Orally Ingested Self-Powered Stimulators for Targeted Gut-Brain Axis Electrostimulation to Treat Obesity and Metabolic Disorders.

Obesity is a significant health concern that often leads to metabolic dysfunction and chronic diseases. This study introduces a novel approach to combat obesity using orally ingested self-powered electrostimulators. These electrostimulators consist of piezoelectric BaTiO3 (BTO) particles conjugated with capsaicin (Cap) and aim to activate the vagus nerve. Upon ingestion by diet-induced obese (DIO) mice, the BTO@Cap particles specifically target and bind to Cap-sensitive sensory nerve endings in the gastric mucosa. In response to stomach peristalsis, these particles generate electrical signals. The signals travel via the gut-brain axis, ultimately influencing the hypothalamus. By enhancing satiety signals in the brain, this neuromodulatory intervention reduces food intake, promotes energy metabolism, and demonstrates minimal toxicity. Over a 3-week period of daily treatments, DIO mice treated with BTO@Cap particles show a significant reduction in body weight compared to control mice, while maintaining their general locomotor activity. Furthermore, this BTO@Cap particle-based treatment mitigates various metabolic alterations associated with obesity. Importantly, this noninvasive and easy-to-administer intervention holds potential for addressing other intracerebral neurological diseases.

Novel chromium (III)-based compound for inhibition of oxaliplatin-resistant colorectal cancer progression.

Colorectal cancer (CRC) ranks as the third leading cause of cancer-related mortality worldwide. The current standard of care includes systemic chemotherapy with cytotoxic agents, offering palliative relief for severe CRC cases and serving as the primary therapy for metastatic recurrence. However, the development of chemoresistance poses a substantial obstacle in the realm of chemotherapy. This study delved into the potential of a novel chromium (III)-based compound, hexaacetotetraaquadihydroxochromium (III) diiron (III) nitrate, for CRC treatment. The therapeutic promise of this innovative chromium (III)-based compound was explored by utilizing LoVo colon cancer cells and an in-vivo mouse model of CRC. Various dosages of the compound were administered to LoVo parental cells and LoVo oxaliplatin-resistant cells. Findings unveiled that a concentration of 2000 µg/mL of the chromium (III) compound significantly inhibited mesenchymal transition and the migratory and invasive properties of LoVo oxaliplatin-resistant cells. This novel chromium (III)-based compound also demonstrated similar efficacy in other different CRC cell lines. The tumor growth was in the in-vivo mouse model was reduced by this compound. Moreover, the chromium (III)-based compound induced apoptosis by triggering the endoplasmic reticulum (ER) stress pathway in LoVo oxaliplatin-resistant cells. This study illuminates the capacity of the novel chromium (III)-based compound to impede the progression and growth of chemotherapy-resistant CRC. This discovery instills confidence in the potential of this compound as a therapeutic agent for CRC, even in the face of drug resistance. It holds the promise of serving as a valuable asset in the future treatment of chemotherapy-resistant CRC.

A prospective review of the health-promoting potential of Jing Si Herbal Tea.

Traditional Chinese medicine (TCM) has gained considerable attention over the past few years for its multicomponent, multitarget, and multi-pathway approach to treating different diseases. Studies have shown that TCMs as adjuvant therapy along with conventional treatment may benefit in safely treating various disorders. However, investigations on finding effective herbal combinations are ongoing. A novel TCM formula, "Jing Si Herbal Tea (JSHT)," has been reported recently for their health-promoting effects in improving overall body and mental health. JSHT is a combination of eight herbs recognized in Chinese herbal pharmacopoeia for their anti-viral, anti-aging, and anti-cancer properties as well as protective effects against cardiovascular, metabolic, neural, digestive, and genitourinary diseases. Thus, to better understand the beneficial effects of the ingredients of JSHT on health, this review intends to summarize the preclinical and clinical studies of the ingredients of JSHT on human health and diseases, and possible therapeutic effects with the related mode of actions and future prospects for their application in complementary therapies.

Immunomodulatory Prodrug Micelles Imitate Mild Heat Effects to Reshape Tumor Microenvironment for Enhanced Cancer Immunotherapy.

