Study on Dynamic Liquid-Carrying Process of Foaming Agent and Establishment of Mathematical Model.

The efficiency of foam drainage gas recovery is predominantly dictated by the performance of the foaming agent. To better understand their behavior, a novel testing apparatus was developed to simulate the foam drainage gas recovery process within the wellbore. Through the dynamic liquid-carrying performance tests of four foaming agents under uniform conditions, it was discerned that there existed significant disparities in the liquid-carrying performance and action duration. Further interface performance analysis disclosed that the liquid-carrying capacity and the duration were correlated with their adsorption capacity and interface activity at the gas-liquid interface. Notably, foaming agents with lower adsorption capacity and higher interfacial activity demonstrated superior liquid-carrying performance and longer action duration. By analyzing the consumption of foaming agents during the liquid-carrying process, five dynamic liquid-carrying equations were derived based on first-order reaction kinetics, the Malthusian population model, and the logistic function. The outcomes demonstrated that all these five equations could precisely delineate the dynamic liquid-carrying process of the foaming agent. During the research, we found that the consumption of the foaming agent in the foam drainage gas recovery process is related to its adsorption behavior at the gas-liquid interface, and revealed that the dynamic liquid-carrying process of foaming agent is the increasing process of liquid-carrying capacity under the continuous consumption of limited foaming agent resources. This laid a foundation for the further exploration of the functional mechanism of the foaming agent in the foam drainage gas recovery process.

Treatment Options for Distal Rectal Cancer in the Era of Organ Preservation.

OPINION STATEMENT: The introduction of total mesorectal excision into the radical surgery of rectal cancer has significantly improved the oncological outcome with longer survival and lower local recurrence. Traditional treatment modalities of distal rectal cancer, relying on radical surgery, while effective, take their own set of risks, including surgical complications, potential damage to the anus, and surrounding structure owing to the pursuit of thorough resection. The progress of operating methods as well as the integration of systemic therapies and radiotherapy into the peri-operative period, particularly the exciting clinical complete response of patients after neoadjuvant treatment, have paved the way for organ preservation strategy. The non-inferiority oncological outcome of "watch and wait" compared with radical surgery underscores the potential of organ preservation not only to control local recurrence but also to reduce the need for treatments followed by structure destruction, hopefully improving the long-term quality of life. Radical radiotherapy provides another treatment option for patients unwilling or unable to undergo surgery. Organ preservation points out the direction of treatment for distal rectal cancer, while additional researches are needed to answer remaining questions about its optimal use.

Task-State Functional MRI of Brain Regions with Reduced Activation in Aphasia Patients: A Meta-analysis.

OBJECTIVE: Language is one of the most celebrated hallmarks of human cognition. With the continuous improvement of medical technology, functional MRI (fMRI) has been used in aphasia. Although many related studies have been carried out, most studies have not extensively focused on brain regions with reduced activation in aphasic patients. The aim of this study was to identify brain regions normally activated in healthy controls but with reduced activation in aphasic patients during fMRI language tasks. METHODS: We collected all previous task-state fMRI studies of secondary aphasia. The brain regions showed normal activation in healthy controls and reduced activation in aphasic patients were conducted activation likelihood estimation (ALE) meta-analysis to obtain the brain regions with consistently reduced activation in aphasic patients. RESULTS: The ALE meta-analysis revealed that the left inferior frontal gyrus, left middle temporal gyrus, left superior temporal gyrus, left fusiform gyrus, left lentiform nucleus and the culmen of the cerebellum were the brain regions with reduced activation in aphasic patients. DISCUSSION: These findings from the ALE meta-analysis have significant implications for understanding the language network and the potential for recovery of language functions in individuals with aphasia.

Novel Germline KIT Variants in Families With Severe Piebaldism: Case Series and Literature Review.

