Non-destructive testing (NDT) and structural health monitoring (SHM) are widely used for this purpose. Different types of NDT techniques have been proposed for the damage detection, such as optical image, ultrasound wave, thermography, eddy current, and microwave. The focus in this study is on the wave-based detection method, which is grouped into two major categories: feature-based damage detection and model-assisted damage detection. Both damage detection approaches have their own pros and cons. Feature-based damage detection is usually very fast and doesn’t involve in the solution of the physical model. The key idea is the dimension reduction of signals to achieve efficient damage detection. The disadvantage is that the loss of information due to the feature extraction can induce significant uncertainties and reduces the resolution. The resolution of the feature-based approach highly depends on the sensing path density. Model-assisted damage detection is on the opposite side. Model-assisted damage detection has the ability for high resolution imaging with limited number of sensing paths since the entire signal histories are used for damage identification. Model-based methods are time-consuming due to the requirement for the inverse wave propagation solution, which is especially true for the large 3D structures.
The motivation of the proposed method is to develop efficient and accurate model-based damage imaging technique with limited data. The special focus is on the efficiency of the damage imaging algorithm as it is the major bottleneck of the model-assisted approach. The computational efficiency is achieved by two complimentary components. First, a fast forward wave propagation solver is developed, which is verified with the classical Finite Element(FEM) solution and the speed is 10-20 times faster. Next, efficient inverse wave propagation algorithms is proposed. Classical gradient-based optimization algorithms usually require finite difference method for gradient calculation, which is prohibitively expensive for large degree of freedoms. An adjoint method-based optimization algorithms is proposed, which avoids the repetitive finite difference calculations for every imaging variables. Thus, superior computational efficiency can be achieved by combining these two methods together for the damage imaging. A coupled Piezoelectric (PZT) damage imaging model is proposed to include the interaction between PZT and host structure. Following the formulation of the framework, experimental validation is performed on isotropic and anisotropic material with defects such as cracks, delamination, and voids. The results show that the proposed method can detect and reconstruct multiple damage simultaneously and efficiently, which is promising to be applied to complex large-scale engineering structures.
Recent studies suggest a role for the microbiota in autism spectrum disorders (ASD), potentially arising from their role in modulating the immune system and gastrointestinal (GI) function or from gut–brain interactions dependent or independent from the immune system. GI problems such as chronic constipation and/or diarrhea are common in children with ASD, and significantly worsen their behavior and their quality of life. Here we first summarize previously published data supporting that GI dysfunction is common in individuals with ASD and the role of the microbiota in ASD. Second, by comparing with other publically available microbiome datasets, we provide some evidence that the shifted microbiota can be a result of westernization and that this shift could also be framing an altered immune system. Third, we explore the possibility that gut–brain interactions could also be a direct result of microbially produced metabolites.
Background: Autism spectrum disorders (ASD) are complex neurobiological disorders that impair social interactions and communication and lead to restricted, repetitive, and stereotyped patterns of behavior, interests, and activities. The causes of these disorders remain poorly understood, but gut microbiota, the 1013 bacteria in the human intestines, have been implicated because children with ASD often suffer gastrointestinal (GI) problems that correlate with ASD severity. Several previous studies have reported abnormal gut bacteria in children with ASD. The gut microbiome-ASD connection has been tested in a mouse model of ASD, where the microbiome was mechanistically linked to abnormal metabolites and behavior. Similarly, a study of children with ASD found that oral non-absorbable antibiotic treatment improved GI and ASD symptoms, albeit temporarily. Here, a small open-label clinical trial evaluated the impact of Microbiota Transfer Therapy (MTT) on gut microbiota composition and GI and ASD symptoms of 18 ASD-diagnosed children.
Results: MTT involved a 2-week antibiotic treatment, a bowel cleanse, and then an extended fecal microbiota transplant (FMT) using a high initial dose followed by daily and lower maintenance doses for 7–8 weeks. The Gastrointestinal Symptom Rating Scale revealed an approximately 80% reduction of GI symptoms at the end of treatment, including significant improvements in symptoms of constipation, diarrhea, indigestion, and abdominal pain. Improvements persisted 8 weeks after treatment. Similarly, clinical assessments showed that behavioral ASD symptoms improved significantly and remained improved 8 weeks after treatment ended. Bacterial and phage deep sequencing analyses revealed successful partial engraftment of donor microbiota and beneficial changes in the gut environment. Specifically, overall bacterial diversity and the abundance of Bifidobacterium, Prevotella, and Desulfovibrio among other taxa increased following MTT, and these changes persisted after treatment stopped (followed for 8 weeks).