Physical stimulation with mild heat possesses the notable ability to induce immunomodulation within the tumor microenvironment (TME). It transforms the immunosuppressive TME into an immune-active state, making tumors more receptive to immune checkpoint inhibitor (ICI) therapy. Transient receptor potential vanilloid 1 (TRPV1), which can be activated by mild heat, holds the potential to induce these alterations in the TME. However, achieving precise temperature control within tumors while protecting neighboring tissues remains a significant challenge when using external heat sources. Taking inspiration from the heat sensation elicited by capsaicin-containing products activating TRPV1, this study employs capsaicin to chemically stimulate TRPV1, imitating immunomodulatory benefits akin to those induced by mild heat. This involves developing a glutathione (GSH)-responsive immunomodulatory prodrug micelle system to deliver capsaicin and an ICI (BMS202) concurrently. Following intravenous administration, the prodrug micelles accumulate at the tumor site through the enhanced permeability and retention effect. Within the GSH-rich TME, the micelles disintegrate and release capsaicin and BMS202. The released capsaicin activates TRPV1 expressed in the TME, enhancing programmed death ligand 1 expression on tumor cell surfaces and promoting T cell recruitment into the TME, rendering it more immunologically active. Meanwhile, the liberated BMS202 blocks immune checkpoints on tumor cells and T cells, activating the recruited T cells and ultimately eradicating the tumors. This innovative strategy represents a comprehensive approach to fine-tune the TME, significantly amplifying the effectiveness of cancer immunotherapy by exploiting the TRPV1 pathway and enabling in situ control of immunomodulation within the TME.

Associations between paraben exposure, thyroid capacity, homeostasis and pituitary thyrotropic function in the general Taiwanese: Taiwan Environmental Survey for Toxicants (TEST) 2013.

Several studies have suggested that some endocrine disruptors such as synthetic phenols, parabens and phthalates may disrupt thyroid hormone signaling and associated negative feed-backs with the central hypothalamic-pituitary-thyroid (HPT) axis. Therefore, we investigated urinary paraben and blood thyroid hormone levels in the Taiwanese population. Our sample comprised 264 adults (aged 18-97 years) and 75 minors (aged 7-17 years) from Taiwan Environmental Survey for Toxicants 2013. Urinary levels of methylparaben (MeP), ethylparaben (EtP), propylparaben (PrP), and butylparaben (BuP) were assessed. Hormones of particular interest include: thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4). We sought integrated parameters to describe the transfer of thyroid hormones in homeostatic models. The geometric mean urinary paraben levels of the adults were higher than those of the minors (adults vs. minors; MeP: 383 vs. 62.4 ng/mL; PrP: 109 vs. 8.00 ng/mL; EtP: 39.5 vs. 2.38 ng/mL, and BuP: 6.36 vs. 2.13 ng/mL). In the male adults, we discovered that 0.253% (p = 0.032), 0.256% (p = 0.041) and 0.257% (p = 0.037) decreases in the TSH, TSH/T4 and TSH/FreeT4 ratio was associated with 1% EtP increases, respectively. In the female minors, 0.093% (p = 0.044), 0.072% (p = 0.047) and 0.156 (p = 0.004) increases in the TSH ratios were associated with a 1% MeP, EtP and BuP increase, respectively. Moreover, 0.151% (p = 0.008) and 0.177% (p = 0.001) increases in TSH/T4 and TSH/free T4 ratios were associated with a BuP 1% increase, respectively. Finally, EtP was positively associated with SPINA-GT (ß: 15.66, p = 0.036) in the male adults. By contrast, EtP were positively associated with Jostel's TSH index and sTSHI (ß: 0.072, p = 0.049; ß: 0.107, p = 0.049) in the female minors. The Taiwanese population is commonly exposed to parabens, which can potentially lead to alteration of thyroid hormone homeostasis.