INTRODUCTION: Piebaldism is a rare autosomal dominant disorder characterized by congenital white forelock and depigmented patches, which is most commonly caused by deleterious variants in the KIT gene. METHODS: Four KIT variants were identified in a piebaldism case series by whole-exome sequencing. Functional experiments, including in vitro minigene reporter assay and enzyme-linked immunosorbent assay, were carried out to elucidate the pathogenicity of the variants. The genotype-phenotype correlation was summarized through extensive literature reviewing. RESULTS: All the four cases had severe piebaldism presented with typical white forelock and diffuse depigmentation on the ventral trunk and limbs. Four germline variants at the tyrosine kinase (TK) domains of the KIT gene were identified: two novel variants c.1990+1G>A (p.Pro627_Gly664delinsArg) and c.2716T>C (p.Cys906Arg), and two known variants c.1879+1G>A (p.Gly592_Pro627delinsAla) and c.1747G>A (p.Glu583Lys). Both splicing variants caused exon skipping and inframe deletions in the TK1 domain. The missense variants resided at the TK1 and TK2 domains respectively impairing PI3K/AKT and MAPK/ERK signaling pathways, the downstream of KIT. All severe cases were associated with variants in the TK domains, eliciting a major dominant-negative mechanism of the disease. CONCLUSION: Our data expand the mutation spectrum of KIT, emphasized by a dominant-negative effect of variants in the critical TK domains in severe cases. We also share the experience of prenatal diagnosis and informed reproductive choices for the affected families.

Evaluation of left ventricular stiffness with echocardiography.

Half of patients with heart failure are presented with preserved ejection fraction (HFpEF). The pathophysiology of these patients is complex, but increased left ventricular (LV) stiffness has been proven to play a key role. However, the application of this parameter is limited due to the requirement for invasive catheterization for its measurement. With advances in ultrasound technology, significant progress has been made in the noninvasive assessment of LV chamber or myocardial stiffness using echocardiography. Therefore, this review aims to summarize the pathophysiological mechanisms, correlations with invasive LV stiffness constants, applications in different populations, as well as the limitations of echocardiography-derived indices for the assessment of both LV chamber and myocardial stiffness. Indices of LV chamber stiffness, such as the ratio of E/e' divided by left ventricular end-diastolic volume (E/e'/LVEDV), the ratio of E/SRe (early diastolic strain rates)/LVEDV, and diastolic pressure-volume quotient (DPVQ), are derived from the relationship between echocardiographic parameters of LV filling pressure (LVFP) and LV size. However, these methods are surrogate and lumped measurements, relying on E/e' or E/SRe for evaluating LVFP. The limitations of E/e' or E/SRe in the assessment of LVFP may contribute to the moderate correlation between E/e'/LVEDV or E/SRe/LVEDV and LV stiffness constants. Even the most validated measurement (DPVQ) is considered unreliable in individual patients. In comparison to E/e'/LVEDV and E/SRe/LVEDV, indices like time-velocity integral (TVI) measurements of pulmonary venous and transmitral flows may demonstrate better performance in assessing LV chamber stiffness, as evidenced by their higher correlation with LV stiffness constants. However, only one study has been conducted on the exploration and application of TVI in the literature, and the accuracy of assessing LV chamber stiffness remains to be confirmed. Regarding echocardiographic indices for LV myocardial stiffness evaluation, parameters such as epicardial movement index (EMI)/ diastolic wall strain (DWS), intrinsic velocity propagation of myocardial stretch (iVP), and shear wave imaging (SWI) have been proposed. While the alteration of DWS and its predictive value for adverse outcomes in various populations have been widely validated, it has been found that DWS may be better considered as an overall marker of cardiac function performance rather than pure myocardial stiffness. Although the effectiveness of iVP and SWI in assessing left ventricular myocardial stiffness has been demonstrated in animal models and clinical studies, both indices have their limitations. Overall, it seems that currently no echocardiography-derived indices can reliably and accurately assess LV stiffness, despite the development of several parameters. Therefore, a comprehensive evaluation of LV stiffness using all available parameters may be more accurate and enable earlier detection of alterations in LV stiffness.

