Efficient nitrite accumulation in partial sulfide autotrophic denitrification (PSAD) system: insights of S/N ratio, pH and temperature.

To provide the necessary nitrite for the Anaerobic Ammonium Oxidation (ANAMMOX) process, the effect of nitrite accumulation in the partial sulfide autotrophic denitrification (PSAD) process was investigated using an SBR reactor. The results revealed that the effectiveness of nitrate removal was unsatisfactory when the S/N ratio (mol/mol) fell below 0.6. The optimal conditions for nitrate removal and nitrite accumulation were achieved within the S/N ratio range of 0.7-0.8, resulting in an average Nitrate Removal Efficiency (NRE) of 95.84%±4.89% and a Nitrite Accumulation Rate (NAR) of 75.31%±6.61%, respectively. It was observed that the nitrate reduction rate was three times faster than that of nitrite reduction during a typical cycle test. Furthermore, batch tests were conducted to assess the influence of pH and temperature conditions. In the pH tests, it became evident that the PSAD process performed more effectively in alkaline environment. The highest levels of nitrate removal and nitrite accumulation were achieved at an initial pH of 8.5, resulting in a NRE of 98.30%±1.93% and a NAR of 85.83%±0.47%, respectively. In the temperature tests, the most favourable outcomes for nitrate removal and nitrite accumulation were observed at 22±1 ℃, with a NRE of 100.00% and a NAR of 81.03%±1.64%, respectively. Moreover, a comparative analysis of 16S rRNA sequencing results between the raw sludge and the sulfide-enriched culture sludge sample showed that Proteobacteria (49.51%) remained the dominant phylum, with Thiobacillus (24.72%), Prosthecobacter (2.55%), Brevundimonas (2.31%) and Ignavibacterium (2.04%) emerging as the dominant genera, assuming the good nitrogen performance of the system.

Effect of glucose pretreatment on Cu-ZnO-Al2O3 catalyzed CO2 hydrogenation to methanol.

A series of Cu-ZnO-Al2O3 catalysts (CZA) were prepared by glucose pretreatment and applied for methanol synthesis from CO2 hydrogenation. The advantages of the glucose pretreatment and the effects of glucose content were investigated by XRD, N2 physisorption, SEM, N2O chemisorption, CO2-TPD, H2-TPR, TG, and XPS characterization techniques. The influence of glucose pretreatment on the average Cu particle size and the interaction between different components, as well as the effects of the amount of glucose on the Cu specific surface area, the ratio of Cu0/Cu+ and the performance of the catalysts were discussed. The results showed that the catalysts prepared by glucose pretreatment increased the number of basic sites and had a significant advantage in methanol yield. The optimum content of glucose was beneficial to improve the catalytic performance of the CZA catalyst. The maximum space-time yield of methanol was obtained by 2 wt% glucose pretreatments at 200 °C, which was 57.0 g kg-1 h-1.

Patients with Asian-type DEL can safely be transfused with RhD-positive blood.

Red blood cells (RBCs) of Asian-type DEL phenotype express few RhD proteins and are typed as serologic RhD-negative (D-) phenotype in routine testing. RhD-positive (D+) RBC transfusion for patients with Asian-type DEL has been proposed but has not been generally adopted because of a lack of direct evidence regarding its safety and the underlying mechanism. We performed a single-arm multicenter clinical trial to document the outcome of D+ RBC transfusion in patients with Asian-type DEL; none of the recipients (0/42; 95% confidence interval, 0-8.40) developed alloanti-D after a median follow-up of 226 days. We conducted a large retrospective study to detect alloanti-D immunization in 4045 serologic D- pregnant women throughout China; alloanti-D was found only in individuals with true D- (2.63%, 79/3009), but not in those with Asian-type DEL (0/1032). We further retrospectively examined 127 serologic D- pregnant women who had developed alloanti-D and found none with Asian-type DEL (0/127). Finally, we analyzed RHD transcripts from Asian-type DEL erythroblasts and examined antigen epitopes expressed by various RHD transcripts in vitro, finding a low abundance of full-length RHD transcripts (0.18% of the total) expressing RhD antigens carrying the entire repertoire of epitopes, which could explain the immune tolerance against D+ RBCs. Our results provide multiple lines of evidence that individuals with Asian-type DEL cannot produce alloanti-D when exposed to D+ RBCs after transfusion or pregnancy. Therefore, we recommend considering D+ RBC transfusion and discontinuing anti-D prophylaxis in patients with Asian-type DEL, including pregnant women. This clinical trial is registered at www.clinicaltrials.gov as #NCT03727230.

