Capsaicin alleviates acute alcohol-induced pyroptosis by activating ESCRT-III-dependent cell membrane repair in hepatocytes.

Capsaicin (CAP), the active ingredient in hot chilli peppers, has anti-inflammatory and hepatoprotection effects. Acute alcoholic liver injury (AALI) is liver damage caused by acute alcohol abuse, which can lead to severe liver lesions and even be life-threatening. Pyroptosis is inflammation-related programmed cell death characterized by membrane rupture and plays a key role in AALI. The endosomal sorting complexes required for transport (ESCRT) proteins can gather at damaged areas of the membrane to facilitate the process of sealing the membrane. In this study, we found that CAP could relieve acute alcohol-induced pyroptosis of hepatocytes in vitro and in vivo. Mechanically, we found that CAP could alleviate acute alcohol-induced pyroptosis by activating the ESCRT-III-dependent membrane repair machinery. Furthermore, the data showed that CAP induced ESCRT-III protein expression by activating transient receptor potential vanilloid member 1 (TRPV1) on the cell membrane and Ca2+ influx. TRPV1 inhibitor capsazepine (CPZ) inhibited the relief effect of CAP on acute alcohol-induced pyroptosis. Overall, these results showed that CAP might activate ESCRT-III-dependent membrane repair machinery through Ca2+ influx, which is regulated by TRPV1 calcium channels, therefore mitigating acute alcohol-induced pyroptosis. Our research provides a new perspective on a naturally active food product to promote cell repair and relieve AALI.

Preventive effects of lactoferrin on acute alcohol-induced liver injury via iron chelation and regulation of iron metabolism.

Lactoferrin is widely found in milk and has the ability to bind iron. Previous studies have reported that lactoferrin was effective in the prevention and treatment of acute alcohol-induced liver injury (AALI). Ferroptosis is a recently discovered cell death and is involved in the development of AALI. However, the potential role of lactoferrin in acute alcohol-induced ferroptosis is still unclear. In this study, we observed that lactoferrin (10, 20, and 40 µg/mL) significantly mitigated alcohol (300 mM)-induced injury in vitro. Additionally, lactoferrin (100 and 200 mg/kg BW) significantly alleviated alcohol (4.8 g/kg BW)-induced injury in vivo. Our results showed that lactoferrin inhibited alcohol-induced upregulation of the ferroptosis marker protein ACSL4 and downregulation of GPX4. Meanwhile, lactoferrin treatment successfully reversed the elevated malondialdehyde (MDA) levels and the reduced glutathione (GSH) levels caused by alcohol treatment. These results may indicate that lactoferrin significantly decreased ferroptosis in vivo and in vitro. Lactoferrin has the potential to chelate iron, and our results showed that lactoferrin (20 µg/mL) significantly reduced iron ions and the expression of the ferritin heavy chain (FTH) under FeCl3 (100 µM) treatment. It was demonstrated that lactoferrin had a significant iron-chelating effect and reduced iron overload caused by FeCl3 in AML12 cells. Next, we examined iron content and the expression of iron metabolism marker proteins transferrin receptor (TFR), divalent metal transporter 1 (DMT1), FTH, and ferroportin (FPN). Our results showed that lactoferrin alleviated iron overload induced by acute alcohol. The expression of TFR and DMT1 was downregulated, and FPN and FTH were upregulated after lactoferrin treatment in vivo and in vitro. Above all, the study suggested that lactoferrin can alleviate AALI by mitigating acute alcohol-induced ferroptosis. Lactoferrin may offer new strategies for the prevention or treatment of AALI.

Sodium sulfite triggered hepatic apoptosis, necroptosis, and pyroptosis by inducing mitochondrial damage in mice and AML-12 cells.