Incidence and prognostic factors of residual back pain in patients treated for osteoporotic vertebral compression fractures: a systematic review and meta-analysis.

BACKGROUND: Osteoporotic vertebral compression fracture (OVCF) is a common consequence of osteoporosis and can significantly impact the quality of life for affected individuals. Despite treatment options such as vertebroplasty and kyphoplasty, many patients continue to experience residual back pain (RBP) even after the fracture has healed. The incidence of RBP after OVCF treatment varies among studies, and there is a need for further research to understand the risk factors associated with RBP. METHODS: A systematic review and meta-analysis were conducted following the PRISMA guidelines. Electronic databases were searched, and relevant studies were selected based on inclusion and exclusion criteria. Data extraction and quality assessment were performed independently by two authors. Statistical analysis included single-proportion meta-analyses and pooling of odds ratios (OR) using the inverse-variance method, to calculate the overall incidences of RBP and cement leakage and identify risk factors associated with RBP. RESULTS: A total of 19 studies were included in the analysis. The overall incidences of RBP and cement leakage were found to be 16% and 18%, respectively. Several risk factors were identified, including gender, bone mineral density, depression, baseline visual analog scale (VAS) score, intravertebral vacuum cleft, number of fractured segments, cement distribution, history of vertebral fracture, thoracolumbar fascial injury, and fracture non-union. CONCLUSIONS: This study provides potential value within the scope of the incidence and risk factors of RBP following treatment of OVCFs. The identified risk factors can help clinicians identify high-risk patients and tailor appropriate interventions. Future research should focus on standardizing the definition of RBP and patient selection criteria to improve the accuracy of estimates and facilitate better management strategies for OVCF patients.

Using nomogram scores to predict the early regression of coronary artery aneurysms of Kawasaki disease.

BACKGROUND: Coronary artery aneurysms have been considered the most serious complication of Kawasaki disease. However, some coronary artery aneurysms do regress. Therefore, the ability to predict the expected time of coronary artery aneurysm regression is critical. Herein, we have created a nomogram prediction system to determine the early regression (<1 month) among patients with small to medium coronary artery aneurysms. METHODS: Seventy-six Kawasaki disease patients identified with coronary artery aneurysms during the acute or subacute phase were included. All the patients who met inclusion criteria demonstrated regression of coronary artery aneurysms within the first-year post Kawasaki disease diagnosis. The clinical and laboratory parameters were compared between the groups of coronary artery aneurysms regression duration within and beyond 1 month. Multivariate logistic regression analysis was used to identify the independent parameters for early regression based on the results from the univariable analysis. Then nomogram prediction systems were established with associated receiver operating characteristic curves. RESULTS: Among the 76 included patients, 40 cases recovered within 1 month. Haemoglobin, globulin, activated partial thromboplastin time, the number of lesions, location of the aneurysm, and coronary artery aneurysm size were identified as independent factors for early regression of coronary artery aneurysms in Kawasaki disease patients. The predictive nomogram models revealed a high efficacy in predicting early regression of coronary artery aneurysms. CONCLUSION: The size of coronary artery aneurysms, the number of lesions, and the location of aneurysms presented better predictive value for predicting coronary artery aneurysms regression. The nomogram system created from the identified risk factors successfully predicted early coronary artery aneurysm regression.

[Expert consensus on the genetic counseling for Dystrophinopathies].

Dystrophinopathies caused by variants of DMD gene are a group of muscular diseases including Duchenne muscular dystrophy, Becker muscular dystrophy, and DMD-associated dilated cardiomyopathy. With the advancement of genetic testing techniques and wider implementation of genetic screening, especially the expanded carrier screening, more and more individuals carrying DMD gene variants have been identified, whereas the genetic counseling capacity is relatively insufficient. Currently there is still a lack of professional norms for genetic counseling on dystrophinopathies. In this consensus, the main points to be covered in the pre- and post-test consultation have been discussed, with an aim to provide genetic counseling guidance for the disease diagnosis, treatment, and family reproduction.

