Cloning, expression and characterization of the maltooligosyl trehalose synthase from the archaeon Sulfolobus tokodaii.

The maltooligosyl trehalose synthase gene from the hyperthermophilic archaeon Sulfolobus tokodaii strain 7 was cloned and the recombinant peotein was expressed in E. coli. The protein was purified to homogeneity by nickel column chromatography. The archaeal enzyme could catalyze an intramolecular transglycosylation reaction and convert the glycosidic bond at the reducing end of dextrins from α-1, 4 (reducing end) into α-1, 1 (non-reducing end). The most suitable temperature was 75°C and the optimal pH was 5. Substrate specificity investigation revealed that maltodextrin and maltooligosaccharide were used as substrates by the enzyme but maltose, chitooligosaccharide, sucrose and ß-cyclodextrin weren't used.

Synchronous ganglioneuroma and schwannoma of the vagal inferior ganglion.

Neurogenic neoplasms resulting from autonomic nerves are considerably rare. In this paper, we report a case of a 41-year-old woman with composite tumor of synchronous ganglioneuroma and schwannoma in the vagal inferior ganglion. Ultrasonography and computed tomography showed a well-defined mass, which extruded from the internal and external carotid arteries. Two tumors were closely attached but with an evident boundary. The small tumor was composed of spindle cells and numerous mature ganglion cells, and the large one consisted entirely of differentiated neoplastic Schwann cells. Results showed that these tumors were a schwannoma arising in a ganglioneuroma of the vagal inferior ganglion. Our case is the first to demonstrate the occurrence of schwannoma in benign ganglioneuroma. We also provided clinical and pathological evidence that such transformation can occur spontaneously.
.

Resveratrol restores sirtuin 1 (SIRT1) activity and pyruvate dehydrogenase kinase 1 (PDK1) expression after hemorrhagic injury in a rat model.

Severe hemorrhage leads to decreased blood flow to tissues resulting in decreased oxygen and nutrient availability affecting mitochondrial function. A mitoscriptome profiling study demonstrated alteration in several genes related to mitochondria, consistent with the mitochondrial functional decline observed after trauma hemorrhage (T-H). Our experiments led to the identification of sirtuin 1 (SIRT1) as a potential target in T-H. Administration of resveratrol (a naturally occurring polyphenol and activator of SIRT1) after T-H improved left ventricular function and tissue ATP levels. Our hypothesis was that mitochondrial function after T-H depends on SIRT1 activity. In this study, we evaluated the activity of SIRT1, a mitochondrial functional modulator, and the mitochondrial-glycolytic balance after T-H. We determined the changes in protein levels of pyruvate dehydrogenase kinase (PDK)-1 and nuclear c-Myc, peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and NF-E2-related factor (NRF)2 after T-H and after treatment with resveratrol or a combination of sirtinol (a SIRT1 inhibitor) and resveratrol. We have also tested the activity of mitochondrial complex 1. SIRT1 enzyme activity was significantly decreased after T-H, whereas resveratrol treatment restored the activity. We found elevated PDK1 and c-Myc levels and decreased PGC-1α, NRF2 and mitochondrial complex I activity after T-H. The reduced SIRT1 activity after T-H may be related to declining mitochondrial function, since resveratrol was able to reinstate SIRT1 activity and mitochondrial function. The elevated level of PDK1 (an inhibitor of pyruvate dehydrogenase complex) after T-H indicates a possible shift in cellular energetics from mitochondria to glycolysis. In conclusion, SIRT1 modulation alters left ventricular function after T-H through regulation of cellular energetics.

Regulation and photocatalytic degradation mechanism of a hydroxyl modified UiO-66 type metal organic framework.