Development and evaluation of a novel chromium III-based compound for potential inhibition of emerging SARS-CoV-2 variants.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused 403 million cases of coronavirus disease (COVID-19) and resulted in more than 5.7 million deaths worldwide. Extensive research has identified several potential drug treatments for COVID-19. However, the development of new compounds or therapies is necessary to prevent the emergence of drug resistance in SARS-CoV-2. In this study, a novel compound based on hexaacetotetraaquadihydroxochromium(III)diiron(III) nitrate, which contains small amounts of chromium (III), was synthesised and evaluated for its effectiveness against multiple variants of COVID-19 using both in vitro and in vivo models. This innovative compound demonstrated interference with the interaction between the spike protein of SARS-CoV-2 and angiotensin-converting enzyme 2 (ACE2). Furthermore, in vitro experiments showed that this compound downregulated the expression of ACE2 and transmembrane serine protease 2 (TMPRSS2). It also exhibited a reduction in the activity of 3-chymotrypsin-like protease (3CL) and RNA-dependent RNA polymerase (RdRp). Pretreatment with this small chromium (III)-based compound resulted in reduced ACE2-rich cell infection by various variants of SARS-CoV-2 spike protein-pseudotyped lentivirus. Finally, the compound effectively inhibited viral infection by multiple variants of SARS-CoV-2 spike protein-pseudotyped lentivirus in both the abdominal and thoracic regions of mice. In conclusion, this compound lowers the likelihood of SARS-CoV-2 entry into cells, inhibits viral maturation and replication in vitro, and reduces infection levels of multiple variants of SARS-CoV-2 spike protein-pseudotyped lentivirus in the abdomen and thorax following pretreatment. Small chromium (III)-based compounds have the potential to restrict the progression of SARS-CoV-2 infections.

Gemcitabine resistance in non-small cell lung cancer is mediated through activation of the PI3K/AKT/NF-κB pathway and suppression of ERK signaling by reactive oxygen species.

Lung cancer is one of the most common cancers in the world. Chemotherapy is a standard clinical treatment. However, tumor cells often develop multidrug resistance after chemotherapy, an inevitable bottleneck in cancer treatment. Therefore, this study used gemcitabine-resistant (GEM-R) CL1-0 lung cancer cells. First, we used flow cytometry and western blot analysis to examine differences in performance between resistant and parental cells. The results showed that compared with parental cells, GEM-R CL1-0 cells significantly enhanced the activation of the AKT pathway, which promoted survival and growth, and decreased the activation of the reactive oxygen species-extracellular signal-regulated kinase (ROS)-ERK pathway. Next, the AKT and ERK pathways' role in tumor growth was further explored in vivo using a xenograft model. The results showed that enhancing AKT and inhibiting ERK activation reduced GEM-induced inhibition of tumor growth. Finally, combining the above results, we found that GEM-R CL1-0 cells showed reduced sensitivity to GEM by activating the phosphatidylinositol 3-kinase/AKT/NF-kB pathway and inhibiting the ROS-ERK pathway leading to resistance against GEM. Therefore, the AKT and ERK pathways are potential targets for improving the sensitivity of cancer cells to anticancer drugs.

A low-energy emulsification platform based on a Diet Coke-Mentos reaction-derived bubbly flow for formulating various emulsions as drug carriers.

The formulation of a drug using high-energy emulsification commonly causes drug deterioration. Exploiting the well-known Diet Coke-Mentos reaction (DCMR), a U-shaped tube reactor that can generate an eruption of bubbly flow that can serve as a low-energy emulsification platform, is proposed. The liquid in the U-tube reactor is a supersaturated solution of aqueous CO2, which mimics Diet Coke. When glass beads with rough surfaces, mimicking Mentos, are dropped into the carbonated water, an eruptive bubbly flow is spontaneously created, mediating effective emulsification at a compound water-oil interface. Experimental results demonstrate that DCMR-mediated bubbly flow may provide a versatile platform for the production of "oil-in-water" or "water-in-oil" droplets and Pickering emulsion composite particles as drug carriers. The DCMR-derived bubbly flow is generated without significant temperature elevation, so the activity of the drug to be emulsified is unaffected. In vivo results reveal the feasibility of using this low-energy emulsification platform to formulate an emulsion system that contains catalase, a temperature-sensitive oxidoreductase, to mitigate an experimentally formed paw inflammation in mice. The as-proposed emulsification platform is attractive for formulating numerous drug delivery systems on a small-scale in a customized manner to meet the needs of each individual for personalized medicine.

Macrophage-Hitchhiked Orally Administered ß-Glucans-Functionalized Nanoparticles as "Precision-Guided Stealth Missiles" for Targeted Pancreatic Cancer Therapy.