Current and emerging molecular and epigenetic disease entities in acute myeloid leukemia and a critical assessment of their therapeutic modalities.

Acute myeloid leukemia (AML) is the most frequently diagnosed acute leukemia, and its incidence increases with age. Although the etiology of AML remains unknown, exposure to genotoxic agents or some prior hematologic disorders could lead to the development of this condition. The pathogenesis of AML involves the development of malignant transformation of hematopoietic stem cells that undergo successive genomic alterations, ultimately giving rise to a full-blown disease. From the disease biology perspective, AML is considered to be extremely complex with significant genetic, epigenetic, and phenotypic variations. Molecular and cytogenetic alterations in AML include mutations in those subsets of genes that are involved in normal cell proliferation, maturation and survival, thus posing significant challenge to targeting these pathways without attendant toxicity. In addition, multiple malignant cells co-exist in the majority of AML patients. Individual subclones are characterized by unique genetic and epigenetic abnormalities, which contribute to the differences in their response to treatment. As a result, despite a dramatic progress in our understanding of the pathobiology of AML, not much has changed in therapeutic approaches to treat AML in the past four decades. Dose and regimen modifications with improved supportive care have contributed to improved outcomes by reducing toxicity-related side effects. Several drug candidates are currently being developed, including targeted small-molecule inhibitors, cytotoxic chemotherapies, monoclonal antibodies and epigenetic drugs. This review summarizes the current state of affairs in the pathobiological and therapeutic aspects of AML.

A novel variant in the FBP1 gene causes fructose-1,6-bisphosphatase deficiency through increased ubiquitination.

Fructose-1,6-bisphosphatase (FBPase) deficiency is an autosomal recessive disorder characterized by impaired gluconeogenesis caused by mutations in the fructose-1,6-bisphosphatase 1 (FBP1) gene. The molecular mechanisms underlying FBPase deficiency caused by FBP1 mutations require investigation. Herein, we report the case of a Chinese boy with FBPase deficiency who presented with hypoglycemia, ketonuria, metabolic acidosis, and repeated episodes of generalized seizures that progressed to epileptic encephalopathy. Whole-exome sequencing revealed compound heterozygous variants, c.761 A > G (H254R) and c.962C > T (S321F), in FBP1. The variants, especially the novel H254R, reduced protein stability and enzymatic activity in patient-derived leukocytes and transfected HepG2 and U251 cells. Mutant FBP1 undergoes enhanced ubiquitination and proteasomal degradation. NEDD4-2 was identified as an E3 ligase for FBP1 ubiquitination in transfected cells and the liver and brain of Nedd4-2 knockout mice. The H254R mutant FBP1 interacted with NEDD4-2 at significantly higher levels than the wild-type control. Our study identified a novel H254R variant of FBP1 underlying FBPase deficiency and elucidated the molecular mechanism underlying the enhanced NEDD4-2-mediated ubiquitination and proteasomal degradation of mutant FBP1.

Measurable residual disease detected by flow cytometry independently predicts prognoses of NPM1-mutated acute myeloid leukemia.

