Biodiesel production and properties estimation from food waste and domestic wastewater by Rhodosporidium toruloides.

Producing biodiesel from food waste (FW) would benefit both environment and economy. Current study investigated biodiesel production from food waste and domestic wastewater by utilizing the oleaginous yeast Rhodosporidium toruloides under non-sterile condition. The potential of biolipid production from the mixture of effluents of existing local FW treatment facilities and domestic wastewater was firstly evaluated. Then, to increase the nutrient recovery efficiency, FW hydrolysis process by crude enzymes produced from solid FWs by Aspergillus oryzae was introduced and the conditions were further optimized. The optimized hydrolysis process resulted in reducing sugar (RS) yield of 251.81 ± 8.09 mg gdryFW-1 and free amino nitrogen (FAN) yield of 7.70 ± 0.74 mg gdryFW-1 while waste oil with the RS yield of 93.54 ± 0.01 mg gdryFW-1 was easily separated without solvent usage. Compared to the hydrolysate only used, when mixed with domestic wastewater, the results showed obvious enhancement on biomass yield, biolipid yield, and wastewater treatment efficiency. The maximum biolipid yield was 29.80 ± 0.50 mg gdryFW-1 and the estimated quality of biodiesel produced from the biolipid met both EN 14214 and ASTM D6751 standards.

Rosin Derivative IDOAMP Inhibits Prostate Cancer Growth via Activating RIPK1/RIPK3/MLKL Signaling Pathway.

Rosin derivatives such as dehydroabietic acid and dehydroabietic amine belonging to diterpenoids have similar structure with androgen that inhibited the occurrence and development of prostate cancer. In this study, the effects and possible mechanism of the rosin derivative IDOAMP on prostate cancer were investigated. Our results showed that IDOAMP effectively inhibited cell viabilities of LNCaP, PC3, and DU145 prostate cells. After the treatment with IDOAMP, the levels of cleaved-PARP, LC3BII/I, and HMGB1 were increased, whereas the expression of GPX4 was decreased. Interestingly, cell viability was reversed by the supplements of necrostatin-1 and necrosulfonamide. Meanwhile, the IDOAMP downregulated the expression of human Aurora kinase A that was overexpressed in prostate cancer. In addition, co-IP results showed that IDOAMP inhibited the binding of Aurora kinase A to the receptor-interacting serine/threonine kinase 1 (RIPK1) and RIPK3. However, the binding of RIPK1 to FADD, RIPK3, or MLKL was significantly promoted. Further studies showed that the phosphorylation levels of RIPK1, RIPK, and MLKL were increased in a concentration-dependent manner. In in vivo model, IDOAMP reduced the tumor volumes and weights. In conclusion, IDOAMP directly inhibited Aurora kinase A and promoted the RIPK1/RIPK3/MLKL necrosome activation to inhibit the prostate cancer.

Effect of thermophilic bacterium HB27 manganese superoxide dismutase in a rat model of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).

We investigated the therapeutic effects of superoxide dismutase (SOD) from thermophilic bacterium HB27 on chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and its underlying mechanisms. A Sprague-Dawley rat model of CP/CPPS was prepared and then administered saline or Thermus thermophilic (Tt)-SOD intragastrically for 4 weeks. Prostate inflammation and fibrosis were analyzed by hematoxylin and eosin staining, and Masson staining. Alanine transaminase (ALT), aspartate transaminase (AST), serum creatinine (CR), and blood urea nitrogen (BUN) levels were assayed for all animals. Enzyme-linked immunosorbent assays (ELISA) were performed to analyze serum cytokine concentrations and tissue levels of malondialdehyde, nitric oxide, SOD, catalase, and glutathione peroxidase. Reactive oxygen species levels were detected using dichlorofluorescein diacetate. The messenger ribonucleic acid (mRNA) expression of tissue cytokines was analyzed by reverse transcription polymerase chain reaction (RT-PCR), and infiltrating inflammatory cells were examined using immunohistochemistry. Nuclear factor-κB (NF-κB) P65, P38, and inhibitor of nuclear factor-κBα (I-κBα) protein levels were determined using western blot. Tt-SOD significantly improved histopathological changes in CP/CPPS, reduced inflammatory cell infiltration and fibrosis, increased pain threshold, and reduced the prostate index. Tt-SOD treatment showed no significant effect on ALT, AST, CR, or BUN levels. Furthermore, Tt-SOD reduced inflammatory cytokine expression in prostate tissue and increased antioxidant capacity. This anti-inflammatory activity correlated with decreases in the abundance of cluster of differentiation 3 (CD3), cluster of differentiation 45 (CD45), and macrophage inflammatory protein 1α (MIP1α) cells. Tt-SOD alleviated inflammation and oxidative stress by reducing NF-κB P65 and P38 protein levels and increasing I-κBα protein levels. These findings support Tt-SOD as a potential drug for CP/CPPS.

The protective effect of manganese superoxide dismutase from thermophilic bacterium HB27 on hydrochloric acid-induced chemical cystitis in rats.