The prognosis in cases of pancreatic ductal adenocarcinoma (PDAC) with current treatment modalities is poor owing to the highly desmoplastic tumor microenvironment (TME). Herein, a ß-glucans-functionalized zinc-doxorubicin nanoparticle system (ßGlus-ZnD NPs) that can be orally administered, is developed for targeted PDAC therapy. Following oral administration in PDAC-bearing mice, ßGlus-ZnD NPs actively target/transpass microfold cells, overcome the intestinal epithelial barrier, and then undergo subsequent phagocytosis by endogenous macrophages (ßGlus-ZnD@Mϕ). As hitchhiking cellular vehicles, ßGlus-ZnD@Mϕ transits through the intestinal lymphatic system and enters systemic circulation, ultimately accumulating in the tumor tissue as a result of the tumor-homing and "stealth" properties that are conferred by endogenous Mϕ. Meanwhile, the Mϕ that hitchhikes ßGlus-ZnD NPs is activated to produce matrix metalloproteinases, destroying the desmoplastic stromal barrier, and differentiates toward the M1 -like phenotype, modulating the TME and recruiting effector T cells, ultimately inducing apoptosis of the tumor cells. The combination of ßGlus-ZnD@Mϕ and immune checkpoint blockade effectively inhibits the growth of the primary tumor and suppresses the development of metastasis. It thus represents an appealing approach to targeted PDAC therapy.

Protective effects of Scoparia dulcis L. extract on high glucose-induced injury in human retinal pigment epithelial cells.

Diabetic retinopathy (DR) is a major cause of vision loss in diabetic patients. Hyperglycemia-induced oxidative stress and the accumulation of inflammatory factors result in blood-retinal barrier dysfunction and the pathogenesis of DR. Scoparia dulcis L. extract (SDE), a traditional Chinese medicine, has been recently recognized for its various pharmacological effects, including anti-diabetic, anti-hyperlipidemia, anti-inflammatory, and anti-oxidative activities. However, there is no relevant research on the protective effect of SDE in DR. In this study, we treated high glucose (50 mM) in human retinal epithelial cells (ARPE-19) with different concentrations of SDE and analyzed cell viability, apoptosis, and ROS production. Moreover, we analyzed the expression of Akt, Nrf2, catalase, and HO-1, which showed that SDE dose-dependently reduced ROS production and attenuated ARPE-19 cell apoptosis in a high-glucose environment. Briefly, we demonstrated that SDE exhibited an anti-oxidative and anti-inflammatory ability in protecting retinal cells from high-glucose (HG) treatment. Moreover, we also investigated the involvement of the Akt/Nrf2/HO-1 pathway in SDE-mediated protective effects. The results suggest SDE as a nutritional supplement that could benefit patients with DR.

Magnetic anaerobic granular sludge for sequestration and immobilization of Pb.

The development of magnetic adsorbents with high capacity to capture heavy metals has been the subject of intense research, but the process usually involves costive synthesis steps. Here, we propose a green approach to obtaining a magnetic biohybrid through in situ grown anaerobic granular sludge (AGS) with the help of magnetite, constituting a promising adsorbent for sequestration and immobilization of Pb in aqueous solutions and soils. The resultant magnetite-embedded AGS (M-AGS) was not only capable of promoting methane production but also conducive to Pb adsorption because of the large surface area and abundant function groups. The uptake of Pb on M-AGS followed the pseudo-second order, having a maximum adsorption capacity of 197.8 mg gDS-1 at pH 5.0, larger than 159.7, 170.3, and 178.1 mg gDS-1 in relation to AGS, F-AGS (ferrihydrite-mediated), and H-AGS (hematite-mediated), respectively. Mechanistic investigations showed that Pb binding to M-AGS proceeds via surface complexation, mineral precipitation, and lattice replacement, which promotes heavy metal capture and stabilization. This was evident from the increased proportion of structural Pb sequestrated from the aqueous solution and the enhanced percentage of the residual fraction of Pb extracted from the contaminated soils.

Phosphorylation of Bcl-2 by JNK confers gemcitabine resistance in lung cancer cells by reducing autophagy-mediated cell death.