Acute myeloid leukemia (AML) with NPM1 mutation is a distinct genetic entity with favorable outcomes. Nevertheless, emerging evidence suggests that NPM1-mutated AML is still a highly heterogeneous disorder. In this study, 266 patients with AML with NPM1 mutations were retrospectively analyzed to evaluate the associations between variant allele frequency (VAF) of NPM1 mutations, co-mutated genes, measurable residual disease (MRD), and patient outcomes. Multiparameter flow cytometry (MFC) and real-time quantitative polymerase chain reaction (RT-PCR) were used for monitoring MRD. Ultimately, 106 patients were included in the long-term follow-up period. Patients with high NPM1 VAF (≥ 42.43%) had poorer 2-year relapse-free survival (RFS) (55.7% vs. 70.2%, P = 0.017) and overall survival (OS) (63.7% vs. 82.0%, P = 0.027) than those with low VAF. DNMT3A mutations negatively influenced the outcomes of patients with NPM1 mutations. Patients with high DNMT3A VAF or NPM1/DNMT3A/FLT3-ITD triple mutations had shorter RFS and significantly lower OS than that in controls. After two cycles of chemotherapy, patients with positive MFC MRD results had lower RFS (MRD+ vs. MRD-:44.9% vs. 67.6%, P = 0.007) and OS (61.5% vs. 76.6%, P = 0.011) than those without positive MFC MRD results. In multivariate analysis, high NPM1 VAF (hazard ratio [HR] = 2.045; P = 0.034) and positive MRD after two cycles of chemotherapy (HR = 3.289; P = 0.003) were independent risk factors for RFS; MRD positivity after two cycles of chemotherapy (HR = 3.293; P = 0.008) independently predicted the OS of the patients. These results indicate that VAF of both NPM1 gene itself or certain co-occurring gene pre-treatment and MRD post-treatment are potential markers for restratifying the prognoses of patients AML having NPM1 mutations.

Impact of a novel prognostic model on allogeneic hematopoietic stem cell transplantation outcomes in patients with CMML.

Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell malignancy, and allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only curable treatment. The outcomes after transplant are influenced by both disease characteristics and patient comorbidities. To develop a novel prognostic model to predict the post-transplant survival of CMML patients, we identified risk factors by applying univariable and multivariable Cox proportional hazards regression to a derivation cohort. In multivariable analysis, advanced age (hazard ratio [HR] 3.583), leukocyte count (HR 3.499), anemia (HR 3.439), bone marrow blast cell count (HR 2.095), and no chronic graft versus host disease (cGVHD; HR 4.799) were independently associated with worse survival. A novel prognostic model termed ABLAG (Age, Blast, Leukocyte, Anemia, cGVHD) was developed and the points were assigned according to the regression equation. The patients were categorized into low risk (0-1), intermediate risk (2, 3), and high risk (4-6) three groups and the 3-year overall survival (OS) were 93.3% (95%CI, 61%-99%), 78.9% (95%CI, 60%-90%), and 51.6% (95%CI, 32%-68%; p < .001), respectively. In internal and external validation cohort, the area under the receiver operating characteristic (ROC) curves of the ABLAG model were 0.829 (95% CI, 0.776-0.902) and 0.749 (95% CI, 0.684-0.854). Compared with existing models designed for the nontransplant setting, calibration plots, and decision curve analysis showed that the ABLAG model revealed a high consistency between predicted and observed outcomes and patients could benefit from this model. In conclusion, combining disease and patient characteristic, the ABLAG model provides better survival stratification for CMML patients receiving allo-HSCT.

A rare case with fetal autoimmune heart block and KNCH2 variant-induced long QT syndrome: a controversial opinion on prenatal management strategy.

BACKGROUND: Among all fetal heart block patients, > 50% cases are associated with maternal autoimmune diseases, and such patients should receive treatment. However, nearly half of fetal heart block cases involve a mother with negative results following autoimmune antibody screening. A few studies have reported long QT syndrome (LQTS) can also present as a severe fetal bradycardia, which does not respond to fetal treatment. Herein, we reported a rare case of an infant who presented with high-degree autoimmune-mediated fetal atrioventricular block (AVB) with LQTS induced by a novel KCNH2 variant. This case led us to review our prenatal therapeutic strategy. CASE PRESENTATION: A 1-year-old boy presented to our heart center having experienced syncope 5 times in the past year. He had previously presented with fetal bradycardia during the fetal stage from 27 + 3 gestational weeks. The fetal echocardiography demonstrated AVB (2:1 transmission). As the maternal autoimmune antibody results were positive, his mother had received dexamethasone treatment during pregnancy; subsequently, the fetal AVB had changed from 2:1 to 4:3 transmission with elevated ventricular beating rates. However, this patient was identified to have complete AVB after birth. The initial electrocardiogram and Holter measurements at hospital administration showed complete AVB, pleomorphic ventricular tachycardia, a prolonged QT interval (QT = 602 ms, corrected QT = 538 ms), and wide and deep inverted T-waves. Meanwhile, torsades de pointes could be observed in several transit ventricular tachycardias based on Holter monitoring review. Genetic testing revealed KCNH2 c.2483G > A variant-induced LQTS. An implantable cardioverter defibrillator device and permanent pacemaker were both considered as therapeutic alternations; his parents ultimately accepted the implantation of a permanent pacemaker. CONCLUSIONS: For fetuses with autoimmune-mediated AVB, intrauterine treatment should still be pursued immediately. However, once the treatment outcomes are deemed unacceptable or unexpected, other genetic variant-related channelopathies should be highly suspected. If the fetus lacks a positive family history, fetal genetic testing should be recommended to improve the prognosis of such patients by introducing integrative therapeutic strategies between the prenatal and postnatal phases.

