Effects of Methyl Sulfonyl Methane and Selenium Yeast on Fatty Liver Syndrome in Laying Hens and Their Biological Mechanisms.

The purpose of this study was to explore the effects of MSM and Se-Y on FLS in laying hens during the late peak laying period and the underlying biological mechanisms. Therefore 240 55-week-old Jing-fen No. 6 laying hens were randomly divided into five groups, with eight replicates in each group and six laying hens in each replicate. The hens were fed a basal diet (Control) and diets supplemented with 350 and 700 mg/kg MSM and 25 and 50 mg/kg Se-Y, respectively, for four weeks. The results showed that MSM and Se-Y had no significant effects on the performance of laying hens. With the increasing dosage of MSM and Se-Y, the symptoms of liver steatosis in laying hens were reduced, and MSM and Se-Y could significantly reduce the content of malondialdehyde (MDA) in serum and liver (p < 0.05) and increase the contents of total superoxide dismutase (T-SOD) and glutathione peroxidase (GPX) in serum and liver (p < 0.05). The RNA-seq results showed that 700 mg/kg MSM significantly downregulated the expression levels of the ATP5I, ATP5G1, CYCS, and UQCRQ genes in the liver, and 50 mg/kg Se-Y significantly downregulated the expression levels of MAPK10, SRC, BMP2, and FGF9 genes in the liver. In conclusion, dietary supplementation with MSM and Se-Y can effectively reduce the FLS of laying hens in the late peak laying period and increase their antioxidant capacity. The underlying biological mechanism may be related to the downregulation of genes involved in liver oxidative phosphorylation and inflammation-related pathways.

Pinus massoniana needle extracts attenuate oxidative stress injury in cerebral ischemia reperfusion rats by regulating JNK3/caspase-3 signal transduction.

OBJECTIVE: To investigate the effect and mechanism of Pinus massoniana needle extracts (PNE) on oxidative stress injury in cerebral ischemia reperfusion rats. METHODS: The SD male rats were randomly divided into sham group, model control group, Edaravone (3 mg/kg) group, PNE low-dose (200 mg/kg), medium-dose (400 mg/kg) and high-dose (800 mg/kg) groups. PNE was administered by gavage for 7 d before modeling and 6 h after modeling in PNE treatment groups; Edaravone was given by intraperitoneal injection 7 d before modeling and 6 h after reperfusion. The rat model of cerebral ischemia reperfusion injury was established by middle cerebral artery occlusion method. After 24 h of reperfusion, the neurological deficit score, brain water content and cerebral infarction volume of rats were measured. The pathological changes of cerebral cortex and hippocampus were observed by HE staining, and the number of normal nerve cells was counted. The apoptosis rate of neurons in cerebral cortex was detected by TUNEL method. The content of nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) activity in ischemic brain tissue were detected. The protein expression of c-Jun N-terminal kinase (JNK) 3, phosphorylated JNK3 (p-JNK3), B-cell lymphoma protein(Bcl) -2, Bcl-2 associated X (Bax), cytochrome C and caspase-3 in cerebral cortex were detected by Western blotting method. RESULTS: Compared with the model control group, the behavioral score, brain water content and cerebral infarction volume in PNE groups were significantly reduced (all P<0.05), the pathological damage of cerebral cortex and hippocampal CA1 area was significantly alleviated, and the number of normal nerve cells in ischemic cortex and hippocampal CA1 area was increased (all P<0.05). The medium-dose PNE group had the best effect. Compared with the model control group, the apoptosis rate of cortical neurons, the content of NO and MDA in cerebral cortex, the ratio of p-JNK3/JNK3, the expression level of cytochrome C and caspase-3 protein in PNE medium-dose group were significantly reduced , and the activity of SOD, the Bcl-2/Bax ratio were significantly improved (all P<0.05). CONCLUSION: PNE ameliorates brain injury after cerebral ischemia reperfusion in rats, which may be related to scavenging NO and MDA, inhibiting oxidative stress-mediated JNK3/caspase-3 signsal transduction to inhibit neuronal apoptosis.

Rehmannioside A improves cognitive impairment and alleviates ferroptosis via activating PI3K/AKT/Nrf2 and SLC7A11/GPX4 signaling pathway after ischemia.