Photocatalytic performance can be effectively improved by modifying the functional groups on the organic ligands of metal organic frameworks (MOFs). Herein, the hydroxyl-modified UiO-66 type MOF: UIO-66-2OH(2,3), was successfully synthesized by the method of ligand exchange by the 2,3-dihydroxyterephthalic acid and UIO-66 as raw materials. The mechanism of photocatalytic degradation of methylene blue (MB) by UIO-66-2OH(2,3) shows that the hydroxyl functional group on the organic ligand regulates its electronegativity and expands its light absorption range. The decomposition of MB is carried out in multiple steps under the oxidation of the hydroxyl radical (˙OH). This research result shows the direction for guiding the synthesis of efficient photocatalysts and clarifying the light absorption of MOFs regulated by hydroxyl functional groups.

Reproductive toxicity of micro- and nanoplastics.

Large-scale plastic pollution occurs in terrestrial and marine environments and degrades into microparticles (MP) and nanoparticles (NP) of plastic. Micro/nanoplastics (MP/NPs) are found throughout the environment and different kinds of marine organisms and can enter the human body through inhalation or ingestion, particularly through the food chain. MPs/NPs can enter different organisms, and affect different body systems, including the reproductive, digestive, and nervous systems via the induction of different stresses such as oxidative stress and endoplasmic reticulum stress. This paper summarizes the effects of MPs/NPs of different sizes on the reproduction of different organisms including terrestrial and marine invertebrates and vertebrates, the amplification of toxic effects between them through the food chain, the serious threat to biodiversity, and, more importantly, the imminent challenge to human reproductive health. There is a need to strengthen international communication and cooperation on the remediation of plastic pollution and the protection of biodiversity to build a sustainable association between humans and other organisms.

Influence of aging and hemorrhage injury on Sirt1 expression: possible role of myc-Sirt1 regulation in mitochondrial function.

Trauma-hemorrhage (T-H) causes hypoxia and organ dysfunction. Mitochondrial dysfunction is a major factor for cellular injury due to T-H. Aging also has been known to cause progressive mitochondrial dysfunction. In order to study the effect of aging on T-H-induced mitochondrial dysfunction, we recently developed a rodent mitochondrial genechip with probesets representing mitochondrial and nuclear genes contributing to mitochondrial structure and function. Using this chip we recently identified signature mitochondrial genes altered following T-H in 6 and 22 month old rats; augmented expression of the transcription factor c-myc was the most pronounced. Based on reports of c-myc-IL6 collaboration and c-myc-Sirt1 negative regulation, we further investigated the expression of these regulatory factors with respect to aging and injury. Rats of ages 6 and 22 months were subjected to T-H or sham operation and left ventricular tissues were tested for cytosolic cytochrome c, mtDNA content, Sirt1 and mitochondrial biogenesis factors Foxo1, Ppara and Nrf-1. We observed increased cardiac cytosolic cytochrome c (sham vs T-H, p<0.03), decreased mitochondrial DNA content (sham vs T-H, p<0.05), and decreased Sirt1 expression (sham vs TH, p<0.05) following T-H and with progressing age. Additionally, expression of mitochondrial biogenesis regulating transcription factors Foxo1 and Nrf-1 was also decreased with T-H and aging. Based upon these observations we conclude that Sirt1 expression is negatively modulated by T-H causing downregulation of mitochondrial biogenesis. Thus, induction of Sirt1 is likely to produce salutary effects following T-H induced injury and hence, Sirt1 may be a potential molecular target for translational research in injury resolution.

Resveratrol improves cardiac contractility following trauma-hemorrhage by modulating Sirt1.