Reprogramming of arachidonate metabolism confers temozolomide resistance to glioblastoma through enhancing mitochondrial activity in fatty acid oxidation.

BACKGROUND: Sp1 is involved in the recurrence of glioblastoma (GBM) due to the acquirement of resistance to temozolomide (TMZ). Particularly, the role of Sp1 in metabolic reprogramming for drug resistance remains unknown. METHODS: RNA-Seq and mass spectrometry were used to analyze gene expression and metabolites amounts in paired GBM specimens (primary vs. recurrent) and in paired GBM cells (sensitive vs. resistant). ω-3/6 fatty acid and arachidonic acid (AA) metabolism in GBM patients were analyzed by targeted metabolome. Mitochondrial functions were determined by Seahorse XF Mito Stress Test, RNA-Seq, metabolome and substrate utilization for producing ATP. Therapeutic options targeting prostaglandin (PG) E2 in TMZ-resistant GBM were validated in vitro and in vivo. RESULTS: Among the metabolic pathways, Sp1 increased the prostaglandin-endoperoxide synthase 2 expression and PGE2 production in TMZ-resistant GBM. Mitochondrial genes and metabolites were obviously increased by PGE2, and these characteristics were required for developing resistance in GBM cells. For inducing TMZ resistance, PGE2 activated mitochondrial functions, including fatty acid ß-oxidation (FAO) and tricarboxylic acid (TCA) cycle progression, through PGE2 receptors, E-type prostanoid (EP)1 and EP3. Additionally, EP1 antagonist ONO-8713 inhibited the survival of TMZ-resistant GBM synergistically with TMZ. CONCLUSION: Sp1-regulated PGE2 production activates FAO and TCA cycle in mitochondria, through EP1 and EP3 receptors, resulting in TMZ resistance in GBM. These results will provide us a new strategy to attenuate drug resistance or to re-sensitize recurred GBM.

Virus-specific editing identification approach reveals the landscape of A-to-I editing and its impacts on SARS-CoV-2 characteristics and evolution.

Upon SARS-CoV-2 infection, viral intermediates specifically activate the IFN response through MDA5-mediated sensing and accordingly induce ADAR1 p150 expression, which might lead to viral A-to-I RNA editing. Here, we developed an RNA virus-specific editing identification pipeline, surveyed 7622 RNA-seq data from diverse types of samples infected with SARS-CoV-2, and constructed an atlas of A-to-I RNA editing sites in SARS-CoV-2. We found that A-to-I editing was dynamically regulated, varied between tissue and cell types, and was correlated with the intensity of innate immune response. On average, 91 editing events were deposited at viral dsRNA intermediates per sample. Moreover, editing hotspots were observed, including recoding sites in the spike gene that affect viral infectivity and antigenicity. Finally, we provided evidence that RNA editing accelerated SARS-CoV-2 evolution in humans during the epidemic. Our study highlights the ability of SARS-CoV-2 to hijack components of the host antiviral machinery to edit its genome and fuel its evolution, and also provides a framework and resource for studying viral RNA editing.

Excess soluble alkalis to prepare highly efficient MgO with relative low surface oxygen content applied in DMC synthesis.

The activities of various MgO catalysts, which were prepared from different methods such as hydration synthesis, thermal decomposition, combustion, sol-gel and co-precipitation, were conducted in dimethyl carbonate (DMC) synthesis via transesterification of ethylene carbonate with methanol. MgO-P-Na2CO3-3.14 synthesized by the excess Na2CO3 precipitation compared the best catalytic activity and stability, which could be reused for seven times without obvious deactivation. The DMC yield was as high as 69.97% at 68 °C. The transesterification reaction could be separated into two steps, and the samples obtained by NaOH precipitant exhibited better ring-opening capability, while the catalysts acquired by Na2CO3 precipitant displayed superior transesterification ability. The structure-performance relationship was evaluated by multiple characterization methods. The results indicated that the as-synthesized catalyst derived from dried precursors with more crystalline magnesium carbonate was favorable for the promotion of DMC yield, and MgO-P-Na2CO3-3.14 with more Mg-O pairs, which were the active center for the transesterification of 2-hydroxyethyl methyl carbonate (HEMC) intermediate with methanol, resulted in more moderately basic sites left that was in accordance with the DMC yield variation. MgO-P-Na2CO3-3.14 with greater BET surface area and mesopore volume, relative low surface oxygen content and larger moderately basic sites amount compared the excellent activity in DMC synthesis.

