μg DA. Astrocyte swelling was increased by DA. Astrocytic protein tyrosine nitration (PTN) was induced by DA. DA-induced PTN was insensitive to l -NMMA but was blunted by apocynin, superoxide dismutase, catalase and uric acid. Exposure to DA substantially increased levels of astrocytic NADPH oxidase subunits and induced p47 phox phosphorylation and reactive oxygen species production but decreased the expression and activity of neuronal-type nitric oxide synthase (nNOS). Conclusions PTN induced by DA, which was attributed to NADPH oxidase and not to nNOS, may alter astrocyte function and thereby contribute to the precipitation of MHE episodes.

The amount of books has been one of the important indexes to measure the libraries' level. While the books' daily management work in library such as how to classify and place books has aggravated the burden of the librarians. The rapid development of mobile-robot technology and multi-agent give a new possible method to solve this problem. therefore, this paper provides a mobile-robot model based on multi-agent technology, which can recognize, classify and place books automatically, and navigate the walk route by improved BUG algorithm which can complete the work of classify and arrange books quickly and correctly. This model can simplify the traditional manual work and lighten the heavy and repeated labor, which produces the far-reaching realistic meaning for introducing the artificial intelligence technology into daily life.