Mitochondria play a critical role in metabolic homeostasis of a cell. Our recent studies, based on the reported interrelationship between c-Myc and Sirt1 (mammalian orthologue of yeast sir2 [silent information regulator 2]) expression and their role in mitochondrial biogenesis and function, demonstrated a significant downregulation of Sirt1 protein expression and an upregulation of c-Myc following trauma-hemorrhage (T-H). Activators of Sirt1 are known to improve mitochondrial function and the naturally occurring polyphenol resveratrol (RSV) has been shown to significantly increase Sirt1 activity by increasing its affinity to both NAD+ and the acetylated substrate. In this study we tested the salutary effect of RSV following T-H and its influence on Sirt1 expression. Rats were subjected to T-H or sham operation. RSV (8 mg/kg body weight, intravenously) or vehicle was administered 10 min after the onset of resuscitation, and the rats were killed 2 h following resuscitation. Sirtinol, a Sirt1 inhibitor, was administered 5 min prior to RSV administration. Cardiac contractility (±dP/dt) was measured and heart tissue was tested for Sirt1, Pgc-1α, c-Myc, cytosolic cytochrome C expression and ATP level. Left ventricular function, after T-H, was improved (P < 0.05) following RSV treatment, with significantly elevated expression of Sirt1 (P < 0.05) and Pgc-1α (P < 0.05), and decreased c-Myc (P < 0.05). We also observed significantly higher cardiac ATP content, declined cytosolic cytochrome C and decreased plasma tumor necrosis factor-α in the T-H-RSV group. The salutary effect due to RSV was abolished by sirtinol, indicating a Sirt1-mediated effect. We conclude that RSV may be a useful adjunct to resuscitation fluid following T-H.

In Situ Synthesis Mechanism and Photocatalytic Performance of Cyano-Bridged Cu (I)/Cu (II) Ultrathin Nanosheets.

In situ synthesis of cyano-bridged Cu (I)/Cu (II) complexes usually requires organometallic catalysts or is carried out under high-temperature and high-pressure conditions. Herein, the cyano-bridged two-dimensional Cu (I)/Cu (II) photocatalyst, [Cu2 (Py)3(CN)3]n (1), is synthesized in situ at room temperature. The in situ synthesis mechanism of 1 shows that the partial Cu (II) complex catalyzed the C-C bond cleavage of 1,3-isophthalonitrile (L) to introduce -CN and generate Cu (I)/Cu (II). Its ultrathin nanosheets can be obtained by adding sodium dodecyl benzene sulfonate and performing ultrasonic synthesis in the process of synthesis 1. The ultrathin nanosheets of 1 have a lattice distance of about 0.31 nm, and it can rapidly decompose methylene blue (MB) (K = 0.25 mg L-1 min-1 at pH = 3). This research work is beneficial for in situ synthesis of cyano-bridged Cu (I)/Cu (II) complexes at room temperature and explores their synthesis and photocatalytic mechanism.

Insight into the promoting effect of support pretreatment with sulfate acid on selective catalytic reduction performance of CeO2/ZrO2 catalysts.

In this paper, sulfated ZrO2 were synthesized via precipitation and impregnation method, and the promoting effects of support sulfation on selective catalytic reduction (SCR) performance of CeO2/ZrO2 catalysts were investigated. The results revealed that sulfated ZrO2 could significantly enhance the SCR activity of CeO2/ZrO2 catalysts in a wide temperature range. Especially when S/Zr molar ratio was 0.1, CeO2/ZrO2-0.1S catalyst exhibited a large operating temperature window of 251 âˆ¼ 500 °C and its N2 selectivity was 100 % in the temperature range of 150 âˆ¼ 500 °C. Moreover, CeO2/ZrO2-0.1S catalyst possessed a superior low-temperature activity over 0.1S-CeO2/ZrO2 catalyst. After exposing to 100 ppm SO2 for 15 h, a high NO conversion efficiency of CeO2/ZrO2-0.1S catalyst (90.7 %) could still be reached. The characterization results indicated that ZrO2 treated with a proper dosage of sulfate acid was beneficial to enlarge the specific surface area greatly. Sulfated ZrO2 was also in favor of promoting the transformation of CeO2 from crystalline state to highly-dispersed amorphous state, and inhibiting the transformation of ZrO2 from tetragonal to monoclinic phase. It could also enhance the total surface acidity greatly with an increase in both Brønsted acid sites and Lewis acid sites, thus significantly improving NH3 adsorption on catalyst surface. Besides, the promoting effect of support sulfation on SCR performance of CeO2/ZrO2 catalysts was also related with the enhanced redox property, higher Ce3+/(Ce3++Ce4+) ratio and abundant surface chemisorbed labile oxygen. The in-situ DRIFTS results implied that nitrate species coordinated on the surface of CeO2/ZrO2-0.1S catalyst could participate in the Selective catalytic reduction with ammonia (NH3-SCR) reactions at either medium or high temperature, suggesting that both Eley-Rideal (E-R) and Langmuir-Hinshelwood (L-H) mechanisms might be followed in SCR reactions.