The most common cancer-related death in the world is non-small cell lung cancer (NSCLC). Gemcitabine (GEM) is a common and effective first-line chemotherapeutic drug for the treatment of NSCLC. However, the long-term use of chemotherapeutic drugs in patients usually induces cancer cell drug resistance, leading to poor survival, and prognosis. In this study, to observe and explore the key targets and potential mechanisms of NSCLC resistance to GEM, we first cultured lung cancer CL1-0 cells in a GEM-containing medium to induce CL1-0 cells to develop GEM resistance. Next, we compared protein expression between the parental and GEM-R CL1-0 cell groups. We observed significantly lower expression of autophagy-related proteins in GEM-R CL1-0 cells than in parental CL1-0 cells, indicating that autophagy is associated with GEM resistance in CL1-0 cells. Furthermore, a series of autophagy experiments revealed that GEM-R CL1-0 cells had significantly reduced GEM-induced c-Jun N-terminal kinase phosphorylation, which further affected the phosphorylation of Bcl-2, thereby reducing the dissociation of Bcl-2 and Beclin-1 and ultimately reducing the generation of GEM-induced autophagy-dependent cell death. Our findings suggest that altering the expression of autophagy is a promising therapeutic option for drug-resistant lung cancer.

Recuperative herbal formula Jing Si maintains vasculature permeability balance, regulates inflammation and assuages concomitants of "Long-Covid".

Coronavirus disease 2019 (COVID-19) is a worldwide health threat that has long-term effects on the patients and there is currently no efficient cure prescribed for the treatment and the prolonging effects. Traditional Chinese medicines (TCMs) have been reported to exert therapeutic effect against COVID-19. In this study, the therapeutic effects of Jing Si herbal tea (JSHT) against COVID-19 infection and associated long-term effects were evaluated in different in vitro and in vivo models. The anti-inflammatory effects of JSHT were studied in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and in Omicron pseudotyped virus-induced acute lung injury model. The effect of JSHT on cellular stress was determined in HK-2 proximal tubular cells and H9c2 cardiomyoblasts. The therapeutic benefits of JSHT on anhedonia and depression symptoms associated with long COVID were evaluated in mice models for unpredictable chronic mild stress (UCMS). JSHT inhibited the NF-ƙB activities, and significantly reduced LPS-induced expression of TNFα, COX-2, NLRP3 inflammasome, and HMGB1. JSHT was also found to significantly suppress the production of NO by reducing iNOS expression in LPS-stimulated RAW 264.7 cells. Further, the protective effects of JSHT on lung tissue were confirmed based on mitigation of lung injury, repression in TMRRSS2 and HMGB-1 expression and reduction of cytokine storm in the Omicron pseudotyped virus-induced acute lung injury model. JSHT treatment in UCMS models also relieved chronic stress and combated depression symptoms. The results therefore show that JSHT attenuates the cytokine storm by repressing NF-κB cascades and provides the protective functions against symptoms associated with long COVID-19 infection.

Nanocontroller-mediated dissolving hydrogel that can sustainably release cold-mimetic menthol to induce adipocyte browning for treating obesity and its related metabolic disorders.

Obesity leads to the development of many metabolic diseases, causing severe health problems. Menthol can induce adipocyte browning and thus has been used to combat obesity. To deliver menthol with a sustained effect, an injectable hydrogel that comprises carboxymethyl chitosan and aldehyde-functionalized alginate that are crosslinked through dynamic Schiff-base linkages is developed to load menthol-cyclodextrin inclusion complexes (IC). To render the as-developed hydrogel soluble after its payload is released, amino acid-loaded liposomes, functioning as nanocontrollers, are covalently grafted onto networks of the hydrogel. Upon subcutaneous injection in mice with diet-induced obesity, the as-developed hydrogel absorbs body fluids and spontaneously swells, expanding and stretching its networks, gradually releasing the loaded IC. Menthol then disassociates from the released IC to induce adipocyte browning, triggering fat consumption and increasing energy expenditure. Meanwhile, the expanded hydrogel networks destabilize the grafted liposomes, which function as built-in nanocontrollers, unleashing their loaded amino acid molecules to disrupt the dynamic Schiff-base linkages, causing hydrogel to dissolve. The thus-developed nanocontroller-mediated dissolving hydrogel realizes the sustained release of menthol for treating obesity and its related metabolic disorders without leaving exogenous hydrogel materials inside the body, and thereby preventing any undesired adverse effects.

Lymphocytopenia and survival after whole-brain radiotherapy in patients with small-cell lung cancer.