ETHNOPHARMACOLOGICAL RELEVANCE: Rehmannioside A is derived from Rehmannia glutinosa Libosch, which is widely used as an important ingredient in diverse traditional Chinese medicines to treat diseases caused by "kidney deficiency" such as cerebral arteriosclerosis, aging-related stroke and dementia in China. Recent studies have proved that Rehmannia glutinosa Libosch and Rehmannioside A can improve memory capability and recover nerve damage. AIM OF THE STUDY: To investigate the effect of Rehmannioside A on cognitive impairment after ischemia in rats and SH-SY5Y cells, and further evaluate the anti-oxidative and anti-ferroptosis mechanisms. MATERIALS AND METHODS: Differentially expressed proteins (DEPs) in patients after cerebral ischemic stroke were revealed by a RayBio protein array. Cognitive impairment model was established by middle cerebral artery occlusion and reperfusion (MCAO) 14 days in rats. Rehmannioside A was administered intraperitoneally injection at dose of 80 mg/kg. The SH-SY5Y cells were exposed to H2O2 for 24 h and treated with Rehmannioside A (80 µM) for 24 h. The neuroprotecion of Rehmannioside A were evaluated by infarct volume (TTC), neurological defects (Garcia score) and learning memory (Morris water maze test) in vivo, and cell viability (CCK-8 or LDH) in vitro. Superoxide dismutase (SOD), malondialdehyde (MDA) and myeloperoxidase (MPO) activity of rats, glutathione (GSH), oxidized glutathione (GSSG) and nicotinamide adenine dinucleotide phosphate (NADPH) of cells were detected by biochemical assay. Intracellular reactive oxygen species (ROS) were measured by DCFH-DA assay. Myeloperoxidase (MPO), PI3 kinase (PI3K), p-PI3K, Akt, p-Akt, heme oxygenase-1 (HO-1), nuclear factor-E2-related factor 2 (Nrf2), SLC7A11, glutathione peroxidase 4 (GPX4) of the cerebral cortex in rats or SH-SY5Y cells were examined by western blotting. RESULTS: Compared with model group, the cognitive impairment and neurological deficits of Rehmannioside A group were significantly improved, and the cerebral infarction was reduced in MCAO rats. Moreover, the cell viability obviously increased and the H2O2-induced toxicity was reduced in Rehmannioside A group. Further research indicated that the expression of p-PI3K, p-Akt, nuclear Nrf2, HO-1 and SLC7A11 in Rehmannioside A group was significantly higher than model group. CONCLUSION: Rehmannioside A has neuroprotection effect and improves cognitive impairment after cerebral ischemia by inhibiting ferroptosis and activating PI3K/AKT/Nrf2 and SLC7A11/GPX4 signaling pathway. These findings provide valuable insight into the pathogenesis and therapeutic target of ischemic stroke.

Source profiles, emission factors and associated contributions to secondary pollution of volatile organic compounds (VOCs) emitted from a local petroleum refinery in Shandong.

An in-depth study was conducted to quantify and characterize VOC emissions from a petroleum refinery located in Shandong, China. The VOC emission inventory established in this study showed that storage tanks were the largest emission source, accounting for 56.4% of total emissions, followed by loading operations, wastewater collection and treatment system, process vents, and equipment leaks. Meanwhile, the localization factors for refining, storage tanks and loading operations were calculated, which were 1.33, 0.75 and 0.31g VOCs/kg crude oil refined. Furthermore, the characteristics of fugitive and organized emissions were determined for various processes and emission sources using a gas chromatography-mass spectrometry/flame ionization detection (GC-MS/FID) system. Most samples contained mainly alkanes, but the total VOC concentrations and key species varied greatly among processes. The source profile of the refinery, synthesized using the weighted average method, indicated that cis-2-butene (14.5%), n-pentane (10.2%), n-butane (7.4%), isopentane (6.5%) and MTBE (5.9%) were the major species released by this refinery. Assessment of O3 and secondary organic aerosol formation potentials were completed, and the results indicated that cis-2-butene, m/p-xylene, toluene, n-pentane, isopentane, benzene, o-xylene and ethylbenzene were the active species for which treatment should be prioritized.

In vitro cultured calculus bovis attenuates cerebral ischaemia-reperfusion injury by inhibiting neuronal apoptosis and protecting mitochondrial function in rats.

ETHNOPHARMACOLOGICAL RELEVANCE: In vitro cultured calculus bovis (ICCB), which is produced based on the formation mechanism of bovine gallstones, is used to replace the natural bezoar. It has been used in the clinic to treat brain diseases, including stroke, Alzheimer's disease and depression. AIM OF STUDY: ICCB is used to treat encephalopathy in the clinic. We explored the effects of ICCB on cerebral ischaemia-reperfusion injury (CIRI) and the potential associated mechanisms. MATERIALS AND METHODS: Rats were subjected to middle cerebral artery occlusion for 90 min, followed by 24 h of reperfusion, after being given different concentrations of ICCB once a day for 3 days. Subsequently, the neurological scores, brain oedema and volume of cerebral infarction were measured, and the histopathological changes in the cortex neurons were observed by haematoxylin and eosin staining (H&E). Apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL). Ultrastructural changes in the mitochondria of the cortex were assessed by transmission electron microscopy (TEM). The apoptosis-related proteins Bax, Bcl-2, caspase-9, caspase-3, Mito-Cyt C and Cyto-Cyt C were detected by Western blotting. RESULTS: Compared with those in the control group, the neurological scores, the volumes of cerebral infarction, and the brain water contents were significantly decreased in the ICCB groups at doses of 50 and 100 mg/kg. The ICCB treatment effectively decreased the neuronal apoptosis resulting from the CIRI-induced neuron injury. In addition, the histopathological damage and the mitochondria ultrastructure injury were partially improved in the CIRI rats after ICCB treatment. Western blotting analysis indicated that ICCB significantly decreased the expression of Bax, caspase-9, caspase-3 and Cyto-Cyt C protein levels while increasing the expression of Bcl-2 and Mito-Cyt C protein levels. CONCLUSION: The ICCB protected against CIRI by suppressing the mitochondria-mediated apoptotic signalling pathway.