Aging influences cardiac mitochondrial gene expression and cardiovascular function following hemorrhage injury.

Cardiac dysfunction and mortality associated with trauma and sepsis increase with age. Mitochondria play a critical role in the energy demand of cardiac muscles, and thereby on the function of the heart. Specific molecular pathways responsible for mitochondrial functional alterations after injury in relation to aging are largely unknown. To further investigate this, 6- and 22-month-old rats were subjected to trauma-hemorrhage (T-H) or sham operation and euthanized following resuscitation. Left ventricular tissue was profiled using our custom rodent mitochondrial gene chip (RoMitochip). Our experiments demonstrated a declined left ventricular performance and decreased alteration in mitochondrial gene expression with age following T-H and we have identified c-Myc, a pleotropic transcription factor, to be the most upregulated gene in 6- and 22-month-old rats after T-H. Following T-H, while 142 probe sets were altered significantly (39 up and 103 down) in 6-month-old rats, only 66 were altered (30 up and 36 down) in 22-month-old rats; 36 probe sets (11 up and 25 down) showed the same trend in both groups. The expression of c-Myc and cardiac death promoting gene Bnip3 were increased, and Pgc1-α and Ppar-α a decreased following T-H. Eleven tRNA transcripts on mtDNA were upregulated following T-H in the aged animals, compared with the sham group. Our observations suggest a c-myc-regulated mitochondrial dysfunction following T-H injury and marked decrease in age-dependent changes in the transcriptional profile of mitochondrial genes following T-H, possibly indicating cellular senescence. To our knowledge, this is the first report on mitochondrial gene expression profile following T-H in relation to aging.

Ethinyl estradiol sulfate acts without fluid resuscitation through estrogen receptors to rapidly protect the cardiovascular system from severe hemorrhage.

BACKGROUND: Our in vivo rodent and pig model evidenced that estrogen and its derivative, ethinyl estradiol sulfate (EES), promote survival following hemorrhagic shock. To determine its mechanism, we first confirmed EES binding to estrogen receptor (ER) and improving/restoring cellular signaling, countering the assumption that EES, an ethinyl estradiol metabolite, is inactive. In addition, we examined if EES acts rapidly, consistent with nongenomic signaling. We selected the biomarkers of cardiovascular performance, reduction of apoptosis and proinflammatory responses, and elaboration of nitric oxide (NO) to validate efficacy. METHODS: A rat trauma-hemorrhage model, consisting of a midline laparotomy and controlled bleeding (60% blood loss) without fluid resuscitation, was used. At 30 minutes after hemorrhage, heart performance was monitored, and Western blots were used to quantify biochemical analytes. The specificity of EES for ER was profiled with ER antagonists. Binding studies by Sekisui XenoTech (Kansas City, KS) determined an LD50 value for EES binding the rat ER. RESULTS: The EES IC50 value was 1.52 × 10-8 Mol/L, consistent with pharmacologic efficacy. Ethinyl estradiol sulfate raised mean arterial pressure and ±derivative of pressure over time (dP/dT) significantly (but did not fully restore) within a 30-minute window. Levels of apoptosis and activation of NF-κB were dramatically reduced, as was elaboration of nitric oxide (NO) by inducible nitric oxide synthase. Phospho-endothelial nitric oxide synthase (eNOS) was restored to physiological levels. The restoration of cellular signaling occurs before restoration of cardiac contractility. CONCLUSION: Ethinyl estradiol sulfate is a potent drug for improving heart performance, which also dramatically reduces damage by apoptosis, proinflammatory activity, and NO production, validating that EES can blunt multiple harmful outcomes arising from hypoxia and hypovolemia. The actions are dependent on receptor engagement, where specificity is confirmed by ER antagonists. The constraint of a 30-minute sampling window affirms that the responses are nongenomic and very likely restricted to cell-surface receptor engagement. The rapidity of these responses makes EES promising for intervention in the "golden hour."

