Molecular dynamics simulation of CO2 dissolution-diffusion in multi-component crude oil

In order to study the dissolution-diffusion process and mechanism of CO2 in multi-component crude oil, a model of multi-component crude oil system with octane as the main component and 16 other alkanes as a compound was constructed by using molecular dynamics simulation method. We estimated the CO2 density distribution in crude oil model and the shift in crude oil model volume change. We then investigated the microscopic influence mechanism of CO2 dissolution-diffusion on the volume expansion of crude oil by simulating the action of CO2 dissolution-diffusion in the multi-component crude oil model. Based on the variation law of mean square displacement between crude oil molecules, the dissolution and diffusion coefficients of CO2 were predicted, and the influence of CO2 dissolution-diffusion on crude oil mobility was analyzed. It is found that temperature intensifies the molecular thermal motion and increases the voids between alkane molecules, which promotes the dissolution of CO2 and encourages CO2 molecules to transmit, making the crude oil expand and viscosity decrease, and improving the flow ability of crude oil; with the enhancement of given pressure, the potential energy difference between the inside and outside of the crude oil model becomes larger, and the voids between alkane molecules become larger, which is favorable to the dissolution of CO2. Nevertheless, the action of CO2 molecules’ diffusing in the crude oil sample is significantly limited or even tends to zero, besides, the mobility of crude oil is affected due to the advance of external pressure. The mechanism of CO2 dissolution and diffusion in multi-component crude oil is revealed at the microscopic level, and provides theoretical guidance for the development of CO2 flooding

Endobronchial optical coherence tomography helps to estimate the cartilage damage of the central airway in TBTB patients

PurposeAt present, there are few examination methods used to evaluate tracheobronchial cartilage damage. In our study, we explored whether endobronchial optical coherence tomography (EB-OCT) can be used to estimate central airway cartilage damage in tracheobronchial tuberculosis (TBTB) patients.MethodsIn our study, we used the OCTICS Imaging system to perform EB-OCT scanning for TBTB patients. The thickness of the central airway wall and cartilage was measured by the OCTICS software system workstation.ResultsThere were 102 TBTB patients included in our study cohort. Their EB-OCT images of the central airway cartilage showed that abnormal cartilage manifests as thinning of the cartilage, cartilage damage, cartilage destruction, and even cartilage deficiency. The cartilage morphology becomes irregular and discontinuous. Some parts of the cartilage become brighter in grayscale. The intima of the cartilage is thickened and discontinuous, and the boundary with submucosa and mucosa is unclear.ConclusionOur study conducted EB-OCT examination of the central airway cartilage of TBTB patients in vivo for the first time. EB-OCT helps to estimate the cartilage damage of the central airway in TBTB patients to some extent

Recent progress in 2D group-VA semiconductors: from theory to experiment

This review provides recent theoretical and experimental progress in the fundamental properties, electronic modulations, fabrications and applications of 2D group-VA materials.</p

PRPF3

Purpose. To characterize the clinical and molecular genetic characteristics of a large, multigenerational Chinese family showing different phenotypes. Methods. A pedigree consisted of 56 individuals in 5 generations was recruited. Comprehensive ophthalmic examinations were performed in 16 family members affected. Mutation screening of CYP4V2 was performed by Sanger sequencing. Next-generation sequencing (NGS) was performed to capture and sequence all exons of 47 known retinal dystrophy-associated genes in two affected family members who had no mutations in CYP4V2. The detected variants in NGS were validated by Sanger sequencing in the family members. Results. Two compound heterozygous CYP4V2 mutations (c.802-8_810del17insGC and c.992A>C) were detected in the proband who presented typical clinical features of BCD. One missense mutation (c.1482C>T, p.T494M) in the PRPF3 gene was detected in 9 out of 22 affected family members who manifested classical clinical features of RP. Conclusions. Our results showed that two compound heterozygous CYP4V2 mutations caused BCD, and one missense mutation in PRPF3 was responsible for adRP in this large family. This study suggests that accurate phenotypic diagnosis, molecular diagnosis, and genetic counseling are necessary for patients with hereditary retinal degeneration in some large mutigenerational family