BACKGROUND: To investigate whether whole-brain radiotherapy (WBRT) decreases lymphocyte counts and evaluate the impact of treatment-related lymphopenia on survival in patients with brain metastasis. METHODS: Medical records from 60 small-cell lung cancer patients treated with WBRT from January 2010 to December 2018 were included in the study. Total lymphocyte count (TLC) was obtained pre and post treatment (within 1 month). We performed linear and logistic regression analyses to identify predictors of lymphopenia. The association between lymphopenia and survival was analyzed using Cox regression analysis. RESULTS: Thirty-nine patients (65%) developed treatment-related lymphopenia. The median TLC decrease was -374 cells/µL (interquartile range -50 to -722, p < 0.001). Baseline lymphocyte count was a significant predictor of TLC difference and percentage change in TLC. Logistic regression analysis found male sex (odds ratio [OR] 0.11, 95% confidence interval [CI] 0.00-0.79, p = 0.033) and higher baseline lymphocyte count (OR 0.91, 95% CI 0.82-0.99, p = 0.005) were associated with a lower risk of developing ≥grade 2 treatment-related lymphopenia. Cox regression analysis showed that age at brain metastasis (hazard ratio [HR] 1.03, 95% CI 1.01-1.05, p = 0.013), ≥grade 2 treatment-related lymphopenia, and percentage change in TLC (per 10%, HR 0.94, 95% CI 0.89-0.99, p = 0.032) were prognostic factors of survival. CONCLUSIONS: WBRT decreases TLC and the magnitude of treatment-related lymphopenia is an independent predictor of survival in small-cell lung cancer patients.

Ginkgolide A improves the pleiotropic function and reinforces the neuroprotective effects by mesenchymal stem cell-derived exosomes in 6-OHDA-induced cell model of Parkinson's disease.

Parkinson's disease (PD) is a common disorder attributed to the loss of midbrain dopamine (mDA) neurons and reduced dopamine secretion. Currently, the treatment regimes for PD comprise deep brain stimulations, however, it attenuates the PD progression marginally and does not improve neuronal cell death. We investigated the function of Ginkgolide A (GA) to reinforce Wharton's Jelly-derived mesenchymal stem cells (WJMSCs) for treating the in vitro model of PD. GA enhanced the self-renewal, proliferation, and cell homing function of WJMSCs as assessed by MTT and transwell co-culture assay with a neuroblastoma cell line. GA pre-treated WJMSCs can restore 6-hydroxydopamine (6-OHDA)-induced cell death in a co-culture assay. Furthermore, exosomes isolated from GA pre-treated WJMSCs significantly rescued 6-OHDA-induced cell death as determined by MTT assay, flow cytometry, and TUNEL assay. Western blotting showed that apoptosis-related proteins were decreased following GA-WJMSCs exosomal treatment which further improved mitochondrial dysfunction. We further demonstrated that exosomes isolated from GA-WJMSCs could restore autophagy using immunofluorescence staining and immunoblotting assay. Finally, we used the alpha-synuclein recombinant protein and found that exosomes derived from GA-WJMSCs led to the reduced aggregation of alpha-synuclein compared to that in control. Our results suggested that GA could be a potential candidate for strengthening stem cell and exosome therapy for PD.

A coupled electrochemical process for schwertmannite recovery from acid mine drainage: Important roles of anodic reactive oxygen species and cathodic alkaline.

The increasing need for sustainable acid mine drainage (AMD) treatment has spurred much attention to strategic development of resource recovery. Along this line, we envisage that a coupled electrochemical system involving anodic Fe(II) oxidation and cathodic alkaline production will facilitate in situ synthesis of schwertmannite from AMD. Multiple physicochemical studies showed the successful formation of electrochemistry-induced schwertmannite, with its surface structure and chemical composition closely related to the applied current. A low current (e.g., 50 mA) led to the formation of schwertmannite having a small specific surface area (SSA) of 122.8 m2 g-1 and containing small amounts of -OH groups (formula Fe8O8(OH)4.49(SO4)1.76), whereas a large current (e.g., 200 mA) led to schwertmannite high in SSA (169.5 m2 g-1) and amounts of -OH groups (formula Fe8O8(OH)5.16(SO4)1.42). Mechanistic studies revealed that the reactive oxygen species (ROS)-mediated pathway, rather than the direct oxidation pathway, plays a dominant role in accelerating Fe(II) oxidation, especially at high currents. The abundance of •OH in the bulk solution, along with the cathodic production of OH-, were the key to obtaining schwertmannite with desirable properties. It was also found to function as a powerful sorbent in removal of arsenic species from the aqueous phase.