Generic and Flexible Unmanned Sailboat for Innovative Education and World Robotic Sailing Championship.

Over the past two decades, scholars developed various unmanned sailboat platforms, but most of them have specialized designs and controllers. Whereas these robotic sailboats have good performance with open-source designs, it is actually hard for interested researchers or fans to follow and make their own sailboats with these open-source designs. Thus, in this paper, a generic and flexible unmanned sailboat platform with easy access to the hardware and software architectures is designed and tested. The commonly used 1-m class RC racing sailboat was employed to install Pixhawk V2.4.8, Arduino Mega 2,560, GPS module M8N, custom-designed wind direction sensor, and wireless 433 Mhz telegram. The widely used open-source hardware modules were selected to keep reliable and low-cost hardware setup to emphasize the generality and feasibility of the unmanned sailboat platform. In software architecture, the Pixhawk V2.4.8 provided reliable states' feedback. The Arduino Mega 2,560 received estimated states from Pixhawk V2.4.8 and the wind vane sensor, and then controlled servo actuators of rudder and sail using simplified algorithms. Due to the complexity of introducing robot operating system and its packages, we designed a generic but real-time software architecture just using Arduino Mega 2,560. A suitable line-of-sight guidance strategy and PID-based controllers were used to let the autonomous sailboat sail at user-defined waypoints. Field tests validated the sailing performance in facing WRSC challenges. Results of fleet race, station keeping, and area scanning proved that our design and algorithms could control the 1-m class RC sailboat with acceptable accuracy. The proposed design and algorithms contributed to developing educational, low-cost, micro class autonomous sailboats with accessible, generic, and flexible hardware and software. Besides, our sailboat platform also facilitates readers to develop similar sailboats with more focus on their missions.

Application of 3D Printing Technology in Bone Tissue Engineering: A Review.

Clinically, the treatment of bone defects remains a significant challenge, as it requires autogenous bone grafts or bone graft substitutes. However, the existing biomaterials often fail to meet the clinical requirements in terms of structural support, bone induction, and controllable biodegradability. In the treatment of bone defects, 3D porous scaffolds have attracted much attention in the orthopedic field. In terms of appearance and microstructure, complex bone scaffolds created by 3D printing technology are similar to human bone. On this basis, the combination of active substances, including cells and growth factors, is more conducive to bone tissue reconstruction, which is of great significance for the personalized treatment of bone defects. With the continuous development of 3D printing technology, it has been widely used in bone defect repair as well as diagnosis and rehabilitation, creating an emerging industry with excellent market potential. Meanwhile, the diverse combination of 3D printing technology with multi-disciplinary fields, such as tissue engineering, digital medicine, and materials science, has made 3D printing products with good biocompatibility, excellent osteoinductive capacity, and stable mechanical properties. In the clinical application of the repair of bone defects, various biological materials and 3D printing methods have emerged to make patient-specific bioactive scaffolds. The microstructure of 3D printed scaffolds can meet the complex needs of bone defect repair and support the personalized treatment of patients. Some of the new materials and technologies that emerged from the 3D printing industry's advent in the past decade successfully translated into clinical practice. In this article, we first introduced the development and application of different types of materials that were used in 3D bioprinting, including metal, ceramic materials, polymer materials, composite materials, and cell tissue. The combined application of 3D bioprinting and other manufacturing methods used for bone tissue engineering are also discussed in this article. Finally, we discussed the bottleneck of 3D bioprinting technique and forecasted its research orientation and prospect.