Sodium sulfite (SS) is a biological derivative of the air pollutant sulfur dioxide, and is often used as a food and pharmaceutical additive. Improper or excessive SS exposure in liver cell death. The phenomenon of simultaneous regulation of apoptosis, necroptosis, and pyroptosis is defined as PANoptosis. However, the specific types of programmed cell death (PCD) caused by SS and their interconnections remain unclear. In the present study, C57BL/6 mice were orally administered SS for 30 d, consecutively, to establish an in vivo mouse exposure model. AML-12 cells were treated with SS for 24 h to establish an in vitro exposure model. The results showed that SS-induced mitochondrial reactive oxygen species (mtROS) accumulation activated the BAX/Bcl-2/caspase 3 pathway to trigger apoptosis and RIPK1/RIPK3/p-MLKL to trigger necroptosis. Interestingly, ROS-activated p-MLKL perforated not the cell membrane as well as the lysosomal membrane. We determined that p-MLKL mediates lysosomal membrane permeabilization (LMP), resulting in cathepsin B (CTSB) release. Furthermore, knockdown of MLKL, a CTSB inhibitor (CA074-ME) and an NLRP3 inhibitor (MCC950) alleviated SS-induced pyroptosis. In summary, our study showed that SS induced apoptosis and necroptosis though mtROS accumulation, whereas the activation of p-MLKL mediated NLRP3-dependent pyroptosis by causing CTSB leakage through LMP. This study comprehensively explored the mechanism unerlying SS-induced PCD and provided an experimental basis for p-MLKL as a potential regulatory protein in PANoptosis.

The roles of FXYD family members in ovarian cancer: an integrated analysis by mining TCGA and GEO databases and functional validations.

BACKGROUND: The FXYD family of ion transport regulators have emerged as important modulators of cancer progression and metastasis. However, their expression and roles in ovarian cancer (OCa) have not been systematically investigated. METHODS: The expression of FXYD genes in OCa was analyzed using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), as well as independent clinical samples. The prognostic values of FXYD genes were evaluated by Kaplan-Meier and Cox regression analysis. To explore potential mechanisms, bioinformatics approaches including Gene Ontology, KEGG pathway analysis, GSEA and drug sensitivity correlation analysis were performed. OCa cell lines overexpressing FXYD1, FXYD5 or FXYD7 were also generated and their impacts on proliferation, migration and invasion were assessed. RESULTS: FXYD1 and FXYD6 were significantly downregulated while FXYD3, FXYD4 and FXYD5 were upregulated in OCa tissues compared to normal tissues. FXYD1, FXYD5 and FXYD7 were independent adverse prognostic factors for OCa patients. Pathway and drug correlation analysis revealed that FXYD1, FXYD5 and FXYD7 genes regulated diverse oncogenic signaling cascades and modulated the response to various chemotherapeutic agents. Overexpression of FXYD1, FXYD5 or FXYD7 enhanced OCa cell motility and invasiveness in vitro. CONCLUSION: Our results demonstrate aberrant expression patterns, prognostic values, and oncogenic activities of FXYD genes in OCa. FXYD1, FXYD5 and FXYD7 may serve as biomarkers and therapeutic targets for this disease. Targeting FXYD-mediated signaling represents a promising therapeutic strategy against OCa.

Sodium Sulfite-Triggered Hepatocyte Ferroptosis via mtROS/Lysosomal Membrane Permeabilization-Mediated Lysosome Iron Efflux.

Sodium sulfite is a widely used preservative in the food industry. Ferroptosis has been a newly discovered form of iron-dependent oxidative cell death in recent years. However, the potential connection between sodium sulfite and ferroptosis has not been explored. In our study, we observed the abnormal expression of ferroptosis marker protein in vivo, suggesting that sodium sulfite caused ferroptosis in vivo. Next, our study revealed that sodium sulfite caused the overproduction of mitochondrial reactive oxygen species (mtROS) in the AML-12 cells. It is well established that reactive oxygen species (ROS) can induce lysosomal membrane permeabilization. After lysosomal membrane permeabilization occurs, the outflow of Fe2+ in lysosomes triggers the Fenton reaction and subsequently results in the increase of intracellular ROS level, which is closely related to ferroptosis. As speculated, acridine orange (AO) staining and LysoTracker red staining showed that sodium sulfite-induced lysosomal membrane permeabilization could be alleviated by mtROS scavenger TEMPO. In addition, TEMPO, lysosomal stabilizer mannose, and lysosomal iron chelator deferoxamine (DFO) inhibited sodium sulfite-induced ferroptosis. Overall, the results showed that sodium sulfite induced lysosomal iron efflux through the mtROS-lysosomal membrane permeabilization pathway and eventually led to ferroptosis. Our study might provide a new mechanism for the hepatotoxicity of sodium sulfite and a theoretical basis for the risk assessment of sodium sulfite as a food additive.

