Magnetite particles accelerate methanogenic degradation of highly concentrated acetic acid in anaerobic digestion process.

The anaerobic digestion (AD) process has become significant for its capability to convert organic wastewater into biogas, a valuable energy source. Excessive acetic acid accumulation in the anaerobic digester can inhibit methanogens, ultimately leading to the deterioration of process performance. Herein, the effect of magnetite particles (MP) as an enhancer on the methanogenic degradation of highly-concentrated acetate (6 g COD/L) was examined through long-term sequential AD batch tests. Bioreactors with (AM) and without (AO) MP were compared. AO experienced inhibition and its methane production rate (qm) converged to 0.45 L CH4/g VSS/d after 10 sequential batches (AO10, the 10th batch in a series of the sequential batch tests conducted using bioreactors without MP addition). In contrast, AM achieved 3-425% higher qm through the sequential batches, indicating that MP could counteract the inhibition caused by the highly-concentrated acetate. MP addition to inhibited bioreactors (AO10) successfully restored them, achieving qm of 1.53 L CH4/g VSS/d, 3.4 times increase from AO10 after 8 days lag time, validating its potential as a recovery strategy for inhibited digesters with acetate accumulation. AM exhibited higher microbial populations (1.8-3.8 times) and intracellular activity (9.3 times) compared to AO. MP enriched Methanosaeta, Peptoclostridium, Paraclostridium, OPB41, and genes related to direct interspecies electron transfer and acetate oxidation, potentially driving the improvement of qm through MP-mediated methanogenesis. These findings demonstrated the potential of MP supplementation as an effective strategy to accelerate acetate-utilizing methanogenesis and restore an inhibited anaerobic digester with high acetate accumulation.

PINK1 siRNA-loaded poly(lactic-co-glycolic acid) nanoparticles provide neuroprotection in a mouse model of photothrombosis-induced ischemic stroke.

PTEN-induced kinase 1 (PINK1) is a well-known critical marker in the pathway for mitophagy regulation as well as mitochondrial dysfunction. Evidence suggests that mitochondrial dynamics and mitophagy flux play an important role in the development of brain damage from stroke pathogenesis. In this study, we propose a treatment strategy using nanoparticles that can control PINK1. We used a murine photothrombotic ischemic stroke (PTS) model in which clogging of blood vessels is induced with Rose Bengal (RB) to cause brain damage. We targeted PINK1 with poly(lactic-co-glycolic acid) (PLGA)-based nanoparticles loaded with PINK1 siRNA (PINK1 NPs). After characterizing siRNA loading in the nanoparticles, we assessed the efficacy of PINK1 NPs in mice with PTS using immunohistochemistry, 1% 2,3,5-triphenyltetrazolium chloride staining, measurement of motor dysfunction, and Western blot. PINK1 was highly expressed in microglia 24 h after PTS induction. PINK1 siRNA treatment increased phagocytic activity, migration, and expression of an anti-inflammatory state in microglia. In addition, the PLGA nanoparticles were selectively taken up by microglia and specifically regulated PINK1 expression in those cells. Treatment with PINK1 NPs prior to stroke induction reduced expression of mitophagy-inducing factors, infarct volume, and motor dysfunction in mice with photothrombotic ischemia. Experiments with PINK1-knockout mice and microglia depletion with PLX3397 confirmed a decrease in stroke-induced infarct volume and behavioral dysfunction. Application of nanoparticles for PINK1 inhibition attenuates RB-induced photothrombotic ischemic injury by inhibiting microglia responses, suggesting that a nanomedical approach targeting the PINK1 pathway may provide a therapeutic avenue for stroke treatment.

Targeting spinal microglia with fexofenadine-loaded nanoparticles prolongs pain relief in a rat model of neuropathic pain.

