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Using Co-Culture to Functionalize Clostridium Fermentation
Clostridium fermentations have been developed for producing butanol and other value-added chemicals, but their development is constrained by some limitations, such as relatively high substrate cost and the need to maintain an anaerobic condition. Recently, co-culture is emerging as a popular way to address these limitations by introducing a partner strain with Clostridium. Generally speaking, the co-culture strategy enables the use of a cheaper substrate, maintains the growth of Clostridium without any anaerobic treatment, improves product yields, and/or widens the product spectrum. Herein, we review recent developments of co-culture strategies involving Clostridium species according to their partner stains’ functions with representative examples. We also discuss research challenges that need to be addressed for the future development of Clostridium co-cultures.
Clostridium co-culture has emerged as a solution to some problems faced by Clostridium monoculture.Co-culturing Clostridium with cellulolytic strains or acetogens enables the production of butanol from cheaper substrates such as lignocellulosic biomass and syngas.Aerotolerance is possible in anaerobic Clostridium fermentation in co-cultures with oxygen-consuming microbes.Co-culturing solventogenic Clostridium with acetogens can improve the production of butanol and its derivatives by increasing carbon recovery and relieving solvent toxicity.Other products, such as H2 or fatty acids, can be efficiently produced by the co-culture of Clostridium and other H2-producing strains (such as PNS bacteria), or chain-elongating strains respectively.
Journal Article
A sequential two-step priming scheme reproduces diversity in synaptic strength and short-term plasticity
Glutamatergic synapses display variable strength and diverse short-term plasticity (STP), even for a given type of connection. Using nonnegative tensor factorization and conventional state modeling, we demonstrate that a kinetic scheme consisting of two sequential and reversible steps of release–machinery assembly and a final step of synaptic vesicle (SV) fusion reproduces STP and its diversity among synapses. Analyzing transmission at the calyx of Held synapses reveals that differences in synaptic strength and STP are not primarily caused by variable fusion probability (pfusion
) but are determined by the fraction of docked synaptic vesicles equipped with a mature release machinery. Our simulations show that traditional quantal analysis methods do not necessarily report pfusion
of SVs with a mature release machinery but reflect both pfusion
and the distribution between mature and immature priming states at rest. Thus, the approach holds promise for a better mechanistic dissection of the roles of presynaptic proteins in the sequence of SV docking, two-step priming, and fusion. It suggests a mechanism for activity-induced redistribution of synaptic efficacy.
Journal Article
Canine tumor mutational burden is correlated with TP53 mutation across tumor types and breeds
Spontaneous canine cancers are valuable but relatively understudied and underutilized models. To enhance their usage, we reanalyze whole exome and genome sequencing data published for 684 cases of >7 common tumor types and >35 breeds, with rigorous quality control and breed validation. Our results indicate that canine tumor alteration landscape is tumor type-dependent, but likely breed-independent. Each tumor type harbors major pathway alterations also found in its human counterpart (e.g., PI3K in mammary tumor and p53 in osteosarcoma). Mammary tumor and glioma have lower tumor mutational burden (TMB) (median < 0.5 mutations per Mb), whereas oral melanoma, osteosarcoma and hemangiosarcoma have higher TMB (median ≥ 1 mutations per Mb). Across tumor types and breeds, TMB is associated with mutation of
TP53
but not
PIK3CA
, the most mutated genes. Golden Retrievers harbor a TMB-associated and osteosarcoma-enriched mutation signature. Here, we provide a snapshot of canine mutations across major tumor types and breeds.
Genomic studies of canine tumours have been done for individual cancer types or dog breeds. Here the authors analyse canine tumour genomics data across multiple breeds and cancer types, finding that mutational burden is associated with TP53 mutations and that Golden Retrievers are enriched for particular signatures.