Changes in the characteristics of dental emergencies under the influence of SARS-CoV-2 pandemic: a retrospective study.

BACKGROUND: Further understanding of the distribution and changing characteristics of dental diseases is of great significance for all dental emergency centers for strengthening the medical staff's treatment knowledge abilities and effective use of emergency resources in the face of public health emergencies involving highly infectious respiratory diseases. METHODS: The medical records of 4158 dental emergency patients in 2019 and 2020 were retrospectively analyzed and divided into pre-SARS-COV-2 group and SARS-COV-2 group according to time. The demographic data, date and time, diagnosis, and treatment methods of the two groups were statistically described, and the chi-squared test was used to analyze the differences. The medical records of 4158 dental emergency patients during the same period of two years in 2019 and 2020 were retrospectively analyzed and divided into SARS-COV-2 pre-group and SARS-COV-2 group according to time. The demographic data, date and time, diagnosis and treatment methods of the two groups were statistically described, and the chi-square test was used to determine the differences. RESULTS: During the SARS-COV-2 pandemic, the number of dental emergency visits increased by 29.7%. During the pandemic, males (n = 286, 58.1%) were more likely to visit dental emergency centers for trauma than females (n = 206, 41.9%) (P < 0.05); females (n = 242, 60.8%) were more likely to visit dental emergency centers for acute gingivitis and acute pericoronitis than males (n = 156, 39.2%) (P < 0.05). A major change in diagnosis was related to acute pulpitis (K04.0) and acute apical periodontitis (K04.4), which increased by 9.2%; acute gingivitis (K05.0) and acute pericoronitis (K05.2) increased by 3.5%; open wound of the lip and oral cavity (S01.5) decreased by 17.9%; other conditions (non-emergency diseases) increased by 6.8%, compared with the pre-SARS-COV-2 period. Among the treatment modalities, during the pre-SARS-COV-2 period, 304 patients (17.7%) received a prescription for antibiotics and analgesics, and 1485 (86.5%) received a prescription for local treatment. During the SARS-COV-2 period, 958 (39.2%) received a prescription for antibiotics and analgesics, and 1636 (67.0%) received a prescription for local treatment. CONCLUSION: SARS-COV-2 pandemic led to changes in the characteristics of dental emergency patients. Trauma, acute pulpitis, and acute periodontitis are the leading reasons patients refer to dental emergency centers. Dental emergency centers should optimize treatment procedures, optimize the staff, and reasonably allocate materials according to the changes to improve the on-site treatment capacity and provide adequate dental emergency care.

On Change of Soil Moisture Distribution With Vegetation Reconstruction in Mu Us Sandy Land of China, With Newly Designed Lysimeter.

BACKGROUND: China's so-called Three North Shelterbelt Program (3NSP) has produced a vast area of lined forest reconstruction in the semi-arid regions. This study uses the lined rain-fed Pinus sylvestris var. mongolica (PSM) sand-fixing forest in the eastern part of Mu Us Sandy Land in Northwestern China as an example to investigate the ecohydrological process in this region. Rain gauges, newly designed lysimeters and soil moisture sensors are used to monitor precipitation, deep soil recharge (DSR) and soil water content, where DSR specifically refers to recharge that can reach a depth more than 200 cm and eventually replenish the underneath groundwater reservoir. RESULTS: This study shows that there are two obvious moisture recharge processes in an annual base for the PSM forest soil: a snowmelt-related recharge process in the spring and a precipitation-related recharge process in the summer. The recharge depth of the first process can reach 180 cm without DSR occurring (in 2018). The second process results in noticeable DSR in 2018. Specifically, the DSR values over 2016-2018 are 1, 0.2, and 1.2 mm, respectively. To reach the recharge depths of 20, 40, 80, 120, 160, and 200 cm, the required precipitation intensities have to be 2.6, 3.2, 3.4, 8.2, 8.2, and 13.2 mm/d, respectively. The annual evapotranspiration in the PSM forest is 466.94 mm in 2016, 324.60 mm in 2017, and 183.85 mm in 2018. CONCLUSION: This study concludes that under the current precipitation conditions (including both dry- and wet-years such as 2016-2018), water consumption of PSM somewhat equals to the precipitation amount, and PSM has evolved over years to regulate its evapotranspiration in response to annual precipitation fluctuations in Mu Us Sandy Land of China.