Ovarian mucinous cystic tumor associated with sarcomatous mural nodule and benign Brenner tumor: A case report and literature review.

RATIONALE: Ovarian mucinous tumor with malignant mural nodule is exceedingly rare. We report a case of ovarian mucinous cystic tumor associated with sarcomatous mural nodule and benign Brenner tumor and accompanied by nodular histiocytic aggregates in the greater omentum. PATIENT CONCERNS: A 60-year-old postmenopausal woman was presented with a history of one month of lower abdominal discomfort, abdominal distension, nausea, and vomiting. A physical examination revealed a hard, palpable mass with mild tenderness in her right lower abdomen. DIAGNOSES: The mucinous tumor was solid and cystic and contained benign, borderline, and malignant elements. Within the solid areas, two nodules representing pleomorphic undifferentiated sarcoma and benign Brenner tumor were identified. The diagnosis of malignant mural nodule was based on vascular invasion and marked nuclear atypia, including atypical mitoses and mitotic activity. INTERVENTIONS: Bilateral salpingo-oophorectomy and partial omentectomy were performed. Malignant cells were not found on cytologic examination of the peritoneal washing fluid. The patient underwent three cycles of chemotherapy with 210 mg paclitaxel liposome via an intravenous drip, 20 mg nedaplatin via an intravenous drip, and 80 mg nedaplatin via intraperitoneal perfusion. OUTCOMES: The patient has been followed up for 3 years without evidence of tumor recurrence and metastasis. LESSONS: Careful classification of a mural nodule is important to triage patients in need of aggressive adjuvant treatment.

Distinct expression pattern and prognostic values of pituitary tumor transforming gene family genes in non-small cell lung cancer.

Members of the pituitary tumor transforming gene (PTTG) family, including PTTG1, PTTG2 and PTTG3P, exhibit pivotal roles in the onset and progression of certain types of human cancer. However, to the best of our knowledge, a systematic study regarding the expression pattern and the prognostic values of PTTG family genes in non-small cell lung cancer (NSCLC) remains to be performed. The expression levels of PTTG family genes in NSCLC were successively determined using the Gene Expression Profiling Interactive Analysis, UALCAN and Oncomine databases. Subsequently, the Kaplan-Meier plotter database was used to assess the prognostic value of the PTTG family genes in patients with NSCLC, and to determine the associations between PTTG expression levels and the prognosis of patients based on different clinicopathological features, including cancer stage, grade, chemotherapy, radiotherapy, lymph node status, smoking history, and sex. PTTG1 was identified to be significantly upregulated in NSCLC in all three databases, whereas PTTG2 and PTTG3P were significantly upregulated in NSCLC in only the UALCAN database. Patients with NSCLC with higher expression levels of the three PTTG genes demonstrated shorter overall survival times. In summary, the results of the present study suggested that increased expression of PTTG family genes may serve as promising prognostic biomarkers for patients with NSCLC.

The protective effects of PUGNAc on cardiac function after trauma-hemorrhage are mediated via increased protein O-GlcNAc levels.