Nacre-mimetic cerium-doped nano-hydroxyapatite/chitosan layered composite scaffolds regulate bone regeneration via OPG/RANKL signaling pathway.

Autogenous bone grafting has long been considered the gold standard for treating critical bone defects. However, its use is plagued by numerous drawbacks, such as limited supply, donor site morbidity, and restricted use for giant-sized defects. For this reason, there is an increasing need for effective bone substitutes to treat these defects. Mollusk nacre is a natural structure with outstanding mechanical property due to its notable "brick-and-mortar" architecture. Inspired by the nacre architecture, our team designed and fabricated a nacre-mimetic cerium-doped layered nano-hydroxyapatite/chitosan layered composite scaffold (CeHA/CS). Hydroxyapatite can provide a certain strength to the material like a brick. And as a polymer material, chitosan can slow down the force when the material is impacted, like an adhesive. As seen in natural nacre, the combination of these inorganic and organic components results in remarkable tensile strength and fracture toughness. Cerium ions have been demonstrated exceptional anti-osteoclastogenesis capabilities. Our scaffold featured a distinct layered HA/CS composite structure with intervals ranging from 50 to 200 µm, which provided a conducive environment for human bone marrow mesenchymal stem cell (hBMSC) adhesion and proliferation, allowing for in situ growth of newly formed bone tissue. In vitro, Western-blot and qPCR analyses showed that the CeHA/CS layered composite scaffolds significantly promoted the osteogenic process by upregulating the expressions of osteogenic-related genes such as RUNX2, OCN, and COL1, while inhibiting osteoclast differentiation, as indicated by reduced TRAP-positive osteoclasts and decreased bone resorption. In vivo, calvarial defects in rats demonstrated that the layered CeHA/CS scaffolds significantly accelerated bone regeneration at the defect site, and immunofluorescence indicated a lowered RANKL/OPG ratio. Overall, our results demonstrate that CeHA/CS scaffolds offer a promising platform for bone regeneration in critical defect management, as they promote osteogenesis and inhibit osteoclast activation.

Molecular transport in zeolite catalysts: depicting an integrated picture from macroscopic to microscopic scales.

Increasing social sustainability triggers the persistent progress of industrial catalysis in energy transformation and chemical production. Zeolites have been demonstrated to be pivotal catalysts in chemical industries due to their moderate acidity and versatile well-defined pore structures. However, in the context of enhancing the performances of zeolite catalysts, the perspectives on the diffusion regulations within the pores and channels in the bulk phases or external surfaces of the zeolites are often overlooked. Establishing the structure-transport-reactivity relationships in heterogeneous catalysis can provide rational guidelines to design high-performance catalysts. Herein, this tutorial review attempts to systematically depict an integrated picture of molecular transport behaviors in zeolite catalysts from macroscopic to microscopic perspectives. The advances in the accurate diffusion measurements employing both macroscopic and microscopic techniques are briefly introduced. The diffusion characteristics in zeolite catalysts under working conditions (e.g., high temperature, multi-components, and reaction coupling) are then addressed. The macroscopic internal diffusion and the microscopic diffusion occurring in the micro-zones of zeolite crystals (e.g., surface diffusion, diffusion anisotropy, and confined diffusion) are reviewed and discussed in more detail. These diffusion behaviors highly impact the underlying reaction mechanism, catalytic performances, and catalyst optimization strategies. Finally, the multi-type pore systems of practical zeolite catalysts in industrial reactors and their transport behaviors are analyzed. The fully-crystalline monolithic zeolites in the absence of binders are highlighted as rising-star catalytic materials for industrial applications. The research challenges in this field and the potential future development directions are summarized.