Human A-to-I RNA editing SNP loci are enriched in GWAS signals for autoimmune diseases and under balancing selection.

BACKGROUND: Adenosine-to-inosine (A-to-I) RNA editing plays important roles in diversifying the transcriptome and preventing MDA5 sensing of endogenous dsRNA as nonself. To date, few studies have investigated the population genomic signatures of A-to-I editing due to the lack of editing sites overlapping with SNPs. RESULTS: In this study, we applied a pipeline to robustly identify SNP editing sites from population transcriptomic data and combined functional genomics, GWAS, and population genomics approaches to study the function and evolution of A-to-I editing. We find that the G allele, which is equivalent to edited I, is overrepresented in editing SNPs. Functionally, A/G editing SNPs are highly enriched in GWAS signals of autoimmune and immune-related diseases. Evolutionarily, derived allele frequency distributions of A/G editing SNPs for both A and G alleles as the ancestral alleles are skewed toward intermediate frequency alleles relative to neutral SNPs, a hallmark of balancing selection, suggesting that both A and G alleles are functionally important. The signal of balancing selection is confirmed by a number of additional population genomic analyses. CONCLUSIONS: We uncovered a hidden layer of A-to-I RNA editing SNP loci as a common target of balancing selection, and we propose that the maintenance of such editing SNP variations may be at least partially due to constraints on the resolution of the balance between immune activity and self-tolerance.

Sense-antisense miRNA pairs constitute an elaborate reciprocal regulatory circuit.

Antisense transcription of protein-coding genes has been increasingly recognized as an important regulatory mechanism of gene expression. However, less is known about the extent and importance of antisense transcription of noncoding genes. Here, we investigate the breadth and dynamics of antisense transcription of miRNAs, a class of important noncoding RNAs. Because the antisense transcript of a miRNA is likely to form a hairpin suitable as the substrate of ADARs, which convert adenosine to inosine in double-stranded RNAs, we used A-to-I RNA editing as ultrasensitive readout for antisense transcription of the miRNAs. Through examining the unstranded targeted RNA-seq libraries covering all miRNA loci in 25 types of human tissues, we identified 7275 editing events located in 81% of the antisense strand of the miRNA loci, thus uncovering the previously unknown prevalent antisense transcription of the miRNAs. We found that antisense transcripts are tightly regulated, and a substantial fraction of miRNAs and their antisense transcripts are coexpressed. Sense miRNAs have been shown to down-regulate the coexpressed antisense transcripts, whereas the act of antisense transcription, rather than the transcripts themselves, regulates the expression of sense miRNAs. RNA editing tends to decrease the miRNA accessibility of the antisense transcripts, therefore protecting them from being degraded by the sense-mature miRNAs. Altogether, our study reveals the landscape of antisense transcription and editing of miRNAs, as well as a previously unknown reciprocal regulatory circuit of sense-antisense miRNA pairs.

irCLASH reveals RNA substrates recognized by human ADARs.

Adenosine deaminases acting on RNA (ADARs) convert adenosines to inosines in double-stranded RNA (dsRNA) in animals. Despite their importance, ADAR RNA substrates have not been mapped extensively in vivo. Here we develop irCLASH to map RNA substrates recognized by human ADARs and uncover features that determine their binding affinity and editing efficiency. We also observe a dominance of long-range interactions within ADAR substrates and analyze differences between ADAR1 and ADAR2 editing substrates. Moreover, we unexpectedly discovered that ADAR proteins bind dsRNA substrates tandemly in vivo, each with a 50-bp footprint. Using RNA duplexes recognized by ADARs as readout of pre-messenger RNA structures, we reveal distinct higher-order architectures between pre-messenger RNAs and mRNAs. Our transcriptome-wide atlas of ADAR substrates and the features governing RNA editing observed in our study will assist in the rational design of guide RNAs for ADAR-mediated RNA base editing.

Numerical Simulation and Experiment of Electrically-Assisted Incremental Forming of Thin TC4 Titanium Alloy Sheet.