Targeting microglial activation is emerging as a clinically promising drug target for neuropathic pain treatment. Fexofenadine, a histamine receptor 1 antagonist, is a clinical drug for the management of allergic reactions as well as pain and inflammation. However, the effect of fexofenadine on microglial activation and pain behaviors remains elucidated. Here, we investigated nanomedicinal approach that targets more preferentially microglia and long-term analgesics. Fexofenadine significantly abolished histamine-induced microglial activation. The fexofenadine-encapsulated poly(lactic-co-glycolic acid) nanoparticles (Fexo NPs) injection reduced the pain sensitivity of spinal nerve ligation rats in a dose-dependent manner. This alleviation was sustained for 4 days, whereas the effective period by direct fexofenadine injection was 3 h. Moreover, Fexo NPs inhibited microglial activation, inflammatory signaling, cytokine release, and a macrophage phenotype shift towards the alternative activated state in the spinal cord. These results show that Fexo NPs exhibit drug repositioning promise as a long-term treatment modality for neuropathic pain.

Vitamin E reduces spasms caused by prenatal stress by lowering calpain expression.

BACKGROUND: Prenatal stress increases the susceptibility of infants to seizures and is known to be associated with oxidative stress. Recent studies suggest that vitamin E has beneficial effects in various neurological diseases due to its antioxidant properties. In this study, we investigated the relationship between prenatal stress and vitamin E treatment on N-methyl-D-aspartate (NMDA)-induced spasms. METHODS: We used pregnant female Sprague Dawley rats and induced prenatal stress with an injection of betamethasone on G15. They were then treated orally with 200 mg/kg vitamin E or saline twice a day from G15-G21. On postnatal day 15, NMDA was administered to trigger spasms in offspring. The total number of spasms and latency to the first spasm were recorded. We also measured oxidative stress in the medial cortex using western blot, and calpain activity, thiobarbituric acid reactive substances (TBARS), glutathione (GSH)/GSH/glutathione disulfide (GSSG), superoxide dismutase (SOD) activity, catalase activity, and nitric oxide (NO) assays. RESULTS: We observed that rats treated with vitamin E while exposed to prenatal stress demonstrated reduced total number and frequency of spasms. Expression of glutamate decarboxylase 67 (GAD67) and K+/Cl- co-transporter (KCC2) were reduced after prenatal stress; this recovered in the vitamin E treated group. Further, expression of calpain 2 was decreased and various markers of oxidative stress (malondialdehyde (MDA), GSH/GSSG, SOD, catalase, and NO) were reduced in the vitamin E treated group. CONCLUSIONS: Our results provide evidence that vitamin E lowers oxidative stress and decreases seizure susceptibility in rat offspring exposed to prenatal stress. Given the well-known safety profile of vitamin E, these results indicate its potential as a strategy for preventing seizures.

Biophysical properties of striae rubra and striae alba in human skin: Comparison with normal skin.

BACKGROUND: Striae distensae are common dermal lesions that progress through two different stages: the striae rubra, which appears to be erythematous, and striae alba, which is characterized by a hypopigmented feature. The clinical characteristics between striae distensae stages and normal skin remain unknown. OBJECTIVES: We aimed to investigate the clinical characteristics according to stages of striae distensae in terms of their biophysical properties, using objective noninvasive measurements in comparison with adjacent normal skin. METHODS: Sixty-one healthy female subjects with striae distensae were included as follows: 30 with striae rubra and 31 with striae alba on the abdomen and thighs. Hydration of the epidermis and dermis, skin color brightness, and Erythema index were measured. Skin elasticity, roughness, and dermal echo-density of the skin with striae distensae and adjacent normal skin were also measured. RESULTS: Hydration of the epidermis and dermis showed no significant difference between the skin with striae distensae and normal skin. Brightness of skin with striae alba and normal skin was significantly higher than that of skin with striae rubra. Erythema index of skin with striae rubra was significantly higher than that of skin with striae alba and normal skin. Skin with striae rubra and striae alba had a rougher surface than normal skin. Elasticity and dermal echo-density were significantly lower in striae distensae skin. CONCLUSIONS: Striae rubra and striae alba had similar biophysical properties in terms of skin hydration, elasticity, roughness, and dermal density. Moreover, striae distensae have less elasticity, more roughness, and lower dermal density than normal skin.

Age-related biophysical changes of the epidermal and dermal skin in Korean women.