Alcohol induces hepatocytes necroptosis through the LC3/RIPK1/RIPK3 pathway.

Excessive alcohol consumption leads to serious liver injury. Necroptosis is a programmed cell death form, which has been confirmed to be involved in alcoholic liver injury. However, the exact mechanism remains still unclear. In this study, we found that ethanol caused hepatocytes necroptosis by activating receptor-interacting serine/threonine-protein kinase 1 and 3 (RIPK1 and RIPK3). Meanwhile, autophagy was activated in ethanol-treated hepatocytes. Accumulative studies have demonstrated a possible link between autophagy and necroptosis. Microtubule-associated protein 1 light chain 3 (LC3), an autophagy marker protein, is essential for autophagosome biogenesis/maturation. But little attention has been paid to its functional role. In this study, we explored whether LC3 was involved in ethanol-induced necroptosis. The data showed that LC3 interacted with RIPK1 and RIPK3 in ethanol-treated AML12 cells and mice liver by co-immunoprecipitation (co-IP) and colocalization assay. Ethanol-induced necrosome formation and subsequent necroptosis were alleviated in hepatocytes by knockdown of LC3 or autophagy inhibitor 3-methyladenine (3-MA). These results demonstrated that LC3 accumulation facilitated the formation of necrosome by LC3-RIPK1 and LC3-RIPK3 interactions, eventually caused hepatocytes necroptosis after acute ethanol exposure. Our current research could potentially offer a new understanding of the intricate mechanisms involved in the development of acute alcoholic liver injury.

Application of bone alkaline phosphatase and 25-oxhydryl-vitamin D in diagnosis and prediction of osteoporotic vertebral compression fractures.

BACKGROUND: Osteoporosis is a bone metabolic disease that usually causes fracture. The improvement of the clinical diagnostic efficiency of osteoporosis is of great significance for the prevention of fracture. The predictive and diagnostic values of bone alkaline phosphatase (B-ALP) and 25-oxhydryl-vitamin D (25-OH-VD) for osteoporotic vertebral compression fractures (OVCFs) were evaluated. METHODS: 110 OVCFs patients undergoing percutaneous vertebroplasty were included as subjects and their spinal computed tomography (CT) images were collected. After that, deep convolutional neural network model was employed for intelligent fracture recognition. Next, the patients were randomly enrolled into Ctrl group (65 cases receiving postoperative routine treatment) and VD2 group (65 cases injected with vitamin D2 into muscle after the surgery). In addition, 100 healthy people who participated in physical examination were included in Normal group. The differences in Oswestry dysfunction indexes (ODI), imaging parameters, B-ALP and 25-OH-VD expressions, and quality of life (QOL) scores of patients among the three groups were compared. The values of B-ALP and 25-OH-VD in predicting and diagnosing OVCFs and their correlation with bone density were analyzed. RESULTS: It was demonstrated that computer intelligent medical image technique was more efficient in fracture CT recognition than artificial recognition. In contrast to those among patients in Normal group, B-ALP rose while 25-OH-VD declined among patients in Ctrl and VD2 groups (P < 0.05). Versus those among patients in Ctrl group, ODI, Cobb angle, and B-ALP reduced, while bone density, the height ratio of the injured vertebrae, 25-OH-VD, and QOL score increased among patients in VD2 group after the treatment (P < 0.05). The critical values, accuracy, and areas under the curve (AUC) of the diagnosis of OVCFs by B-ALP and 25-OH-VD amounted to 87.8 µg/L versus 30.3 nmol/L, 86.7% versus 83.3%, and 0.86 versus 0.82, respectively. B-ALP was apparently negatively correlated with bone density (r = - 0.602, P < 0.05), while 25-OH-VD was remarkably positively correlated with bone density (r = 0.576, P < 0.05). CONCLUSION: To sum up, deep learning-based computer CT image intelligent detection technique could improve the diagnostic efficacy of fracture. B-ALP rose while 25-OH-VD declined among patients with OVCFs and OVCFs could be predicted and diagnosed based on B-ALP and 25-OH-VD. Postoperative intramuscular injection of VD2 could effectively improve the therapeutic effect on patients with OVCFs and QOL.

Effects of sodium metabisulfite on pyroptosis, mitophagy and degranulation in mast cells.