Journal Article
Detection of Alzheimer’s disease using ECD SPECT images by transfer learning from FDG PET
ObjectiveTo develop a practical method to rapidly utilize a deep learning model to automatically extract image features based on a small number of SPECT brain perfusion images in general clinics to objectively evaluate Alzheimer's disease (AD).MethodsFor the properties of low cost and convenient access in general clinics, Tc-99-ECD SPECT imaging data in brain perfusion detection was used in this study for AD detection. Two-stage transfer learning based on the Inception v3 network model was performed using the ImageNet dataset and ADNI database. To improve training accuracy, the three-dimensional image was reorganized into three sets of two-dimensional images for data augmentation and ensemble learning. The effect of pre-training parameters for Tc-99m-ECD SPECT image to distinguish AD from normal cognition (NC) was investigated, as well as the effect of the sample size of F-18-FDG PET images used in pre-training. The same model was also fine-tuned for the prediction of the MMSE score from the Tc-99m-ECD SPECT image.ResultsThe AUC values of w/wo pre-training parameters for Tc-99m-ECD SPECT image to distinguish AD from NC were 0.86 and 0.90. The sensitivity, specificity, precision, accuracy, and F1 score were 100%, 75%, 76%, 86%, and 86%, respectively for the training model with 1000 cases of F-18-FDG PET image for pre-training. The AUC values for various sample sizes of the training dataset (100, 200, 400, 800, 1000 cases) for pre-training were 0.86, 0.91, 0.95, 0.97, and 0.97. Regardless of the pre-training condition ECD dataset used, the AUC value was greater than 0.85. Finally, predicting cognitive scores and MMSE scores correlated (R2 = 0.7072).ConclusionsWith the ADNI pre-trained model, the sensitivity and accuracy of the proposed deep learning model using SPECT ECD perfusion images to differentiate AD from NC were increased by approximately 30% and 10%, respectively. Our study indicated that the model trained on PET FDG metabolic imaging for the same disease could be transferred to a small sample of SPECT cerebral perfusion images. This model will contribute to the practicality of SPECT cerebral perfusion images using deep learning technology to objectively recognize AD.
Journal Article
Aging shifts mitochondrial dynamics toward fission to promote germline stem cell loss
Changes in mitochondrial dynamics (fusion and fission) are known to occur during stem cell differentiation; however, the role of this phenomenon in tissue aging remains unclear. Here, we report that mitochondrial dynamics are shifted toward fission during aging of Drosophila ovarian germline stem cells (GSCs), and this shift contributes to aging‐related GSC loss. We found that as GSCs age, mitochondrial fragmentation and expression of the mitochondrial fission regulator, Dynamin‐related protein (Drp1), are both increased, while mitochondrial membrane potential is reduced. Moreover, preventing mitochondrial fusion in GSCs results in highly fragmented depolarized mitochondria, decreased BMP stemness signaling, impaired fatty acid metabolism, and GSC loss. Conversely, forcing mitochondrial elongation promotes GSC attachment to the niche. Importantly, maintenance of aging GSCs can be enhanced by suppressing Drp1 expression to prevent mitochondrial fission or treating with rapamycin, which is known to promote autophagy via TOR inhibition. Overall, our results show that mitochondrial dynamics are altered during physiological aging, affecting stem cell homeostasis via coordinated changes in stemness signaling, niche contact, and cellular metabolism. Such effects may also be highly relevant to other stem cell types and aging‐induced tissue degeneration. Aging shifts mitochondrial balance toward fission; fragmented mitochondria with low membrane potential (△Ψ), and ROS levels, along with decreased BMP signaling causing GSC loss. Marf depletion induces highly fragmented mitochondria with low fatty acid (FA) oxidation, causing oil droplet (LD) accumulation, and attenuated BMP signaling that cause GSC loss. Drp1 depletion generates elongated mitochondria and increased E‐cadherin expression to strengthen GSC competitiveness for niche occupancy.
Journal Article
Inhibition of the formation of aluminum–copper intermetallic compounds in direct-bonded aluminum–copper ceramic substrates by using a silver metallic interlayer
A silver metallic interlayer was inserted into a direct-bonded aluminum–copper (DBAC) substrate to inhibit the formation of aluminum–copper intermetallic compounds (IMCs) in the substrate. The Ag caused the dissolution of small quantities of Al and Cu to form a Ag(Al, Cu) metallic layer, which exhibited lower hardness (1.4 ± 0.2 GPa) and a lower elastic modulus (71.7 ± 12.8 GPa) than did Al–Cu IMCs (hardness/elastic modulus: 10.4 ± 0.9 GPa and 193.9 ± 7.2 GPa for Al
4
Cu
9
, 10.6 ± 0.3 GPa and 171.2 ± 10.7 GPa for Al–Cu, and 7.6 ± 1.5 GPa and 121.0 ± 8.4 GPa for Al
2
Cu, respectively). Moreover, the Ag(Al, Cu layer was able to withstand high stress caused by the coefficient of thermal expansion mismatch between Al, Ag, and Cu; thus, this layer prevented crack formation at the Al–Cu bonding interface. The shear strength of the Al–Cu bonding interface was originally 13.3 ± 3.4 MPa. This value then increased to 26.3 ± 3.6 MPa when a Ag metallic interlayer was inserted, and the shear strength was maintained at 21.9 ± 1.1 MPa during 500 thermal cycles between − 50 and 150 °C. At room temperature, the thermal conductivity of DBAC with a Ag metallic layer (280 W/mK) was higher than that of direct-bonded aluminum (233 W/mK) and DBAC without a Ag metallic layer (276 W/mK) because of the high thermal conductivity of Ag and the absence of Al–Cu IMCs in the DBAC with a Ag metallic layer.