In order to integrally manufacture the large TC4 titanium alloy part, an electrically-assisted incremental forming process is cleverly proposed to solve the traditional hot forming disadvantages of expensive heating furnaces and long cycle period. The two-step simulation method including thermal-electricity coupling simulation and thermo-mechanical coupling simulation was selected to predict the temperature variations and the sheet deformation behaviors. The electrically-assisted incremental forming experiment of thin TC4 titanium alloy sheet was performed. The highest prediction error is 6% for springback angles. The thrice forming at 10.9 A/mm2 satisfies the precision requirement of the designed part. Therefore, the two-step simulation method can effectively calculate the electrically-assisted incremental process. The electrically-assisted incremental forming technique is very promising for the integral producing large titanium alloy part.

Titanium dioxide nanoparticles induce mitochondria-associated apoptosis in HepG2 cells.

Widespread applications of nanosized materials over the past decade have prompted investigations of desirable properties and potential hazards to humans and the environment. Titanium dioxide (TiO2) nanoparticles are one of the most widely used nanoparticles. To investigate the effect of biological functions induced by TiO2 nanoparticles (10 nm: TiO2 NPs) on human liver cell lines, normal liver cell line L02 and hepatoma cell line HepG2 were co-cultured with exogenous TiO2 NPs. Cell growth and proliferation, cell cycle, and the apoptosis rate were analyzed. The effects of TiO2 NPs on the expression levels of apoptosis-associated protein caspase-3 and the membrane channel protein αENaC and caspase-3/7 activity were determined. Moreover, the influence of TiO2 NPs on the expression levels of the mitochondria-related proteins SIRT3, VDAC1, and ACSS1, the mitochondrial membrane potential and the ADP/ATP ratio were also examined. Our results revealed that TiO2 NPs inhibited the growth and proliferation of HepG2 cells, suppressed the S phase of cell cycling, and induced apoptosis of HepG2 cells. Following an increase in concentration, the inhibitory effect induced by TiO2 NPs on proliferation and cell cycle was more evident, and the apoptosis rate increased in a significant concentration-dependent manner, whereas there was no significant effect on the growth, proliferation, apoptosis, and cell cycle of L02 cells. In addition, the results of western blot showed that in HepG2 cells, TiO2 NPs upregulated the expressions of the apoptosis-related protein caspase-3 and the membrane channel protein αENaC in a concentration-dependent manner. However, in L02 cells, there was no significant difference in the expression levels of caspase-3 or αENaC. Furthermore, TiO2 NPs induced depolarization of the mitochondrial membrane, upregulated the expression levels of the mitochondria-related proteins SIRT3 and VDAC1, and downregulated the expression level of the key respiratory chain protein ACSS1 in HepG2 cells. However, in L02 cells, the expressions of SIRT3, VDAC1, and ACSS1 exhibited no clear change. The apoptosis of HepG2 cells induced by TiO2 NPs may be achieved by regulating intracellular osmotic pressure; moreover, upregulating the expression of the channel protein αENaC or the mitochondrial porin VDAC1 and depolarizing the mitochondrial membrane of HepG2 cells resulted in the loss of Cyt-c and ATP and further activated caspase-3. To further confirm the above results, a nude mouse xenograft model was employed. After a certain period of treatment with TiO2 NPs, the nude mice were sacrificed, tumors were removed, and the expression of related proteins was detected. Immunohistochemistry and western blot results showed that the expressions of the proteins VDAC1 and SIRT3 were clearly upregulated in tissues treated to TiO2 NPs, whereas the expression of ACSS1 was downregulated. The results were consistent with the above in vitro results. All the above results confirmed that TiO2 NPs can act as a safe antitumor agent.

Fabrication of low-density carbon-bonded carbon fiber composites with an Hf-based coating for high temperature applications.

A novel Hf-based anti-oxidation coating has been prepared on the surface of low-density carbon-bonded carbon fiber composites (CBCFs). The coating exhibits a gradient transition structure, with mainly HfB2, Hf2Si and SiC ceramics. Oxyacetylene torch testing has been utilized to evaluate the ablation resistance under the condition ranging from 1.6 MW m-2 to 2.2 MW m-2 for 300 s. The experimental results show that the as-prepared Hf-based coating can effectively protect CBCFs under high-temperature oxidation conditions. The surface maximum temperature can reach 1616-2037 °C, and the mass ablation rates vary from -3.5 × 10-5 g s-1 cm-2 to 1.5 × 10-5 g s-1 cm-2. The formation of a dense SiO2 glass layer embedded with HfO2 grains or particle accumulation in the HfO2 layer is responsible for the good ablation resistance.