Sodium metabisulphite (SMB) is the most used foods and drugs antioxidant among sulfites. So far, there were few studies about its harm, especially in mast cells. Our study was to investigate the effects of SMB on mitophagy and pyroptosis in mast cells. The results revealed that SMB dose-dependently promoted the expressions of NLRP3, GSDMD-N and other marker proteins of pyroptosis. Knockdown of GSDMD, NLRP3 inhibitor, mitophagy activator and mtROS inhibitor all reversed the changes in pyroptosis indicators caused by SMB. Considering the degranulation characteristics of mast cells and the sensitization of sulfite, we examined the effects of the above inhibitors on the degranulation of mast cells caused by SMB. The results showed that SMB-mediated mast cell degranulation was significantly inhibited by the above inhibitors. Meanwhile, we used immunofluorescence co-localization experiments and found that GSDMD pore-forming protein and histamine co-localized near the cell membrane. Overall, evidence suggested that SMB caused pyroptosis by inhibiting mitophagy, leading to mast cell degranulation. These findings are of great significance to the sensitization mechanism of SMB and provide a new insight into SMB toxicology and mast cell degranulation.

Alliin alleviates LPS-induced pyroptosis via promoting mitophagy in THP-1 macrophages and mice.

Pyroptosis is a new type of programmed cell death associated with inflammation. Excessive pyroptosis can cause body damage. Alliin is an organosulfur compound extracted from garlic, bearing anti-oxidation and anti-inflammatory properties. In this study, we revealed that alliin alleviated LPS-induced macrophage pyroptosis by detecting PI staining, IL-1ß and IL-18 release in vitro and in vivo. In the study of mechanism, we found that alliin might reduce the activation of NLRP3 inflammosome by decreasing intracellular ROS generation. Subsequently, we detected the effect of alliin on mitophagy which degraded damaged mitochondria. The results showed that alliin promoted PINK 1/Parkin-mediated mitophagy. After adding the mitophagy inhibitor CsA, the alleviating effect of alliin on mitochondrial damage and mitochondrial ROS were reversed and the relieving effect of alliin on LPS-induced pyroptosis was inhibited. These results suggested that alliin might reduce intracellular ROS production by promoting mitophagy, thus alleviating LPS-induced macrophages pyroptosis. Our study provides a new perspective and theoretical basis for alliin to alleviate pyroptosis which could further induce body damage.

Sodium Sulfite-Induced Mast Cell Pyroptosis and Degranulation.

Sodium sulfite, a common food additive, has been proved to cause allergic reaction. Pyroptosis is an inflammatory form of programmed cell death with plasma membrane lysis. In this study, we found that sodium sulfite triggered pyroptosis, which depended on reactive oxygen species (ROS)/NOD-like receptor protein 3 (NLRP3) in RBL-2H3 mast cells. Sodium sulfite increased the generation of ROS and the expression of NLRP3, caspase-1, gasdermin D N-terminal (GSDMD-N), interleukin-1ß (IL-1ß), and interleukin-18 (IL-18). The ROS scavenger N-acetyl-L-carnosine (NAC) and the NLRP3 inhibitor MCC950 reversed these effects. Furthermore, using a lactate dehydrogenase kit, propidium iodide staining, scanning electron microscopy, colocalization of GSDMD-N with histamine, and neutral red staining, we found that sodium sulfite notably induced cell membrane rupture. Because ß-Hexosaminidase and histamine play a key role in allergic reactions, we detected the release of ß-Hexosaminidase and histamine. The data showed that the release of ß-Hexosaminidase and histamine induced by sodium sulfite was increased with dose independence, which were inhibited after treatment with NAC or MCC950. Overall, evidence suggested that pyroptosis induced by sodium sulfite may rupture the cell membrane and result in degranulation of mast cells. Our study may provide new insights for the mechanism by which sodium sulfite induces mast cell death and sensitization.

Gas Phase Synthesis of the Elusive Trisilacyclopropyl Radical (Si3H5) via Unimolecular Decomposition of Chemically Activated Doublet Trisilapropyl Radicals (Si3H7).