[Advance of research on endoplasmic reticulum stress and genetic epilepsy].

Epilepsies are a group of chronic neurological disorders characterized by spontaneous recurrent seizures caused by abnormal synchronous firing of neurons and transient brain dysfunction. The underlying mechanisms are complex and not yet fully understood. Endoplasmic reticulum (ER) stress, as a condition of excessive accumulation of unfolded and/or misfolded proteins in the ER lumen, has been considered as a pathophysiological mechanism of epilepsy in recent years. ER stress can enhance the protein processing capacity of the ER to restore protein homeostasis through unfolded protein response, which may inhibit protein translation and promote misfolded protein degradation through the ubiquitin-proteasome system. However, persistent ER stress can also cause neuronal apoptosis and loss, which may aggravate the brain damage and epilepsy. This review has summarized the role of ER stress in the pathogenesis of genetic epilepsy.

Characterization of femtosecond laser-induced grating scattering of a continuous-wave laser light in air.

Nanosecond laser-induced grating scattering/spectroscopy (LIGS) technique has been widely applied for measuring thermodynamic parameters such as temperature and pressure in gaseous and liquid media. Recently, femtosecond (fs) laser was demonstrated to induce the grating and develop the fs-LIGS technique for gas thermometry. In this work, we systematically investigated the fs-LIGS signal generation using 35 fs, 800 nm laser pulses at 1 kHz repetition rate in ambient air by varying the pump laser energies, the probe laser powers and the temporal delays between two pump laser pulses. The stability of single-shot fs-LIGS signal was studied, from which we observed that the signal intensity exhibits a significant fluctuation while the oscillation frequency shows a much better stability. A 4.5% precision of the oscillation frequency was achieved over 100 single-shot signals. By using a previously-developed empirical model, the fs-LIGS signals were fitted using nonlinear least-squares fitting method, by which crucial time constants characterizing the signal decay process were extracted and their dependences on the pump laser energy were studied. From the measured results and theoretical analysis, we found that the appropriate range of the overall pump laser energy for reliable fs-LIGS measurements is approximately located within 80 ∼ 300 µJ. The limitations on the accuracy and precision of the fs-LIGS measurements, the origin of destructive influence of plasma generation on the signal generation as well as the electrostriction contribution were also discussed. Our investigations could contribute to a better understanding of the fs-LIGS process and further applications of the technique in single-shot gas thermometry and pressure measurements in various harsh conditions.

A Fiber Dissection Study of the Anterior Commissure: Correlations with Diffusion Spectrum Imaging Tractography and Clinical Relevance in Gliomas.

The anterior commissure, which connects bilateral temporal lobes and olfactive areas, remains elusive in many aspects of its structure and functional role. To comparatively describe anatomical details of the anterior commissure using cadaveric fiber dissection (FD) and diffusion spectrum imaging (DSI) thus refining our knowledge of the tract and exploring its clinical relevance in glioma migration. Twelve normal postmortem hemispheres were treated with Klingler's method and subjected to FD with medial, inferior, and lateral approaches. The FD findings were correlated with DSI tractography results. To illustrate the clinical relevance, two patients with recurrent temporal high-grade glioma are described. Our FD and DSI tractography of the anterior commissure disclosed a new anatomical paradigm. The FD confirmed that the anterior limb (absent sometimes and variable) and the lateral/temporal extension include the rostral portion and caudal portion, respectively, of the anterior commissure fibers. The shape of the lateral/temporal extension predominantly resembles an 'H'. The DSI tractography findings corresponded to these FD results. According to the FD, the Virchow-Robin space is continuous with the subarachnoid space and very close to the anterior commissure. The two clinical cases presented severe disturbances of consciousness and behavior despite good local tumor control. Subsequent magnetic resonance images showed new lesions infiltrating the contralateral temporal lobes. FD combined with DSI provided anatomical details facilitating a better understanding of the anterior commissure. Glioma migration routes to the contralateral temporal lobe included the anterior commissure, Virchow-Robin space, and subarachnoid space and were clinically relevant.