Prospects for improving cosmological parameter estimation with gravitational-wave standard sirens from Taiji.

Taiji, a space-based gravitational-wave observatory, consists of three satellites forming an equilateral triangle with arm length of 3×106 km, orbiting around the Sun. Taiji is able to observe the gravitational-wave standard siren events of massive black hole binary (MBHB) merger, which is helpful in probing the expansion of the universe. In this paper, we preliminarily forecast the capability of Taiji for improving cosmological parameter estimation with the gravitational-wave standard siren data. We simulate five-year standard siren data based on three fiducial cosmological models and three models of MBHB's formation and growth. It is found that the standard siren data from Taiji can effectively break the cosmological parameter degeneracies generated by the cosmic microwave background (CMB) anisotropies data, especially for dynamical dark energy models. The constraints on cosmological parameters are significantly improved by the data combination CMB + Taiji, compared to the CMB data alone. Compared to the current optical cosmological observations, Taiji can still provide help in improving the cosmological parameter estimation to some extent. In addition, we consider an ideal scenario to investigate the potential of Taiji on constraining cosmological parameters. We conclude that the standard sirens of MBHB from Taiji will become a powerful cosmological probe in the future.

Simultaneous improvements on nutrient and Mg recoveries of microalgal bioremediation for municipal wastewater and nickel laterite ore wastewater.

Effects of different mixing ratios between synthetic municipal wastewater (MW) and magnesium (Mg2+)-enriched nickel laterite ore wastewater (NLOWW) on growth of Chlorella sorokiniana (C. sorokiniana), photosynthetic activities, cellular biocomposition, nutrient and Mg2+ removal were investigated in photobioreactors. In the culture without NLOWW, wrinkled cells were observed with low biomass production. The culture mixed with 0.13% NLOWW obtained 1.89-fold higher biomass yield, 3.77-fold enhanced photosynthetic activity (Fv/Fm value), and improved nutrient removal (nitrogen by 102.2%, phosphorus by 39.3%). However, excessive Mg2+ at 100% NLOWW produced highest reactive oxygen species suppressing microalgal growth. The Mg2+ removal capacity increased with NLOWW loading. Moreover, microalgal assimilation primarily contributed to nutrient removal while absorption was the dominant Mg2+ removal pathway. Carbohydrate content in biomass increased with Mg2+ loading. Finally, the approach for MW/NLOWW treatment was demonstrated as economically feasible with revenue of $75.6 per kilogram biomass through a comprehensive economic model.

Tris(8-Hydroxyquinoline)iron induces apoptotic cell death via oxidative stress and by activating death receptor signaling pathway in human head and neck carcinoma cells.

BACKGROUND: 8-Hydroxyquinoline derivatives have highly sensitive fluorescent chemosensors for metal ions, which are associated with anti-oxidant, anti-tumor and anti-HIV-1 properties. Head and neck squamous cell carcinoma (HNSCC) is associated with a high rate of mortality and novel anti-HNSCC drugs must be developed. Therefore, effective chemotherapy agents are required to address this public health issue. HYPOTHESIS/PURPOSE: The aim of this study was to investigate the inhibitory effect of tris(8-hydroxyquinoline)iron (Feq3) on the HNSCC and the underlying mechanism. STUDY DESIGN/METHODS: A novel 8-hydroxyquinoline derivative, Feq3, was synthesized. The cell viabilities were analyzed using MTT reagent. Apoptosis and the cell cycle distributions were determined by flow cytometer. Reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence, western blot, MitoSOX and CellROX stain assay were used to study the mechanism of Feq3. Feq3 combined with antioxidants NAC (N-acetylcysteine) and BSO (buthionine sulfoximine) measured the cell viability and intracellular ROS. RESULTS: Feq3 induced the death of HNSCC cells and caused them to exhibit the morphological features of apoptosis. Feq3 also induced apoptosis of SCC9 cells by cell cycle arrest during the G2/M phase and the induced arrest of SCC25 cells in the G0/G1 and G2/M phases, which was associated with decreased cyclin B1/cdc2 and cyclin D/cdk4 expressions. Feq3 increases reactive oxygen species (ROS) and reduces glutathione (GSH) levels, and responds to increased p53 and p21 expressions. Feq3 induced apoptosis by mitochondria-mediated Bax and cytochrome c up-expression and down-expression Bcl-2. Feq3 also up-regulated tBid, which interacts with the mitochondrial pathway and tumor necrosis factor-α (TNF-α)/TNF-Rs, FasL/Fas, and TNF-related apoptosis inducing ligand receptors (TRAIL-Rs)/TRAIL-dependent caspases apoptotic signaling pathway in HNSCC cells. However, Feq3 activates Fas but not FasL in SCC25 cells. Feq3 arrests the growth of HNSCC cells and is involved in the mitochondria- and death receptor (DR)-mediated caspases apoptotic pathway. CONCLUSION: This study is the first to suggest that apoptosis mediates the anti-HNSCC of Feq3. Feq3 has potential as a cancer therapeutic agent against HNSCC.

