Molecular cloning, expression profiling, and yeast complementation of 19 β-tubulin cDNAs from developing cotton ovules

Microtubules are a major structural component of the cytoskeleton and participate in cell division, intracellular transport, and cell morphogenesis. In the present study, 795 cotton tubulin expressed sequence tags were analysed and 19 β-tubulin genes (TUB) cloned from a cotton cDNA library. Among the group, 12 cotton TUBs (GhTUBs) are reported for the first time here. Transcription profiling revealed that nine GhTUBs were highly expressed in elongating fibre cells as compared with fuzzless-lintless mutant ovules. Treating cultured wild-type cotton ovules with exogenous phytohormones showed that individual genes can be induced by different agents. Gibberellin induced expression of GhTUB1 and GhTUB3, ethylene induced expression of GhTUB5, GhTUB9, and GhTUB12, brassinosteroids induced expression of GhTUB1, GhTUB3, GhTUB9, and GhTUB12, and lignoceric acid induced expression of GhTUB1, GhTUB3, and GhTUB12. When GhTUBs were transformed into the Saccharomyces cerevisiae inviable mutant, tub2, which is deficient in β-tubulin, one ovule-specific and eight of nine fibre-preferential GhTUBs rescued this lethality. This study suggests that the proteins encoded by cotton GhTUBs are involved during cotton fibre development

Percutaneous closure of postinfarct muscular ventricular septal defects: A multicenter study in China

AbstractBackgroundSurgical repair is an effective method to treat ventricular septal defect (VSD) complicating acute myocardial infarction (AMI). However, the mortality rate remains high. This study was designed to assess the immediate and mid-term results of transcatheter closure of postinfarct muscular VSDs.MethodsData were retrospectively collected from 42 AMI patients who underwent attempted transcatheter VSD closure between 2008 and 2012 in seven heart centers of China.ResultsNine patients underwent emergent VSD closure in the acute phase (within two weeks from VSD) while the others underwent elective closure. The time between VSD occurrence and closure in emergency group and elective group was 7.7±2.3 days and 35±14.5 days, respectively (p<0.01). The percentage of procedure success in the emergency group and elective group was 77.8% (7/9) and 97% (32/33), respectively (p=0.048). The hospital mortality was higher for emergent closure in comparison to elective closure (66.7% vs. 6.1%, p<0.01). During a median follow-up of 25 months (0–58 months), two patients died at 8 and 29 months, respectively, and no serious complications occurred in other patients.ConclusionInterventional postinfarct VSD closure is a safe and effective approach that can be performed with a high procedural success rate, with favorable outcomes if it can be undertaken >14 days postinfarct

Exploring the Mechanism Whereby Sinensetin Delays the Progression of Pulmonary Fibrosis Based on Network Pharmacology and Pulmonary Fibrosis Models

The incidence of pulmonary fibrosis (PF), a progressively fatal disease, has increased in recent years. However, there are no effective medicines available. Previous results have shown that sinensetin probably has some curative effects on PF. Therefore, this paper aims to predict the targets of sinensetin using a network pharmacology method and to confirm its effects and functional targets in PF using a mouse PF model. First, network pharmacology analysis showed that sinensetin has 105 functional targets, and 1,698 gene targets closely relate to PF. The intersection of the functional targets and gene targets produced 52 targets for the treatment of PF with sinensetin. The PPIs (protein–protein interactions) led to several potential key target genes, including MAPK1, EGFR, SRC, and PTGS2. The results of GO and KEGG analyses suggested the crucial function of apoptosis in PF and its involvement in the PI3K signaling pathway. Subsequently, we tested the molecular docking of sinensetin with the PI3K protein using the AutoDock4 software. The results showed that sinensetin could fit well into several binding sites of the PI3K protein. Furthermore, we constructed a PF mouse model through one-off intratracheal instillation of bleomycin and then intragastrically administered different concentrations of sinensetin to the model mice. Twenty-eight days later, the mice were sacrificed, and the lung tissues, serum, and bronchoalveolar lavage fluid (BALF) were collected. The in vivo tests showed that the body weight of model mice increased slightly compared with that of PF mice after intragastric sinensetin. HE and Masson staining suggested a certain extent of reduction in the pathology of lung tissues. The expression of collagens I and III, as well as hydroxyproline in the lung tissues, was reduced to a certain extent. IL-6 levels in the serum and BALF decreased markedly. The expression of vimentin and α-SMA in pulmonary tissues decreased. Cell apoptosis, as well as P-PI3K and P-AKT levels, in lung tissues also reduced. In summary, network pharmacology and in vivo test results suggest sinensetin causes an effective delay in the progression of pulmonary fibrosis, and the functional mechanism is likely related to PI3K-AKT signaling