We have previously shown that administration of glucosamine after trauma-hemorrhage (TH) improved cardiac output and organ perfusion, and this was associated with increased levels of O-linked N-acetylglucosamine (O-GlcNAc) on proteins in the heart and brain. An alternative means of increasing O-GlcNAc levels is by inhibition of O-linked N-acetylglucosaminidase, which catalyzes the removal of N-acetylglucosamine from proteins, with O-(2-acetamido-2-deoxy-d-glucopyranosylidene) amino-N-phenylcarbamate (PUGNAc). The goal of this study, therefore, was to determine whether PUGNAc administration after TH also improves recovery of organ perfusion and function. Fasted male rats were bled to and maintained at a mean arterial blood pressure of 40 mmHg for 90 min, followed by fluid resuscitation. Intravenous administration of PUGNAc (200 micromol/kg body weight) 30 min after the onset of resuscitation significantly improved cardiac output compared with the vehicle controls (12.3 +/- 1.3 mL/min per 100 g body weight vs. 25.5 +/- 2.0 mL/min per 100 g body weight; P < 0.05), decreased total peripheral resistance (6.6 +/- 0.8 mmHg/mL per minute per 100 g body weight vs. 3.7 +/- 0.3 mmHg/mL per minute per 100 g body weight; P < 0.05), and increased perfusion of critical organ systems, including the kidney and liver, determined at 2 h after the end of resuscitation. Treatment with PUGNAc also attenuated the TH-induced increase in plasma IL-6 levels (864 +/- 112 pg/mL vs. 392 +/- 188 pg/mL; P < 0.05) and TNF-alpha levels (216 +/- 21 pg/mL vs. 94 +/- 11 pg/mL; P < 0.05) and significantly increased O-GlcNAc levels in the heart, liver, and kidney. Thus, PUGNAc, like glucosamine, improves cardiac function and organ perfusion and reduced the level of circulating IL-6 and TNF-alpha after TH. The similar effects of glucosamine and PUGNAc support the notion that the protection associated with both interventions is mediated via increased protein O-GlcNAc levels.

Inhibition of cardiac PGC-1alpha expression abolishes ERbeta agonist-mediated cardioprotection following trauma-hemorrhage.

PGC-1alpha (peroxisome proliferator-activated receptor [PPARgamma] coactivator-1alpha) activates PPARalpha and mitochondrial transcription factor A (Tfam), which regulate proteins, fatty acid and ATP metabolism (i.e., FAT/CD36, MCAD, and COX I). Recently we found that the salutary effects of estradiol (E2) on cardiac function following trauma-hemorrhage (T-H) are mediated via estrogen receptor (ER)beta. In this study we tested the hypothesis that ERbeta-mediated cardioprotection is induced via up-regulation of PGC-1alpha through PPARalpha or Tfam-dependent pathway. Male rats underwent T-H and received ERalpha agonist propylpyrazole-triol (PPT), ERbeta agonist diarylpropionitrile (DPN), E2, or vehicle. Another group was treated with antisense PGC-1alpha oligonucleotides prior to administration of DPN. E2 and DPN treatments attenuated the decrease in cardiac mitochondrial ATP, abrogated the T-H-induced lipid accumulation, and normalized PGC-1alpha, PPARalpha, FAT/CD36, MCAD, Tfam, and COX I after T-H. In contrast, PPT administration did not abrogate lipid accumulation. Moreover, in PPT-treated animals mitochondrial ATP remained significantly lower than those observed in DPN- or E2-treated animals. Prior administration of antisense PGC-1alpha prevented DPN-mediated cardioprotection and increase in ATP levels and Tfam but not in PPARalpha following T-H. These findings suggest that the salutary effects of E2 on cardiac function following T-H are mediated via ERbeta up-regulation of PGC-1alpha through Tfam-dependent pathway.

Mechanism of the salutary effects of flutamide on intestinal myeloperoxidase activity following trauma-hemorrhage: up-regulation of estrogen receptor-{beta}-dependent HO-1.