Vitamin D decreases the secretion of eotaxin and RANTES in nasal polyp fibroblasts derived from Taiwanese patients with chronic rhinosinusitis with nasal polyps.

Eosinophils are important inflammatory cells involved in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). Vitamin D and its derivatives, in addition to their classic role as regulators of electrolytes homeostasis, have modulatory effects in immunological and inflammatory responses. Such properties suggest that vitamin D might also play a role in inflammatory airway diseases such as CRSwNP. In this study, we investigated the effect of vitamin D derivatives (calcitriol and tacalcitol) on the secretion of eotaxin and Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES), the two major eosinophil chemoattractants, in fibroblasts derived from the polyps of Taiwanese CRSwNP patients. Patients diagnosed with eosinophilic CRSwNP but without malignancies or asthma and undergoing elective endoscopic sinus surgery were recruited. Three primary fibroblast cultures were established using the polyp specimens obtained from these patients. The third to eighth passages of the fibroblasts were used for in vitro studies. Nasal polyp-derived fibroblasts were stimulated with IL-1ß (10 ng/mL) for 24 hours, followed by replacement with media alone or with calcitriol or tacalcitol (10 µM) and incubation for another 24 hours. After the treatments, the levels of secreted eotaxin and RANTES were evaluated by ELISA assays. The results showed that IL-1ß could substantially stimulate the secretion of eotaxin (p < 0.01) and RANTES (p < 0.01) in nasal polyp-derived fibroblasts. More importantly, this stimulatory effect was significantly suppressed by adding calcitriol (p ≤ 0.002 for eotaxin and p ≤ 0.008 for RANTES) or tacalcitol (p ≤ 0.009 for eotaxin and p ≤ 0.02 for RANTES). Therefore, the inhibitory effect of vitamin D derivatives on eotaxin and RANTES secretion might shed light not only on the disease mechanism, but also on the potential use of vitamin D in pharmacotherapy of Taiwanese patients with CRSwNP.

Seizure after local anesthesia for nasopharyngeal angiofibroma.

We report a young male patient who experienced seizure after local injection of 3 mL 2% lidocaine with epinephrine 1:200,000 around a recurrent nasal angiofibroma. After receiving 100% oxygen via mask and thiamylal sodium, the patient had no residual neurologic sequelae. Seizure immediately following the injection of local anesthetics in the nasal cavity is probably due to injection into venous or arterial circulation with retrograde flow to the brain circulation. Further imaging study or angiography should be done before head and neck surgeries, especially in such highly vascular neoplasm.

Treatment of laryngeal radionecrosis with hyperbaric oxygen therapy: a case report.

An 81-year-old male with early-stage laryngeal carcinoma had been treated with 60 Gy curative radiotherapy. He complained of a sore throat, foul odor in the mouth, progressive dyspnea, and fever 2 months after the completion of radiotherapy. Direct laryngoscopy revealed narrowing of the glottis with diffuse ulcerative necrotic tissue. Biopsies at multiple sites and pathology revealed intense coagulation necrosis with complete denudation of covering epithelium without any malignancy. Since laryngeal radionecrosis was suspected, the patient received hyperbaric oxygen (HBO) therapy 40 times for 1 hour of 100% O2 at 2 atm absolute pressure. His clinical symptoms gradually improved and repeated endolaryngeal biopsies were undertaken near the end of HBO therapy and again 6 months later. The patient's larynx healed completely with diffuse fibrosis and no malignant cells were found on pathology. Radionecrosis must be differentiated from cancer recurrence following curative radiotherapy for early laryngeal cancer. HBO therapy could be a useful treatment adjunct for laryngeal radionecrosis.