The gas phase reaction of the simplest silicon-bearing radical silylidyne (SiH; X2Π) with disilane (Si2H6; X1A1g) was investigated in a crossed molecular beams machine. Combined with electronic structure calculations, our data reveal the synthesis of the previously elusive trisilacyclopropyl radical (Si3H5)-the isovalent counterpart of the cyclopropyl radical (C3H5)-along with molecular hydrogen via indirect scattering dynamics through long-lived, acyclic trisilapropyl (i-Si3H7) collision complex(es). Possible hydrogen-atom roaming on the doublet surface proceeds to molecular hydrogen loss accompanied by ring closure. The chemical dynamics are quite distinct from the isovalent methylidyne (CH)-ethane (C2H6) reaction, which leads to propylene (C3H6) radical plus atomic hydrogen but not to cyclopropyl (C3H5) radical plus molecular hydrogen. The identification of the trisilacyclopropyl radical (Si3H5) opens up preparative pathways for an unusual gas phase chemistry of previously inaccessible ring-strained (inorgano)silicon molecules as a result of single-collision events.

l-Arginine/l-lysine functionalized chitosan-casein core-shell and pH-responsive nanoparticles: fabrication, characterization and bioavailability enhancement of hydrophobic and hydrophilic bioactive compounds.

This study aimed at developing novel oral self-assembled delivery systems for the encapsulation, protection, and controlled release of hydrophobic and hydrophilic bioactive compounds based on l-arginine (Arg)- or l-lysine (Lys)-functionalized chitosan-casein nanoparticles (NPs). The assembled casein (CA) was modified by NaOH and used as a template core for affinity binding with hydrophobic curcumin and hydrophilic egg white-derived peptides (EWDP) and then coated with Arg- or Lys-functionalized chitosan (CS) to stabilize the systems via electrostatic interaction. Dynamic light scattering and transmission electron microscopy examination revealed Arg/Lys-CS-CA NPs with the smallest particle size of 110/82 nm, pH-responsive properties, excellent storage stability until 28 days, and spherical shape. The encapsulation efficiency of curcumin and EWDP in the NPs ranged from 81-91%, 35-74% in Arg-CS-CA NPs, and 76-87%, 48-87% in Lys-CS-CA NPs varying with different pH values. Fourier transform infrared spectroscopy, X-ray diffraction, and differential scanning calorimetry analysis were conducted to fully characterize the interaction mechanism of Arg/Lys-CS with CA, as well as the NP incorporation with curcumin and EWDP. The in vitro controlled release profile of the core-shell NPs was obtained up to 24 and 48 h for curcumin and EWDP, respectively. The simulated gastrointestinal digestion experiments confirmed that curcumin and EWDP had higher bioaccessibility in Arg/Lys-CS-CA NPs. This work offers a novel approach for producing core-shell and pH-responsive nanocarriers for oral delivery and bioavailability enhancement of both hydrophobic and hydrophilic bioactive compounds.

The Elusive Ketene (H2 CCO) Channel in the Infrared Multiphoton Dissociation of Solid 1,3,5-Trinitro-1,3,5-Triazinane (RDX).

Understanding of the fundamental mechanisms involved in the decomposition of 1,3,5-trinitro-1,3,5-triazinane (RDX) still represents a major challenge for the energetic materials and physical (organic) chemistry communities mainly because multiple competing dissociation channels are likely involved and previous detection methods of the products are not isomer selective. In this study we exploited a microsecond pulsed infrared laser to decompose thin RDX films at 5 K under mild conditions to limit the fragmentation channels. The subliming decomposition products during the temperature programed desorption phase are detected using isomer selective single photoionization time-of-flight mass spectrometry (PI-ReTOF-MS). This technique enables us to assign a product signal at m/z=42 to ketene (H2 CCO), but not to diazomethane (H2 CNN; 42 amu) as speculated previously. Electronic structure calculations support our experimental observations and unravel the decomposition mechanisms of RDX leading eventually to the elusive ketene (H2 CCO) via an exotic, four-membered ring intermediate. This study highlights the necessity to exploit isomer-selective detection schemes to probe the true decomposition products of nitramine-based energetic materials.

Associations between untraditional risk factors, pneumonia/lung cancer, and hospital fatality among hypertensive men in Guangzhou downtown.