Hemeoxygenase (HO)-1 induction following adverse circulatory conditions is known to be protective, and precastrated males have less intestinal damage than sham-operated males following trauma-hemorrhage (T-H). Previous studies have also shown that administration of flutamide up-regulated estrogen receptor (ER) expression in males following T-H. We hypothesized that flutamide administration in males following T-H up-regulates HO-1 via an ER-dependent pathway and protects against intestinal injury. Male Sprague-Dawley rats underwent T-H [mean blood pressure (MBP) 40 mmHg for 90 min and then resuscitation]. A single dose of flutamide (25 mg/kg body weight), with or without an ER antagonist (ICI 182,780), a HO enzyme inhibitor [chromium-mesoporphyrin (CrMP)], or vehicle, was administered subcutaneously during resuscitation. At 2 h after T-H or sham operation, intestinal myeloperoxidase (MPO) activity, intercellular adhesion molecule (ICAM)-1, cytokine-induced neutrophil chemoattractant (CINC)-1, and CINC-3 levels were measured. Intestinal ER-alpha, ER-beta, androgen receptor, and HO-1 mRNA/protein levels were also determined. Results showed that T-H increased intestinal MPO activity, ICAM-1, CINC-1, and CINC-3 levels. These parameters were improved significantly in the flutamide-treated rats subjected to T-H. Flutamide treatment increased intestinal HO-1 and ER-beta mRNA/protein levels as compared with vehicle-treated T-H rats. Administration of the ER antagonist ICI 182,780 or the HO inhibitor CrMP prevented the flutamide-induced attenuation of shock-induced intestinal damage. Thus, the salutary effects of flutamide administration on attenuation of intestinal injury following T-H are mediated via up-regulation of ER-beta-dependent HO-1 expression.

Glucosamine administration during resuscitation improves organ function after trauma hemorrhage.

Stress-induced hyperglycemia is necessary for maximal rates of survival after severe hemorrhage; however, the responsible mechanisms are not clear. One consequence of hyperglycemia is an increase in hexosamine biosynthesis, which leads to increases in levels of O-linked attachment of N-acetyl-glucosamine (O-GlcNAc) on nuclear and cytoplasmic proteins. This modification has been shown to lead to improved survival of isolated cells after stress. In view of this, we hypothesized that glucosamine (GlcNH2), which more selectively increases the levels of O-GlcNAc administration after shock, will have salutary effects on organ function after trauma hemorrhage (TH). Fasted male rats that underwent midline laparotomy were bled to a mean arterial blood pressure of 40 mmHg for 90 min and then resuscitated with Ringer lactate (four times the shed blood volume). Administration of 2.5 mL of 150 mmol L GlcNH2 midway during resuscitation improved cardiac output 2-fold compared with controls that received 2.5 mL of 150 mmol L NaCl. GlcNH2 also improved perfusion of various organs systems, including kidney and brain, and attenuated the TH-induced increase in serum levels of IL-6 (902+/-224 vs. 585+/-103 pg mL) and TNF-alpha (540+/-81 vs. 345+/-110 pg mL) (values are mean+/-SD). GlcNH2 administration resulted in significant increase in protein-associated O-GlcNAc in the heart and brain after TH. Thus, GlcNH2 administered during resuscitation improves recovery from TH, as assessed by cardiac function, organ perfusion, and levels of circulating inflammatory cytokines. This protection correlates with enhanced levels of nucleocytoplasmic protein O-GlcNAcylation and suggests that increased O-GlcNAc could be the mechanism that links stress-induced hyperglycemia to improved outcomes.

An investigation on NO removal by wet scrubbing using NaClO2 seawater solution.

The experiments were conducted to investigate the NO removal by wet scrubbing using NaClO2 seawater solution in a cyclic scrubbing mode. Results show that, when the concentration of NaClO2 in scrubbing solution is higher than 10 mM, a complete removal of NO can be achieved during the cyclic scrubbing process. The breakthrough time for seawater with 15 mM NaClO2 is enhanced by 34.3 % compared with that for NaClO2 freshwater. The extension of the breakthrough time for NaClO2 seawater is mainly ascribed to the improved utilization of NaClO2 in the solution. The good buffering ability of seawater could suppress the acidic decomposition of NaClO2 into ClO2 effectively. The analysis of reaction products indicates that the main anions in the spent liquor are chloride ions and nitrate ions. The calculation of NaClO2 utilization according to the ion chromatography also agrees well with the experimental results of breakthrough times.