Conclusions: This exploratory, extended-duration treatment protocol thus appears to be a promising approach to alter the gut microbiome and virome and improve GI and behavioral symptoms of ASD. Improvements in GI symptoms, ASD symptoms, and the microbiome all persisted for at least 8 weeks after treatment ended, suggesting a long-term impact.
High proportions of autistic children suffer from gastrointestinal (GI) disorders, implying a link between autism and abnormalities in gut microbial functions. Increasing evidence from recent high-throughput sequencing analyses indicates that disturbances in composition and diversity of gut microbiome are associated with various disease conditions. However, microbiome-level studies on autism are limited and mostly focused on pathogenic bacteria. Therefore, here we aimed to define systemic changes in gut microbiome associated with autism and autism-related GI problems. We recruited 20 neurotypical and 20 autistic children accompanied by a survey of both autistic severity and GI symptoms. By pyrosequencing the V2/V3 regions in bacterial 16S rDNA from fecal DNA samples, we compared gut microbiomes of GI symptom-free neurotypical children with those of autistic children mostly presenting GI symptoms. Unexpectedly, the presence of autistic symptoms, rather than the severity of GI symptoms, was associated with less diverse gut microbiomes. Further, rigorous statistical tests with multiple testing corrections showed significantly lower abundances of the genera Prevotella, Coprococcus, and unclassified Veillonellaceae in autistic samples. These are intriguingly versatile carbohydrate-degrading and/or fermenting bacteria, suggesting a potential influence of unusual diet patterns observed in autistic children. However, multivariate analyses showed that autism-related changes in both overall diversity and individual genus abundances were correlated with the presence of autistic symptoms but not with their diet patterns. Taken together, autism and accompanying GI symptoms were characterized by distinct and less diverse gut microbial compositions with lower levels of Prevotella, Coprococcus, and unclassified Veillonellaceae.
Background:
Many pharmaceutical drugs are known to be ineffective or have negative side effects in a substantial proportion of patients. Genomic advances are revealing that some non-synonymous single nucleotide variants (nsSNVs) may cause differences in drug efficacy and side effects. Therefore, it is desirable to evaluate nsSNVs of interest in their ability to modulate the drug response.
Results:
We found that the available data on the link between drug response and nsSNV is rather modest. There were only 31 distinct drug response-altering (DR-altering) and 43 distinct drug response-neutral (DR-neutral) nsSNVs in the whole Pharmacogenomics Knowledge Base (PharmGKB). However, even with this modest dataset, it was clear that existing bioinformatics tools have difficulties in correctly predicting the known DR-altering and DR-neutral nsSNVs. They exhibited an overall accuracy of less than 50%, which was not better than random diagnosis. We found that the underlying problem is the markedly different evolutionary properties between positions harboring nsSNVs linked to drug responses and those observed for inherited diseases. To solve this problem, we developed a new diagnosis method, Drug-EvoD, which was trained on the evolutionary properties of nsSNVs associated with drug responses in a sparse learning framework. Drug-EvoD achieves a TPR of 84% and a TNR of 53%, with a balanced accuracy of 69%, which improves upon other methods significantly.
Conclusions:
The new tool will enable researchers to computationally identify nsSNVs that may affect drug responses. However, much larger training and testing datasets are needed to develop more reliable and accurate tools.
expenditure, and environmental risk. Surfactant treatment to disrupt Scenedesmus biomass was evaluated
as a means to make solvent extraction more efficient. Surfactant treatment increased the recovery of fatty
acid methyl ester (FAME) by as much as 16-fold vs. untreated biomass using isopropanol extraction, and
nearly 100% FAME recovery was possible without any Folch solvent, which is toxic and expensive. Surfactant
treatment caused cell disruption and morphological changes to the cell membrane, as documented by
transmission electron microscopy and flow cytometry. Surfactant treatment made it possible to extract wet
biomass at room temperature, which avoids the expense and energy cost associated with heating
and drying of biomass during the extraction process. The best FAME recovery was obtained from highlipid
biomass treated with Myristyltrimethylammonium bromide (MTAB)- and 3-(decyldimethylammonio)-
propanesulfonate inner salt (3_DAPS)-surfactants using a mixed solvent (hexane : isopropanol = 1 : 1, v/v)
vortexed for just 1 min; this was as much as 160-fold higher than untreated biomass. The critical micelle
concentration of the surfactants played a major role in dictating extraction performance, but the growth
stage of the biomass had an even larger impact on how well the surfactants disrupted the cells and
improved lipid extraction. Surfactant treatment had minimal impact on extracted-FAME profiles and,
consequently, fuel-feedstock quality. This work shows that surfactant treatment is a promising strategy for
more efficient, sustainable, and economical extraction of fuel feedstock from microalgae.