MiR-770-5p inhibits cisplatin chemoresistance in human ovarian cancer by targeting ERCC2

In this study, we examined the role of the miRNA miR-770-5p in cisplatin chemotherapy resistance in ovarian cancer (OVC) patients. miR-770-5p expression was reduced in platinum-resistant patients. Using a 6.128-fold in expression as the cutoff value, miR-770-5p expression served as a prognostic biomarker and predicted the response to cisplatin treatment and survival among OVC patients. Overexpression of miR-770-5p in vitro reduced survival in chemoresistant cell lines after cisplatin treatment. ERCC2, a target gene of miR-770-5p that participates in the NER system, was negatively regulated by miR-770-5p. siRNA-mediated silencing of ERCC2 reversed the inhibition of apoptosis resulting from miR-770-5p downreglation in A2780S cells. A comet assay confirmed that this restoration of cisplatin chemosensitivity was due to the inhibition of DNA repair. These findings suggest that endogenous miR-770-5p may function as an anti-oncogene and promote chemosensitivity in OVC, at least in part by downregulating ERCC2. miR-770-5p may therefore be a useful biomarker for predicting chemosensitivity to cisplatin in OVC patients and improve the selection of effective, more personalized, treatment strategies

Overlapping Mechanisms of Peripheral Nerve Regeneration and Angiogenesis Following Sciatic Nerve Transection

Peripheral nervous system owns the ability of self-regeneration, mainly in its regenerative microenvironment including vascular network reconstruction. More recently, more attentions have been given to the close relationship between tissue regeneration and angiogenesis. To explore the overlap of molecular mechanisms and key regulation molecules between peripheral nerve regeneration and angiogenesis post peripheral nerve injury, integrative and bioinformatic analysis was carried out for microarray data of proximal stumps after sciatic nerve transection in SD rats. Nerve regeneration and angiogenesis were activated at 1 day immediately after sciatic nerve transection simultaneously. The more obvious changes of transcription regulators and canonical pathways suggested a phase transition between 1 and 4 days of both nerve regeneration and angiogenesis after sciatic nerve transection. Furthermore, 16 differentially expressed genes participated in significant biological processes of both nerve regeneration and angiogenesis, a few of which were validated by qPCR and immunofluorescent staining. It was demonstrated that STAT3, EPHB3, and Cdc42 co-expressed in Schwann cells and vascular endothelial cells to play a key role in regulation of nerve regeneration and angiogenesis simultaneously response to sciatic nerve transection. We provide a framework for understanding biological processes and precise molecular correlations between peripheral nerve regeneration and angiogenesis after peripheral nerve transection. Our work serves as an experimental basis and a valuable resource to further understand molecular mechanisms that define nerve injury-induced micro-environmental variation for achieving desired peripheral nerve regeneration

Somatic SF3B1 hotspot mutation in prolactinomas.

The genetic basis and corresponding clinical relevance of prolactinomas remain poorly understood. Here, we perform whole genome sequencing (WGS) on 21 patients with prolactinomas to detect somatic mutations and then validate the mutations with digital polymerase&nbsp;chain&nbsp;reaction (PCR) analysis of tissue samples from 227 prolactinomas. We identify the same hotspot somatic mutation in splicing factor 3 subunit B1 (SF3B1R625H) in 19.8% of&nbsp;prolactinomas. These patients with mutant prolactinomas display higher prolactin (PRL) levels (p = 0.02) and shorter progression-free survival (PFS) (p = 0.02) compared to patients without the mutation. Moreover, we identify that the SF3B1R625H mutation causes aberrant splicing of estrogen related receptor gamma (ESRRG), which results in stronger binding of pituitary-specific positive transcription factor 1 (Pit-1), leading to excessive PRL secretion. Thus our study validates an important mutation and elucidates a potential mechanism underlying the pathogenesis of prolactinomas that may lead to the development of targeted therapeutics