In Situ Reconstruction of Metal Oxide Cathodes for Ammonium Generation from High-Strength Nitrate Wastewater: Elucidating the Role of the Substrate in the Performance of Co3O4-x.

In situ electrochemical reconstruction is important for transition metal oxides explored as electrocatalysts for electrochemical nitrate reduction reactions (ENRRs). Herein, we report substantial performance enhancement of ammonium generation on Co, Fe, Ni, Cu, Ti, and W oxide-based cathodes upon reconstruction. Among them, the performance of a freestanding ER-Co3O4-x/CF (Co3O4 grown on Co foil subjected to electrochemical reduction) cathode was superior to its unreconstructed counterpart and other cathodes; e.g., an ammonium yield of 0.46 mmol h-1 cm-2, an ammonium selectivity of 100%, and a Faradaic efficiency of 99.9% were attained at -1.3 V in a 1400 mg L-1 NO3--N solution. The reconstruction behaviors were found to vary with the underlying substrate. The inert carbon cloth only acted as a supporting matrix for immobilizing Co3O4, without appreciable electronic interactions between them. A combination of physicochemical characterizations and theoretical modeling provided compelling evidence that the CF-promoted self-reconstruction of Co3O4 induced the evolution of metallic Co and the creation of oxygen vacancies, which promoted and optimized interfacial nitrate adsorption and water dissociation, thus boosting the ENRR performance. The ER-Co3O4-x/CF cathode performed well over wide ranges of pH and applied current and at high nitrate loadings, ensuring its high efficacy in treating high-strength real wastewater.

Photoinduced transformation of ferrihydrite in the presence of aqueous sulfite and its influence on the repartitioning of Cd.

The photoinduced transformation of ferrihydrite is an important process that can predict the geochemical cycle of Fe in anoxic environments as well as the fate of trace elements bonded to Fe minerals. We report that the photooxidation of sulfite by UV irradiation produces hydrated electrons (super-reductants), which significantly promote ferrihydrite reduction to Fe(II), and SO3•- (a moderate oxidant), enabling its further oxidation to more crystalline Fe(III) products. The experimental results show that the concentration of sulfite was key in influencing the rate and extent of surface-bound Fe(II) formation, which ultimately determined the distribution of individual products. For example, fitting of the Mössbauer spectroscopy data revealed that the relative abundances of mineral species after 8 h of treatment in the UV/sulfite systems were 41.9% lepidocrocite and 58.1% ferrihydrite at 2 mM SO32-; 41.8% goethite, 28.2% lepidocrocite, and 29.1% ferrihydrite at 5 mM SO32-; and 100% goethite at 10 mM SO32-. The combined results of the chemical speciation analysis and the Cd K-edge EXAFS characterization provided compelling evidence that Cd was firmly incorporated into the structure of newly formed minerals, particularly at high sulfite concentrations. These findings provide an understanding of the role of UV/sulfite in facilitating ferrihydrite transformation and promoting Cd stabilization in oxygen-deficit soils and aquatic environments.

Cryptotanshinone protects against oxidative stress in the paraquat-induced Parkinson's disease model.

Parkinson's disease (PD) is a common neurodegenerative disorder associated with striatal dopaminergic neuronal loss in the Substantia nigra. Oxidative stress plays a significant role in several neurodegenerative diseases. Paraquat (PQ) is considered a potential neurotoxin that affects the brain leading to the death of dopaminergic neurons mimicking the PD phenotype. Various scientific reports have proven that cryptotanshinone possesses antioxidant and anti-inflammatory properties. We hypothesized that cryptotanshinone could extend its neuroprotective activity by exerting antioxidant effects. This study was designed to evaluate the effects of cryptotanshinone in both cellular and animal models of PQ-induced PD. Annexin V-PI double staining and immunoblotting were used to detect apoptosis and oxidative stress proteins, respectively. Reactive oxygen species kits were used to evaluate oxidative stress in cells. For in vivo studies, 18 B6 mice were divided into three groups. The rotarod data revealed the motor function and immunostaining showed the survival of TH+ neurons in SNpc region. Our study showed that cryptotanshinone attenuated paraquat-induced oxidative stress by upregulating anti-oxidant markers in vitro, and restored behavioral deficits and survival of dopaminergic neurons in vivo, demonstrating its therapeutic potential.