INTRODUCTION: The clinical characteristics of skin were investigated to study the inter-relationship and changes in the biophysical properties of the epidermal and dermal layers associated with aging using noninvasive methods. METHODS: Our study included 100 healthy women aged between the early 20s and late 60s. Biophysical characteristics of skin such as color (brightness and spots), transparency, wrinkle on crow's feet, elasticity, hydration, sebum content, glossiness, and transepidermal water loss measured under controlled conditions. RESULTS: This study performed in a Korean population demonstrated that aging significantly affects human skin in terms of parameters such as wrinkles, skin color, elasticity, and epidermal hydration. Age-related changes in skin hydration showed varying patterns between the epidermis and dermis. Skin color showed heterogeneous characteristics between the upper and lower epidermal layers associated with aging. Skin elasticity and wrinkles were observed to show and inversely proportional relationship in the early 40s. CONCLUSIONS: We confirmed the significant influence of aging on the biophysical properties of skin and determined the distinct age-related biophysical changes in the epidermal and dermal layers of skin using noninvasive method. This study indicates the need for further research to investigate the distinctive age-related changes in characteristics of the epidermal and dermal layers of human skin.

Foxp3 plasmid-encapsulated PLGA nanoparticles attenuate pain behavior in rats with spinal nerve ligation.

Microglia play a critical role in neuropathic pain. Since upregulated Foxp3 in microglia enhances tissue repair by resolving neuroinflammation in excitotoxin-induced neuronal death, it may attenuate neuropathic pain in a similar manner. Therefore, this study tests whether Foxp3 introduced with poly (D, L-lactic-co-glycolic acid) (PLGA) nanoparticles (Foxp3 NPs) can alleviate neuropathic pain by inhibiting microglia activity. The prepared Foxp3 NPs had an anti-inflammatory effect on lipopolysaccharide-stimulated BV2 cells in vitro, and localized to spinal microglia in vivo. Further, the Foxp3 NPs significantly attenuated pain behavior induced by spinal nerve ligation in rats for 7 days by suppressing microglial activity, followed by the downregulation of pro-nociceptive genes and the upregulation of anti-nociceptive genes in the spinal dorsal horn. Collectively, these data suggest that Foxp3 NPs effectively relieve neuropathic pain in animals by reducing microglia activity and subsequent modulation of neuroinflammation, and may be of therapeutic value in the treatment of neuropathic pain.

Evans Blue Reduces Neuropathic Pain Behavior by Inhibiting Spinal ATP Release.

Upon peripheral nerve injury, vesicular ATP is released from damaged primary afferent neurons. This extracellular ATP subsequently activates purinergic receptors of the spinal cord, which play a critical role in neuropathic pain. As an inhibitor of the vesicular nucleotide transporter (VNUT), Evans blue (EB) inhibits the vesicular storage and release of ATP in neurons. Thus, we tested whether EB could attenuate neuropathic pain behavior induced by spinal nerve ligation (SNL) in rats by targeting VNUT. An intrathecal injection of EB efficiently attenuated mechanical allodynia for five days in a dose-dependent manner and enhanced locomotive activity in an SNL rat model. Immunohistochemical analysis showed that EB was found in VNUT immunoreactivity on neurons in the dorsal root ganglion and the spinal dorsal horn. The level of ATP in cerebrospinal fluid in rats with SNL-induced neuropathic pain decreased upon administration of EB. Interestingly, EB blocked ATP release from neurons, but not glial cells in vitro. Eventually, the loss of ATP decreased microglial activity in the ipsilateral dorsal horn of the spinal cord, followed by a reduction in reactive oxygen species and proinflammatory mediators, such as interleukin (IL)-1ß and IL-6. Finally, a similar analgesic effect of EB was demonstrated in rats with monoiodoacetate-induced osteoarthritis (OA) pain. Taken together, these data demonstrate that EB prevents ATP release in the spinal dorsal horn and reduces the ATP/purinergic receptor-induced activation of spinal microglia followed by a decline in algogenic substances, thereby relieving neuropathic pain in rats with SNL.

A snapshot of microbial community structures in 20 different field-scale anaerobic bioreactors treating food waste.