Feasibility study on posterior laminar screw fixation techniques in the axis

AbstractObjectiveTo get morphologic parameters of Chinese adults through observation and measurement on axial laminas, to evaluate the feasibility of placing axial laminar screws and to introduce the technique.MethodsRelative parameters of 28 sets of fresh Chinese adults' axial specimens, including distance from the superior and inferior entry points of axial laminar screws to the superior margins of axial laminas, superior, middle, inferior thickness and height of the axial laminas, length and angle of the axial laminar screw trajectories, distance from the entry points of axial laminar screws to the transverse foramen and central points of the inferior articular process, were measured with a digital caliper and a goniometer. Data were statistically analyzed.ResultsAveragely, distance from the superior and inferior entry points of axial laminar screws to the superior margins of axial laminas was 5 mm and 9 mm, superior, middle, inferior thickness and the height of the axial laminas were 3.2 mm, 6.7 mm, 5.5 mm and 12.8 mm respectively, and the length of the superior and inferior axial laminar screw trajectories was 26.2 mm and 25.5 mm, respectively.ConclusionsIt is feasible and reliable to apply posterior laminar screw fixation techniques to the axes of Chinese adults. Also the C2 laminar screw fixation technique can be taken as a supplementary to conventional posterior screw fixations of C2

Full velocities and propagation directions of coronal mass ejections inferred from simultaneous full-disk imaging and Sun-as-a-star spectroscopic observations

Coronal mass ejections (CMEs) are violent ejections of magnetized plasma from the Sun, which can trigger geomagnetic storms, endanger satellite operations and destroy electrical infrastructures on the Earth. After systematically searching Sun-as-a-star spectra observed by the Extreme-ultraviolet Variability Experiment (EVE) onboard the Solar Dynamics Observatory (SDO) from May 2010 to May 2022, we identified eight CMEs associated with flares and filament eruptions by analyzing the blue-wing asymmetry of the O III 52.58 nm line profiles. Combined with images simultaneously taken by the 30.4 nm channel of the Atmospheric Imaging Assembly onboard SDO, the full velocity and propagation direction for each of the eight CMEs are derived. We find a strong correlation between geomagnetic indices (Kp and Dst) and the angle between the CME propagation direction and the Sun-Earth line, suggesting that Sun-as-a-star spectroscopic observations at EUV wavelengths can potentially help to improve the prediction accuracy of the geoeffectiveness of CMEs. Moreover, an analysis of synthesized long-exposure Sun-as-a-star spectra implies that it is possible to detect CMEs from other stars through blue-wing asymmetries or blueshifts of spectral lines.Comment: Accepted by Ap

Identification and functional analysis of a novel PRKAG2 mutation responsible for Chinese PRKAG2 cardiac syndrome reveal an important role of non-CBS domains in regulating the AMPK pathway

AbstractBackgroundPRKAG2 gene encodes the γ2 regulatory subunit of AMP-activated protein kinase (AMPK) that acts as a sensor of cellular energy status, and its germline mutations are responsible for PRKAG2 cardiac syndrome (PCS). The majority of missense mutations of cystathionine beta-synthase (CBS) domains found in PCS impair the binding activity of PRKAG2 to adenosine derivatives, and therefore lead to PRKAG2 function impairment and AMPK activity alteration, resulting in a familial syndrome of ventricular preexcitation, conduction defects, and cardiac hypertrophy. However, it is unclear about the PRKAG2 mutation in the non-CBS domain. Here, a Chinese family exhibiting the cardiac syndrome associated with a novel heterozygous PRKAG2 mutation (Gly100Ser) mapped to exon 3 encoding a non-CBS domain is described and the function of this novel mutation was investigated in vitro.MethodsThe PRKAG2 G100S and R302Q mutations were constructed by a two-step polymerase chain reaction and then transfected into CCL13 cells by lentivirus vectors. Wild-type PRKAG2 gene transfection was used as a negative control. PRKAG2 expression was determined by Western blot. Immunofluorescence was used to localize the intracellular PRKAG2 proteins. MTT assay was performed to explore the effect of mutations on cell proliferation. Periodic acid-Schiff staining was used for detecting glycogen accumulation. AMPK concentration was measured with enzyme-linked immunosorbent assay.ResultsOur results showed neither intracellular localization of PRKAG2 nor cell growth was altered. In contrast, PRKAG2 protein expression levels were significantly reduced by this mutation. Furthermore, PRKAG2-mediated activity of AMPK was attenuated, resulting in glycogen metabolism dysregulation. These findings revealed that non-CBS domains of PRKAG2 were essential to the regulation of AMPK activity, similar to CBS.ConclusionsOur study ascribes a crucial regulatory role to the novel PRKAG2 G100S mutation, and reiterates that PCS occurs as a consequence of AMPK signaling abnormality caused by PRKAG2 gene mutations

A 1-hydroxy-2,4-diformylnaphthalene-based fluorescent probe and its detection of sulfites/bisulfite

A novel 1-hydroxy-2,4-diformylnaphthalene-based fluorescent probe L was synthesized by a Knoevenagel reaction and exhibited excellent sensitivity and selectivity towards sulfite ions (SO32−) and bisulfite ions (HSO3−). The detection limits of the probe L were 0.24 μM using UV-Vis spectroscopy and 9.93 nM using fluorescence spectroscopy, respectively. Furthermore, the fluorescent probe L could be utilized for detection in real water samples with satisfactory recoveries in the range 99.20%~104.30% in lake water and 100.00%~104.80% in tap water by UV-Vis absorption spectrometry, and in the range 100.50%~108.60% in lake water and 102.70%~103.80% in tap water by fluorescence spectrophotometry