Mortality of primary hypertension is high worldwide. Whether untraditional factors exist in modern life and affect the mortality is not well studied. The aim of the study was to evaluate the risk factors for fatality rate of hypertensive men in downtown area. A cross-sectional study was performed on hypertensive men, who were hospitalized into our hospital and lived in eligible urban areas. The characteristics of the patients and factors for the fatality were analyzed and of the risks or the contributors on the status were investigated. 14354 patients were identified. Mean age was 68.9 ± 12.4 year old (y) and dead ones was 75.9 ± 9.5 y. The overall hospitalized fatality was 5.9%, which was increased with age: fatality with 0.7%, 2.2%, 2.9%, 7.1%, 11.1% and 16.6% was for age group ≦ 49 y, 50-59 y, 60-69 y, 70-79 y, 80-89 y and ≧ 90 y respectively. The increased fatality was significantly positively correlated with the incidence of pneumonia, P < 0.05, r = 0.99. Pneumonia was prone to involve in men with older age and severer organ damage by hypertension. Similar to traditional risks such as coronary heart disease and stroke, pneumonia and lung cancer were also significantly associated with the fatality. Odds ratio (95% CI) for pneumonia and lung cancer were 6.18 (4.35-8.78) and 1.55 (1.14-2.11). The study provides evidence that pneumonia and lung cancer are highly associated with fatality of hypertensive men in downtown area, indicating that in order to reduce the fatality of hypertension, these lung diseases should be prevented and treated intensively in modern life.

N-Acetyl-l-cysteine/l-Cysteine-Functionalized Chitosan-ß-Lactoglobulin Self-Assembly Nanoparticles: A Promising Way for Oral Delivery of Hydrophilic and Hydrophobic Bioactive Compounds.

Self-assembled and cross-linked hybrid hydrogels for entrapment and delivery of hydrophilic and hydrophobic bioactive compounds were developed based on N-acetyl-l-cysteine (NAC)- or l-cysteine (CYS)-functionalized chitosan-ß-lactoglobulin nanoparticles (NPs). In both the systems, amphiphilic protein ß-lactoglobulin (ß-lg) was self-assembled by using glutaraldehyde for affinity binding with egg white-derived peptides (EWDP) and curcumin and then coated with NAC- or CYS-functionalized chitosan (CS) by electrostatic interaction. The resulting NPs were characterized in terms of size, polydispersity, and surface charge by dynamic light scattering. Results corroborated pH-sensitive properties of NAC-CS-ß-lg NPs and CYS-CS-ß-lg NPs with the particle size as small as 118 and 48 nm, respectively. The two kinds of NPs also showed excellent entrapment of EWDP and curcumin with the entrapment efficiency (EE) of EWDP and curcumin ranging from 51 to 89% and 42 to 57% in NAC-CS-ß-lg NPs, as well as 50-81% and 41-57% in CYS-CS-ß-lg NPs under different pH values. Fourier transform infrared and molecular docking studies provided support for the interaction mechanism of NAC/CYS-CS with ß-lg as well as the NPs with EWDP and curcumin. Strikingly, the in vitro release kinetics of EWDP and curcumin exhibited the controlled and sustained release properties up to 58 and 70 h from the NPs, respectively. Note that the permeability of QIGLF (pentapeptide, isolated from EWDP) and curcumin passing through Caco-2 cell monolayers were all improved after the entrapment in the NPs. This work offers promising methods for effective entrapment and oral delivery of both hydrophilic and hydrophobic bioactive compounds.

Synthesis of Polycyclic Aromatic Hydrocarbons by Phenyl Addition-Dehydrocyclization: The Third Way.

Polycyclic aromatic hydrocarbons (PAHs) represent the link between resonance-stabilized free radicals and carbonaceous nanoparticles generated in incomplete combustion processes and in circumstellar envelopes of carbon rich asymptotic giant branch (AGB) stars. Although these PAHs resemble building blocks of complex carbonaceous nanostructures, their fundamental formation mechanisms have remained elusive. By exploring these reaction mechanisms of the phenyl radical with biphenyl/naphthalene theoretically and experimentally, we provide compelling evidence on a novel phenyl-addition/dehydrocyclization (PAC) pathway leading to prototype PAHs: triphenylene and fluoranthene. PAC operates efficiently at high temperatures leading through rapid molecular mass growth processes to complex aromatic structures, which are difficult to synthesize by traditional pathways such as hydrogen-abstraction/acetylene-addition. The elucidation of the fundamental reactions leading to PAHs is necessary to facilitate an understanding of the origin and evolution of the molecular universe and of carbon in our galaxy.