This study aimed to identify significant factors shaping the microbial populations in biogas plants treating food waste (FW). Twenty full-scale anaerobic acidogenic/methanogenic bioreactors, located at 11 FW treatment facilities, were compared to find patterns in their microbial community structures and potential interactions with the process parameters. Temperature, hydraulic retention time, and organic loading rate were design parameters that systematically influenced the microbial communities. The latter two clearly separated the acidogenic and methanogenic bioreactors. Lactobacillus was the dominant (69.7 ±â€¯19.8%) bacteria in the acidogenic reactors, while hydrogen-utilizing methanogens, such as Methanoculleus (65.1 ±â€¯33.5%), were the dominant archaea in most methanogenic digesters. Defluiviitoga was the dominant (82.7 ±â€¯1.4%) bacteria in the thermophilic digesters, but was also the most abundant (33.1-33.6%) bacteria in dry mesophilic digesters. The two bioreactor categories had lower bacterial diversities, and also higher propionate concentrations (>5 g/L in 4 out of 5 cases), which may impose potential risks for the management of such digesters. The current 'snapshot' of the microbial communities suggests several bacterial and archaeal taxa as potential indicators of bioreactor categories and/or process variables.

Accumulation of the parkin substrate, FAF1, plays a key role in the dopaminergic neurodegeneration.

This study reports the physical and functional interplay between Fas-associated factor 1 (FAF1), a death-promoting protein, and parkin, a key susceptibility protein for Parkinson's disease (PD). We found that parkin acts as an E3 ubiquitin ligase to ubiquitinate FAF1 both in vitro and at cellular level, identifying FAF1 as a direct substrate of parkin. The loss of parkin function due to PD-linked mutations was found to disrupt the ubiquitination and degradation of FAF1, resulting in elevated FAF1 expression in SH-SY5Y cells. Moreover, FAF1-mediated cell death was abolished by wild-type parkin, but not by PD-linked parkin mutants, implying that parkin antagonizes the death potential of FAF1. This led us to investigate whether FAF1 participates in the pathogenesis of PD. To address this, we used a gene trap mutagenesis approach to generate mutant mice with diminished levels of FAF1 (Faf1(gt/gt)). Using the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mouse model of PD, we found that FAF1 accumulated in the substantia nigra pars compacta (SNc) of MPTP-treated PD mice, and that MPTP-induced dopaminergic cell loss in the SNc was significantly attenuated in Faf1(gt/gt) mice versus Faf1(+/+) mice. MPTP-induced reduction of locomotor activity was also lessened in Faf1(gt/gt) mice versus Faf1(+/+) mice. Furthermore, we found that FAF1 deficiency blocked PD-linked biochemical events, including caspase activation, ROS generation, JNK activation and cell death. Taken together, these results suggest a new role for FAF1: that of a positive modulator for PD.

6-Phenoxy-2-phenylbenzoxazoles, novel inhibitors of receptor for advanced glycation end products (RAGE).

Receptor for advanced glycation end products (RAGE) is known to be involved in the transportation of amyloid ß (Aß) peptides and causes the accumulation of Aß in the brain. Moreover, recent studies suggest that the interactions between RAGE and Aß peptides may be the culprit behind Alzheimer's disease (AD). Inhibitors of the RAGE-Aß interactions would not only prevent the accumulation of toxic Aß in the brain, and but also block the progress of AD, therefore, have the potential to provide a 'disease-modifying therapy'. In this study, we have developed a series of 6-phenoxy-2-phenylbenzoxazole analogs as novel inhibitors of RAGE. Among these derivatives, we found several effective inhibitors that block the RAGE-Aß interactions without causing significant cellular toxicity. Further testing showed that compound 48 suppressed Aß induced toxicity in mouse hippocampal neuronal cells and reduced Aß levels in the brains of a transgenic mouse model of AD after oral administration.

Employing the sustained-release properties of poly(lactic-co-glycolic acid) nanoparticles to reveal a novel mechanism of sodium-hydrogen exchanger 1 in neuropathic pain.