Graphical abstract
Journal Article
Liquid Viscosity Sensor Using a Surface Acoustic Wave Device for Medical Applications Including Blood and Plasma
Blood viscosity is the defining health indicator for hyperviscosity syndrome patients. This paper introduces an alternative approach for the real-time monitoring of blood viscosity by employing a surface-horizontal surface acoustic wave (SH-SAW) device at room temperature. A novel bi-layer waveguide is constructed on top of the SAW device. This device enables the SAW sensing of liquid droplets utilizing a bi-layer waveguide, consisting of a zinc oxide (ZnO) enhancement layer and Parlyene C, that facilitates the promotion of the surface horizontal mode. The ZnO piezoelectric thin-film layer enhanced the local particle displacement and dielectric coupling while the Parylene C layer constrained the wave mode at the interface of the piezoelectric material and polymer material. The device was tested with a liquid drop on the SAW delay-line path. Both experimental and finite element analysis results demonstrated the benefits of the bi-layer waveguide. The simulation results confirmed that the displacement field of local particles increased 9 times from 1.261 nm to 11.353 nm with the Parylene C/ZnO bi-layer waveguide structure. The device demonstrated a sensitivity of 3.57 ± 0.3125 kHz shift per centipoise enabling the potential for high precision blood viscosity monitoring.
Journal Article
Degradation of Acid Azo Dyes Using Oxone Activated by Cobalt Titanate Perovskite
Chemical degradation by sulfate radicals from activation of Oxone is one of the most attractive advanced oxidation processes (AOPs) for treating toxic acid azo dyes. However, development of an effective and recyclable heterogeneous catalyst for activating Oxone is still highly desired. In this study, cobalt titanate perovskite (CoTiO3) was synthesized and employed as a heterogeneous catalyst for activating Oxone to degrade acid azo dyes, Acid Red 27 (AR), Acid Yellow 17 (AY), and Acid Blue 120 (AB). As CoTiO3 does not adsorb these azo dyes, and Oxone alone is ineffective to degrade them, the combination of CoTiO3 and Oxone tremendously improves degradation of acid azo dyes, validating that CoTiO3 can activate Oxone. The analyses of Co species before and after Oxone activation validate that the activation mechanism can attributed to Co2+ of CoTiO3, which transforms between Co2+ and Co3+ to activate Oxone. Through examining the effects of radical scavengers, the degradation of these azo dyes is primarily owing to sulfate radicals and derivative hydroxyl radicals to a lesser extent. In addition, CoTiO3-activated Oxone is much favorable at elevated temperature and under a neutral condition (pH = 7), while the addition of NaCl slightly slows the dye degradation kinetics by CoTiO3-activated Oxone. CoTiO3 can also be reused for multiple cycles (up to 5 cycles) and remains effective to activate Oxone. CoTiO3-activated Oxone exhibits the highest degradation efficiency for AR, followed by AB and finally AY, when AR, AB, and AY co-exist. This study demonstrates that CoTiO3 is a promising catalyst for activating Oxone to degrade typical acid azo dyes. The findings obtained here can provide further understanding and optimized parameters for using CoTiO3 to activate Oxone in treatments of acid azo dye-containing wastewater.
Journal Article
The Paradoxical Role of Uric Acid in Osteoporosis
Because of its high prevalence worldwide, osteoporosis is considered a serious public health concern. Many known risk factors for developing osteoporosis have been identified and are crucial if planning health care needs. Recently, an association between uric acid (UA) and bone fractures had been explored. Extracellular UA exhibits antioxidant properties by effectively scavenging free radicals in human plasma, but this benefit might be disturbed by the hydrophobic lipid layer of the cell membrane. In contrast, intracellular free oxygen radicals are produced during UA degradation, and superoxide is further enhanced by interacting with NADPH oxidase. This intracellular oxidative stress, together with inflammatory cytokines induced by UA, stimulates osteoclast bone resorption and inhibits osteoblast bone formation. UA also inhibits vitamin D production and thereby results in hyper-parathyroidism, which causes less UA excretion in the intestines and renal proximal tubules by inhibiting the urate transporter ATP-binding cassette subfamily G member 2 (ABCG2). At normal or high levels, UA is associated with a reduction in bone mineral density and protects against bone fracture. However, in hyperuricemia or gout arthritis, UA increases bone fracture risk because oxidative stress and inflammatory cytokines can increase bone resorption and decrease bone formation. Vitamin D deficiency, and consequent secondary hyperparathyroidism, can further increase bone resorption and aggravated bone loss in UA-induced osteoporosis.
Journal Article