Lysozyme regulates the extracellular polymer of activated sludge and promotes the formation of electroactive biofilm.

The formation of electroactive biofilm from activated sludge on electrode surface is a key step to construct a bio-electrochemical system, yet it is greatly limited by the poor affinity between the bacteria and the electrode interface. Herein, we report a new method to promote the formation of electroactive biofilm by regulating the extracellular polymeric substance (EPS) content in activated sludge with lysozyme. The investigation of the effect of lysozyme treatment on the content of extracellular polymers and the biofilm formation of electroactive bacteria suggests that lysozyme can improve the permeability of the positive bacterial cell membrane and thus increase the EPS content in the activated sludge. The characterizations of electrochemical activity, surface morphology and community structure of the anode biofilm indicate that increasing EPS content promotes the adhesion of the mixed bacteria in the activated sludge on the electrode and results in denser biofilms with better conductivities. The microbial fuel cell (MFC) inoculated with the sludge of high EPS content exhibits the power density up to 2.195 W/m2, much higher than that inoculated with the untreated sludge (1.545 W/m2). The strategy of adjusting EPS content in activated sludge with a biological enzyme can effectively enhance the ability of the bacterial community to form biofilms and exhibits great application potentials in the construction of high efficiency bio-electrochemical systems.

Syringin Prevents Aß25-35-Induced Neurotoxicity in SK-N-SH and SK-N-BE Cells by Modulating miR-124-3p/BID Pathway.

Alzheimer's disease (AD) is a neurodegenerative disorder disease, disturbing people's normal life. Syringin was mentioned to antagonize Amyloid-ß (Aß)-induced neurotoxicity. However, the action mechanism is still not fully elucidated. This study aimed to explore a molecular mechanism of syringin in defending Aß-induced neurotoxicity. SK-N-SH and SK-N-BE cells were treated with amyloid ß-protein fragment 25-35 (Aß25-35) to induce cell neurotoxicity. The injury effects were distinguished by assessing cell viability and cell apoptosis using cell counting kit-8 (CCK-8) assay and flow cytometry assay, respectively. The expression of Cleaved-caspase3 (Cleaved-casp3), B cell lymphoma/leukemia-2 (Bcl-2), Bcl-2 associated X protein (Bax) and BH3 interacting domain death agonist (BID) at the protein level was determined by western blot. The expression of miR-124-3p and BID was detected using quantitative real-time polymerase chain reaction (qRT-PCR). The interaction between miR-124-3p and BID was predicted by the online database starBase and confirmed by dual-luciferase reporter assay plus RNA pull-down assay. Aß25-35 treatment inhibited cell viability and induced cell apoptosis, while the addition of syringin recovered cell viability and suppressed cell apoptosis. MiR-124-3p was significantly downregulated in Aß25-35-treated SK-N-SH and SK-N-BE cells, and BID was upregulated. Nevertheless, the addition of syringin reversed their expression. BID was a target of miR-124-3p, and its downregulation partly prevented Aß25-35-induced injuries. Syringin protected against Aß25-35-induced neurotoxicity by enhancing miR-124-3p expression and weakening BID expression, and syringin strengthened the expression of miR-124-3p to diminish BID level. Syringin ameliorated Aß25-35-induced neurotoxicity in SK-N-SH and SK-N-BE cells by regulating miR-124-3p/BID pathway, which could be a novel theoretical basis for syringin to treat AD.