Neuropathic pain is caused by injury or disease of the somatosensory system, and its course is usually chronic. Several studies have been dedicated to investigating neuropathic pain-related targets; however, little attention has been paid to the persistent alterations that these targets, some of which may be crucial to the pathophysiology of neuropathic pain. The present study aimed to identify potential targets that may play a crucial role in neuropathic pain and validate their long-term impact. Through bioinformatics analysis of RNA sequencing results, we identified Slc9a1 and validated the reduced expression of sodium-hydrogen exchanger 1 (NHE1), the protein that Slc9a1 encodes, in the spinal nerve ligation (SNL) model. Colocalization analysis revealed that NHE1 is primarily co-localized with vesicular glutamate transporter 2-positive neurons. In vitro experiments confirmed that poly(lactic-co-glycolic acid) nanoparticles loaded with siRNA successfully inhibited NHE1 in SH-SY5Y cells, lowered intracellular pH, and increased intracellular calcium concentrations. In vivo experiments showed that sustained suppression of spinal NHE1 expression by siRNA-loaded nanoparticles resulted in delayed hyperalgesia in naïve and SNL model rats, whereas amiloride-induced transient suppression of NHE1 expression yielded no significant changes in pain sensitivity. We identified Slc9a1, which encodes NHE1, as a key gene in neuropathic pain. Utilizing the sustained release properties of nanoparticles enabled us to elucidate the chronic role of decreased NHE1 expression, establishing its significance in the mechanisms of neuropathic pain.

Rejuvenating aged microglia by p16ink4a-siRNA-loaded nanoparticles increases amyloid-ß clearance in animal models of Alzheimer's disease.

Age-dependent accumulation of amyloid plaques in patients with sporadic Alzheimer's disease (AD) is associated with reduced amyloid clearance. Older microglia have a reduced ability to phagocytose amyloid, so phagocytosis of amyloid plaques by microglia could be regulated to prevent amyloid accumulation. Furthermore, considering the aging-related disruption of cell cycle machinery in old microglia, we hypothesize that regulating their cell cycle could rejuvenate them and enhance their ability to promote more efficient amyloid clearance. First, we used gene ontology analysis of microglia from young and old mice to identify differential expression of cyclin-dependent kinase inhibitor 2A (p16ink4a), a cell cycle factor related to aging. We found that p16ink4a expression was increased in microglia near amyloid plaques in brain tissue from patients with AD and 5XFAD mice, a model of AD. In BV2 microglia, small interfering RNA (siRNA)-mediated p16ink4a downregulation transformed microglia with enhanced amyloid phagocytic capacity through regulated the cell cycle and increased cell proliferation. To regulate microglial phagocytosis by gene transduction, we used poly (D,L-lactic-co-glycolic acid) (PLGA) nanoparticles, which predominantly target microglia, to deliver the siRNA and to control microglial reactivity. Nanoparticle-based delivery of p16ink4a siRNA reduced amyloid plaque formation and the number of aged microglia surrounding the plaque and reversed learning deterioration and spatial memory deficits. We propose that downregulation of p16ink4a in microglia is a promising strategy for the treatment of Alzheimer's disease.

Variations in antibiotic resistance genes and microbial community in sludges passing through biological nutrient removal and anaerobic digestion processes in municipal wastewater treatment plants.

Antimicrobial resistance (AMR) represents a relentless, silent pandemic. Contributing to this are wastewater treatment plants (WWTPs), a potential source of antibiotic resistance genes' (ARGs) transmission to the environment, threatening public health. The presence of ARGs in pathogenic bacteria and their release into the environment by WWTPs threatens the public health. The current study investigated changes in ARGs' abundance in biological nutrient removal (BNR) processes and anaerobic digestion (AD) reactors of two WWTPs. Also, microbial community structure, which is known to shape the distribution and abundance of ARGs, was also analyzed. The relative abundance of eight ARGs (tetX, tetA, tetM, TEM, sul1, sul2, ermB and qnrD) was quantified as ARGs' copies/16 S rRNA gene copies using quantitative polymerase chain reaction (qPCR). Microbial community composition was assessed by 16 S rRNA microbiome sequencing analysis. TetX was prevalent among the eight ARGs, followed by TEM and sul1. However, its abundance was decreased in the AD sludges compared to BNR sludges. Proteobacteria was the major bacterial phylum found in all the sludge samples, while Arcobacter, 12up and Acidovorax were the predominant genera. Acinetobacter and Flavobacterium were significantly more abundant in the BNR sludges, while 12up and Aeromonas were predominant in AD sludges. Principal component analysis (PCA) revealed a clear difference in dominant ARGs and bacteria between the sludges in the processes of BNR and AD of the two WWTPs. Clinically relevant bacterial genera, Klebsiella and Enterococcus, found in both the BNR and AD sludges, were significantly correlated with the tetX gene. Throughout this study, the relationship between microbial communities and specific ARGs was revealed, illustrating that the composition of the microbial community could play a vital role in the abundance of ARGs. These results will better inform future studies aimed at controlling the spread of ARGs and their potential hosts from WWTPs.