Cardiac ß2-Adrenergic Receptor Phosphorylation at Ser355/356 Regulates Receptor Internalization and Functional Resensitization.

Previous studies have demonstrated that ß2-adrenergic receptors (ß2ARs) can be phosphorylated by G protein-coupled receptor kinases (GRKs) and protein kinase A (PKA), affecting ß2AR internalization and desensitization. However, the exact physiological function of ß2ARs in cardiomyocytes is unknown. In this study, we showed that neonatal mouse cardiomyocytes had different contraction and internalization responses to sustained or repeated, transient agonist stimulation. Specifically, short-time stimulation (10 min) with epinephrine or norepinephrine increased the cardiomyocyte contraction rate, reaching a maximum at 5 min, followed by a slow decline. When the agonist was re-added after a 60-min wash-out period, the increase in the cardiomyocyte contraction rate was similar to the initial response. In contrast, when cardiomyocytes were exposed continuously to epinephrine or norepinephrine for 60 min, the second agonist stimulation did not increase the contraction response. These results indicated that continuous ß2AR stimulation caused functional desensitization. Phosphorylation of ß2ARs at serine (Ser)355/356 GRK phosphorylation sites, but not at Ser345/346 PKA phosphorylation sites increased with continuous epinephrine stimulation for 60 min. Accordingly, ß2AR internalization increased. Interestingly, ß2AR internalization was blocked by mutations at the GRK phosphorylation sites, but not by mutations at the PKA phosphorylation sites. Furthermore, inhibition of ß2AR dephosphorylation by okadaic acid, a phosphatase 2A inhibitor, impaired the recovery of internalized ß2ARs and reduced the cardiomyocyte contraction rate in response to epinephrine. Finally, epinephrine treatment induced the physical interaction of ß-arrestin with internalized ß2ARs in cardiomyocytes. Together, these data revealed the essential role of the Ser355/356 phosphorylation status of ß2ARs in regulating receptor internalization and physiological resensitization in neonatal cardiomyocytes to contraction functions.

Comprehensive analysis of temozolomide treatment for patients with glioma.

BACKGROUND: This analysis was conducted to evaluate the efficacy and safety of temozolomide based chemotherapy in treating patients with glioma. METHODS: Clinical studies evaluating the efficacy and safety of temozolomide based regimens for patients with glioma were identified using a predefined search strategy. Pooled response rates (RRs) were calculated. RESULTS: In temozolomide based regimens, 5 clinical studies including 152 patients with advanced glioma were considered eligible for inclusion. Four clinical studies included temozolomide. Systematic analysis suggested that, in all patients, pooled CR was 21% (32/152) , and PR was 21% (32/152). Grade 3/4 toxicity included neutropenia, thrombocytopenia, and anemia. No grade 3 or 4 renal or liver toxicity was observed. No treatment related death occurred with temozolomide based treatment. CONCLUSION: This systematic analysis suggests that temozolomide based regimens are associated with mild response rate and acceptable toxicity for treatment of glioma patients.

Mutations of rat surfactant protein A have distinct effects on its glycosylation, secretion, aggregation and degradation.

AIMS: Surfactant protein A (SP-A) plays critical roles in the innate immune system and surfactant homeostasis of the lung. Mutations in SP-A2 of the carbohydrate recognition domain (CRD) impair its glycosylation and are associated with pulmonary fibrosis in humans. We aim to examine how mutations in SP-A that impair its glycosylation affect its biological properties and lead to disease. MAIN METHODS: We generated rat SP-A constructs with two types of mutations that impair its glycosylation: N-glycosylation site mutations (N21T, N207S and N21T/N207S) and disease-associated CRD mutations (G231V, F198S). We transfected these constructs into Chinese hamster ovary (CHO)-K1 cells and assessed biochemical differences in cellular and secreted wild-type and mutant SP-As by western blot, immunofluorescence, and sensitivity to enzymatic digestion. KEY FINDINGS: Mutations of the CRD completely impaired SP-A secretion, whereas mutations of N-glycosylation sites had little effect. Both types of mutations formed nonidet p-40 (NP-40) insoluble aggregates, but the aggregates only from CRD mutations could be partially rescued by a chemical chaperone, 4-phenylbutyrate acid (4-PBA). The majority of CRD mutant SP-A was retained in the endoplasmic reticulum. Moreover, both types of mutations reduced SP-A stability, with CRD mutant SP-A being more sensitive to chymotrypsin digestion. Both types of soluble mutant SP-A could be degraded by the proteasome pathway, while insoluble aggregates could be additionally degraded by the lysosomal pathway. SIGNIFICANCE: Our data provide evidence that the differential glycosylation of SP-A may play distinct roles in SP-A secretion, aggregation and degradation which may contribute to familial pulmonary fibrosis caused by SP-A2 mutations.