PURPOSE: To evaluate the effects of manganese superoxide dismutase (Mn-SOD) from thermophilic bacterium HB27 (name as Tt-SOD) on chemical cystitis. METHODS: Control and experimental rats were infused by intravesical saline or hydrochloric acid (HCl) on the first day of the experiments. Saline, sodium hyaluronate (SH) or Tt-SOD were infused intravesically once a day for three consequent days. On the fifth day, the rats were weighted and sacrificed following a pain threshold test. The bladder was harvested for histological and biochemical analyses. RESULTS: Tt-SOD could reduce the bladder index, infiltration of inflammatory cells in tissues, serum inflammatory factors and SOD levels, mRNA expression of inflammatory factors in tissues, and increase perineal mechanical pain threshold and serum MDA and ROS levels in HCl-induced chemical cystitis. Furthermore, Tt-SOD alleviated inflammation and oxidative stress by the negative regulation of the NF-κB p65 and p38 MAPK signaling pathway. CONCLUSIONS: Intravesical instillation of Tt-SOD provides protective effects against HCl-induced cystitis.

Changing Antimicrobial Resistance and Epidemiology of Non-Typhoidal Salmonella Infection in Taiwanese Children.

Non-typhoidal Salmonella (NTS) typically causes self-limiting diarrheal disease but may occasionally lead to invasive infection. This study investigated the epidemiology and antimicrobial resistance of children with NTS infection between 2012 and 2019. We retrospectively analyzed pediatric patients with NTS infections, confirmed by positive cultures, in a tertiary medical center in Taiwan in 2012 and 2019. Clinical features and laboratory data of the patients were collected. Changes in the serogroup category and antimicrobial resistance were also analyzed. Of the total 797 isolates collected, 55 had NTS bacteremia. Compared with the resistance rates in 2012, the rates of resistances to third-generation cephalosporin and ciprofloxacin were significantly higher in 2019 (4.1% vs 14.3%, P < 0.001; 1.9% vs 28.6%, P < 0.001), especially in groups B, D, and E. Moreover, we observed significantly higher antimicrobial resistance (25.3%) to third-generation cephalosporin, and approximately half the NTS isolates in the infant group were multidrug resistant - a higher rate than those of other age groups in 2019. Invasive NTS often presented with a longer fever duration, lower hemoglobin level and with no elevated C-reactive protein (P < 0.05). Non-invasive NTS isolates in 2019 were significantly more resistant to ceftriaxone (P < 0.001) and ciprofloxacin (P < 0.001) than those in 2012. The antimicrobial resistance of NTS in children has increased progressively in the past decade, and different serogroups exhibited different resistance patterns. During this period, infants showed the highest risk to get a third-generation cephalosporin-resistant NTS infection. The high rates of antimicrobial resistance among children with NTS in Taiwan merit continual surveillance.

Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells.

Melanoma is a common type of cutaneous tumor, but current drug treatments do not satisfy clinical practice requirements. At present, mitochondrial uncoupling is an effective antitumor treatment. Triclosan, a common antimicrobial, also acts as a mitochondrial uncoupler. The aims of the present study were to investigate the effects of triclosan on melanoma cells and the underlying mechanisms. Mitochondrial membrane potential (MMP), mitochondrial morphology, mitochondrial reactive oxygen species (mito-ROS), intracellular superoxide anion and [Ca2+]i were measured using confocal microscopy. It was found that triclosan application was associated with decreased A375 cell viability in a dose- and time-dependent manner and these effects may have cell specificity. Furthermore, triclosan induced MMP depolarization, ATP content decrease, mito-ROS and [Ca2+]i level increases, excessive mitochondrial fission, AMP-activated protein kinase (AMPK) activation and STAT3 inhibition. Moreover, these aforementioned effects were reversed by acetylcysteine treatment. Triclosan acute treatment also induced mitochondrial swelling, which was reversed after AMPK-knockdown associated with [Ca2+]i overload. Cell death was caused by STAT3 inhibition but not AMPK activation. Moreover, triclosan induced autophagy via the ROS/AMPK/p62/microtubule-associated protein 1A/1B-light chain 3 (LC3) signaling pathway, which may serve a role in feedback protection. Collectively, the present results suggested that triclosan increased mito-ROS production in melanoma cells, following induced cell death via the STAT3/Bcl-2 pathway and autophagy via the AMPK/p62/LC3 pathway.

MKP-1 overexpression is associated with chemoresistance in bladder cancer via the MAPK pathway.

Mitogen activated protein kinase phosphatase-1 (MKP-1) has been revealed to be overexpressed in bladder cancer, particularly in non-muscle invasive bladder cancer. MKP-1 may also be associated with chemotherapy resistance. However, the underlying mechanism is yet to be elucidated. The current study investigated the expression of MKP-1 by performing immunohistochemistry in surgically resected specimens obtained from primary and recurrent patients with bladder cancer. The results revealed that MKP-1 expression increased in recurrent patients. Additionally, a 3D model of the human bladder cancer cell line, RT112, was established to determine the role of MKP-1 in drug resistance. The results demonstrated that MKP-1 overexpression protected bladder cancer cells against cell death. Contrarily, MKP-1 knockdown was revealed to sensitize cells to death. In addition, the application of MAPK inhibitors effectively increased RT112 cell sensitivity to pirarubicin. In conclusion, the results of the current study indicated that MKP-1 treatment resulted in bladder cancer cell chemoresistance via JNK, ERK and p38 pathways. MKP-1 may also serve as a potential therapeutic target for chemoresistance in patients with bladder cancer.