MiR-146a encapsulated liposomes reduce vascular inflammatory responses through decrease of ICAM-1 expression, macrophage activation, and foam cell formation.

Vascular insults can create an inflammatory cascade involving endothelial cell, smooth muscle cell, and macrophage activation which can eventually lead to vascular disease such as atherosclerosis. Several studies have identified microRNA 146a's (miR-146a) anti-inflammatory potential based on its role in regulating the nuclear factor kappa beta (NF-κß) pathway. Therefore, in this study, we introduced exogenous miR-146a encapsulated by liposomes to lipopolysaccharide (LPS) stimulated vascular cells and macrophages to reduce inflammatory responses. First, the miR-146a encapsulated liposomes showed uniform size (radius 96.4 ± 4.22 nm) and round shape, long term stability (at least two months), high encapsulation efficiency (69.73 ± 0.07%), and were well transfected to human aortic endothelial cells (HAECs), human aortic smooth muscle cells (SMCs), and human differentiated monocytes (U937 cells). In addition, we demonstrated that miR-146a encapsulated liposomes reduced vascular inflammation responses in HAECs and SMCs through inhibition of ICAM-1 expression and decreased monocyte adhesion. In macrophages, miR-146a liposome treatment demonstrated decreased production of proinflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1ß), as well as reduced oxidized low-density lipoprotein (ox-LDL) uptake and foam cell formation. Thus, based on these results, miR-146a encapsulated liposomes may be promising for reducing vascular inflammation by targeting its multiple associated mediators.

Effect of magnetite supplementation on mesophilic anaerobic digestion of phenol and benzoate: Methane production rate and microbial communities.

Anaerobic sequential batch tests treating phenol and benzoate were conducted to evaluate the potential of magnetite supplementation to improve methanogenic degradation of phenol and benzoate, and to identify active microbial communities under each condition. Specific CH4 production rates during anaerobic digestion were 218.5 mL CH4/g VSS/d on phenol and 517.6 mL CH4/g VSS/d on benzoate. Magnetite supplementation significantly increased methanogenic degradation of phenol by 9.0-68.0% in CH4 production rate, and decreased lag time by 7.9-48.0%, with no significant reduction in CH4 yield. Syntrophorhabdus, Sporotomaculum, Syntrophus, Syntrophomonas, Peptoclostridium, Soehngenia, Mesotoga, Geobacter, Methanosaeta, Methanoculleus, and Methanospirillum were revealed as active microbial communities involved in anaerobic digestion of phenol and benzoate. Magnetite-mediated direct interspecies electron transfer between Geobacter, Peptoclostridium, and Methanosaeta harundinacea could contribute to this improvement.

Effects of Different pH Control Strategies on Microalgae Cultivation and Nutrient Removal from Anaerobic Digestion Effluent.

This study investigated nutrient removal from anaerobic digestion effluent by cultivating mixed-culture microalgae enriched from anaerobic sludge under different pH conditions: RUC (uncontrolled), R7-8 (maintained at 7-8), and R<8 (maintained below 8). Significant amounts of NH4+-N were lost by volatilization in RUC cultures due to increased pH values (≤8.6) during the early period of cultivation. The pH control strategies significantly affected the biological NH4+-N removal (highest in R7-8), microalgal growth (highest in R7-8), biomass settleability (highest in R<8), and microalgal growth relative to bacteria (highest in R<8) in the cultures. Parachlorella completely dominated the microalgal communities in the inoculum and all of the cultures, and grew well at highly acidic pH (<3) induced by culture acidification with microalgal growth. Microalgae-associated bacterial community structure developed very differently among the cultures. The findings call for more attention to the influence and control of pH changes during cultivation in microalgal treatment of anaerobic digestion effluent.