Spatial element distribution control in a fully solution-processed nanocrystals-based 8.6% Cu2ZnSn(S,Se)4 device.

A fully solution-processed high performance Cu2ZnSn(S,Se)4 (CZTSSe, kesterite) device has been demonstrated. It is based on the rational engineering of elemental spatial distributions in the bulk and particularly near the surface of the film from nanocrystal precursors. The nanocrystals are synthesized through a modified colloidal approach, with excellent solubility over a large compositional window, followed by a selenization process to form the absorber. The X-ray photoluminescence (XPS) depth profiling indicates an undesirable Sn-rich surface of the selenized film. An excessive Zn species was quantitatively introduced through nanocrystals precursor to correct the element distribution, and accordingly a positive correlation between the spatial composition in the bulk/surface film and the resulting device parameter is established. The enhanced device performance is associated with the reduced interfacial recombination. With a Zn content 1.6 times more than the stoichiometry; the optimized device, which is fabricated by employing a full solution process from the absorber to the transparent top electrode, demonstrates a performance of 8.6%. This composition-control approach through stoichiometric adjustments of nanocrystal precursors, and the developed correlation between the spatial composition and device performance may also benefit other multielement-based photovoltaics.

Oral health survey and oral health questionnaire for high school students in Tibet, China.

OBJECTIVES: The aim of this study is to identify the oral health status as well as oral health practices and access for care of graduating senior high school Tibetan students in Shannan prefecture of Tibet. METHODS: Based on standards of the 3rd Chinese National Oral Epidemiological Survey and WHO Oral Health Surveys, 1907 graduating students from three senior high schools were examined for caries, periodontitis, dental fluorosis, and oral hygiene status. The questionnaire to the students addressed oral health practices and present access to oral medical services. RESULTS: Dental caries prevalence (39.96%) and mean DMFT (0.97) were high in Tibetan students. In community periodontal indexes, the detection rate of gingivitis and dental calculus were 59.50% and 62.64%, respectively. Oral hygiene index-simplified was 0.69, with 0.36 and 0.33 in debris index-simplified and calculus index-simplified, respectively. Community dental fluorosis index was 0.29, with 8.13% in prevalence rate. The questionnaire showed students had poor oral health practices and unawareness for their needs for oral health services. It was also noted that the local area provides inadequate oral medical services. CONCLUSIONS: Tibetan students had higher prevalence of dental diseases and lower awareness of oral health needs. The main reasons were geographical environment, dietary habit, students' attitude to oral health, and lack of oral health promotion and education. Oral health education and local dentists training should be strengthened to get effective prevention of dental diseases.

Correlations of MUC15 overexpression with clinicopathological features and prognosis of glioma.

The abnormal expression of MUC15, a novel cell membrane-associated mucin, has been reported to predict poor survival in several cancers. The aim of the present study was to examine the expression of MUC15 in glioma and its correlation with clinicopathological features, including the survival of patients with glioma. The mRNA expression level of MUC15 was determined by RT-PCR, quantitative RT-PCR (RT-qPCR) and Western blotting in seven normal brain tissues and seven glioma tissues, respectively. The protein expression level of MUC15 was immunohistochemically detected in paraffin-embedded samples of 317 glioma tissues and 115 noncancerous brain tissues. The association of MUC15 expression levels with the clinicopathologic features and the prognosis was analyzed. The results showed that both mRNA and protein levels of MUC15 were significantly increased in glioma as compared with those in noncancerous brain tissue. Moreover, MUC15 overexpression was positively correlated with the advanced clinical stages of glioam patients (P<0.01). Furthermore, MUC15 expression levels were significantly correlated with the progression of glioma (P<0.001). Survival analysis indicated that glioma patients with higher MUC15 expression had a significantly shorter overall and 5-year survival time than those with low MUC15 expression. Multivariate analysis suggested that MUC15 overexpression was an independent factor for prognosis (hazard risk: 3.216; P=0.009). It was concluded that MUC15 is overexpressed in glioma tissues. Its overexpression correlates with tumor progression and it is a potentially unfavorable prognostic factor for patients with glioma.