A study on the enzymatic properties and reuse of cellulase immobilized with carbon nanotubes and sodium alginate.

Cellulase has many potential applications in ethanol production, extraction of medicinal ingredients, food, brewing, oil exploration, environmental protection. However, the widespread use of cellulase is limited by its relatively high production costs and low biological activity. Therefore, we studied the enzymatic properties and reusability of cellulase immobilized on multiwalled carbon nanotubes and sodium alginate for the first time. The results showed that the optimum temperature and pH of immobilized cellulase was 40 °C and 3.0, respectively. After 1 month of storage at 4 °C, the enzyme activity of immobilized cellulase dropped to 71.2% of the baseline. Immobilized cellulase was proved to be reusable and maintained ~ 70% of its activity after 7 cycles of repeated use. Versus free cellulase, the immobilized cellulase showed good thermal stability, pH resistance, storage stability and reusability, which could be beneficial in large-scale industrial manufacturing processes.

A vacuum ultraviolet photoionization study on the formation of methanimine (CH2NH) and ethylenediamine (NH2CH2CH2NH2) in low temperature interstellar model ices exposed to ionizing radiation.

Methylamine (CH3NH2) and methanimine (CH2NH) represent essential building blocks in the formation of amino acids in interstellar and cometary ices. In our study, by exploiting isomer selective detection of the reaction products via photoionization coupled with reflectron time of flight mass spectrometry (Re-TOF-MS), we elucidate the formation of methanimine and ethylenediamine (NH2CH2CH2NH2) in methylamine ices exposed to energetic electrons as a proxy for secondary electrons generated by energetic cosmic rays penetrating interstellar and cometary ices. Interestingly, the two products methanimine and ethylenediamine are isoelectronic to formaldehyde (H2CO) and ethylene glycol (HOCH2CH2OH), respectively. Their formation has been confirmed in interstellar ice analogs consisting of methanol (CH3OH) which is ioselectronic to methylamine. Both oxygen-bearing species formed in methanol have been detected in the interstellar medium (ISM), while for methanimine and ethylenediamine only methanimine has been identified so far. In comparison with the methanol ice products and our experimental findings, we predict that ethylenediamine should be detectable in these astronomical sources, where methylamine and methanimine are present.

Leptin upregulates COX-2 and its downstream products in aortic endothelial cells.

The adipocyte-derived hormone leptin is associated with hypertension. The involvement of cyclooxygenase-2 (COX-2) and its downstream vasomotor products prostaglandin (PG) and thromboxane (TX)A2 in the mechanisms of action of leptin have remained elusive. The aim of the present study was to investigate the effects of leptin on the expression of COX-2 by rat aortic endothelial cells (RAECs) and the concentration of its products, represented by 6-keto PGF1α and TXB2, in the culture media. RAECs were isolated, cultured and identified by immunofluorescence staining. The RAECs were incubated with different concentrations of leptin (10-10, 10-9 and 10-8 M) for various durations (36 or 48 h). COX-2 mRNA and protein expression in the cells was detected by reverse-transcription quantitative PCR and western blot analysis, respectively. The vasodilator 6-keto PGF1α and the vasoconstrictor TXB2 were detected in the supernatant by ELISA. The cultured cells displayed specific factor VIII expression in the cytoplasm. Compared with the PBS-treated control group, leptin significantly increased the expression of COX-2 mRNA and protein in a time- and dose-dependent manner (P<0.01). Furthermore, the vasodilator 6-keto PGF1α was increased and the TXB2/6-keto PGF1α ratio decreased only with relatively high concentrations of leptin (10-9 or 10-8 M; P<0.01), but TXB2 levels were not affected (P>0.05). In conclusion, leptin significantly increased the expression of inflammatory marker COX-2 and its downstream product 6-keto PGF1α, while also decreasing the TXB2/6-keto PGF1α ratio in vitro. These observations suggested that COX-2 may have an important role in the effects of leptin on inflammation, such as the low-inflammatory disease hypertension. However, selective COX-2 inhibitors may increase the risk of hypertension due to inhibiting 6-keto PGF1α, the vasodilator product of COX-2.