Responses of Coagulant Type, Dosage and Process Conditions to Phosphate Removal Efficiency from Anaerobic Sludge.

Phosphorus, a crucial component of life, may cause eutrophication if it is discharged untreated into the aquatic ecosystem. Phosphate (PO43-) may exist at an elevated level in anaerobic digestion (AD) effluents and can lead to the clogging of pipes by forming struvite crystals. This study was conducted to assess the responses of coagulant type, dosage and process conditions to phosphate removal efficiency from anaerobic sludge. The experiments were performed in two steps. First, a sensitivity test was conducted to compare five coagulant types (alum, poly-aluminum chloride (PAC), FeCl2, FeCl3 and PAC + FeCl3) at standard coagulation conditions. The results showed that PAC would be the best coagulant among the tested, while a combination of PAC and FeCl3 may be beneficial under circumstances. Second, an optimization study was performed for PAC using response surface methodology employing central composite design. Among the three independent variables (coagulant dosage, slow mixing duration and agitation speed), the dosage was the sole significant variable for phosphate removal efficiency, while the other two had limited effects. A future study to optimize the rapid mixing conditions would give additional insights into the process. The results of this study may be useful to design a process to counteract phosphate discharges from AD plants, as well as to reduce the risks of pipe clogging and maintenance problems due to crystalline struvite formation in the later stage of AD.

Key players in syntrophic propionate oxidation revealed by metagenome-assembled genomes from anaerobic digesters bioaugmented with propionic acid enriched microbial consortia.

Propionic acid (HPr) is frequently accumulated in anaerobic digesters due to its thermodynamically unfavorable degradation reaction. Here, we identify key players in HPr oxidation and organic overloading recovery from metagenome-assembled genomes (MAGs) recovered from anaerobic digesters inoculated with HPr-enriched microbial consortia before initiating organic overloading. Two independent HPr-enrichment cultures commonly selected two uncultured microorganisms represented with high relative abundance: Methanoculleus sp002497965 and JABUEY01 sp013314815 (a member of the Syntrophobacteraceae family). The relative abundance of JABUEY01 sp013314815 was 60 times higher in bioaugmented bioreactors compared to their unaugmented counterparts after recovery from organic overloading. Genomic analysis of JABUEY01 sp013314815 revealed its metabolic potential for syntrophic propionate degradation when partnered with hydrogenotrophic methanogens (e.g., Methanoculleus sp002497965) via the methylmalonyl-CoA pathway. Our results identified at least two key species that are responsible for efficient propionate removal and demonstrate their potential applications as microbial cocktails for stable AD operation.

Evaluation of facial skin age based on biophysical properties in vivo.

OBJECTIVE: The evaluation of skin age, reflecting overall facial characteristics, has not been established. Previous studies focused on visual assessment or individual-specific feature such as wrinkles or skin color. We studied the evaluation model of skin age index (SAI) including the overall aging features including wrinkles, skin color, pigmentation, elasticity, and hydration. METHODS: Total 300 healthy women aged between 20 and 69 years included in this study. Pearson correlation analysis performed to identify the key factors among the biophysical properties with aging and developed the prediction model of SAI. Statistical regression analysis and machine learning technique applied to build the prediction model using the coefficient of determination (R2 ) and root mean square error (RMSE). Validation study of the SAI model performed on 24 women for 6 weeks application with anti-aging product. RESULTS: Prediction model of SAI consisted of skin elasticity, wrinkles, skin color (brightness, Pigmented spot, and Uv spot), and hydration, which are major features for aging. The cforest model to assess a SAI using machine learning identified the highest R2 and lowest RMSE compared to other models, such as svmRadial, gaussprRadial, blackboost, rpart, and statistical regression formula. The cforest prediction model confirmed a significant decrease of predicted SAI after 6 weeks of application of anti-aging product. CONCLUSION: We developed a prediction model to evaluate a SAI using machine learning, and led to accurate predicted age for overall clinical aging. This model can a good standard index for evaluating facial skin aging and anti-aging products.