The mechanism of xylans removal during hydrothermal pretreatment of poplar fibers investigated by immunogold labeling.

MAIN CONCLUSION: Hydrothermal pretreatment initially removed the lignin-free xylan from the middle layer of secondary wall, followed by the lignin-bound xylan, but the cellulose-bound xylan was seldom removed by this pretreatment. An in-depth understanding of the mechanism of xylan removal during hydrothermal pretreatment (HTP) of wood is critical for cost-effective conversion of lignocellulosic biomass to biofuels. Several studies demonstrated the kinetics and mechanism of xylan removal during HTP on molecular scale, but the dissolution mechanism of xylan during HTP remains unclear at ultra-structural level. Our study investigated changes in the micro-distribution of xylan in poplar fiber cell walls during HTP by transmission electron microscopy (TEM) in combination with immunogold labeling. The study revealed that HTP caused greater decline in the density of xylan labeling in the S2 layer of fiber wall than in the S1 layer. There was a greater loss in the density of xylan labeling during HTP in the delignified and enzymatically treated fibers compared to untreated fibers. We propose that in the initial stages of HTP lignin-free xylan in the S2 layer was more readily hydrolyzed than in the S1 layer by hydronium ions. With increasing pretreatment time, the xylan covalently bound to lignin was also removed from the S2 layer due to the dissolution of lignin. The xylan tightly bound to cellulose was seldom removed during HTP, but was hydrolyzed in subsequent enzymatic treatment. This TEM-immunolabeling investigation reveals the manner in which different xylan fractions are removed from fiber cell wall during HTP, and we expect the information to be helpful in developing processes tailored for more effective conversion of cellulosic biomass into fermentable sugars.

Stress Distribution in Superior Labral Complex and Rotator Cuff During In Vivo Shoulder Motion: A Finite Element Analysis.

PURPOSE: To quantitatively and qualitatively evaluate the impingement behavior between structures within the glenohumeral joint under simulated abduction-external rotation (ABER) motion using finite element analysis. METHODS: Computed tomography (CT) scanning of 1 shoulder in a volunteer was performed at 0° and 120° of shoulder abduction with external rotation (ABER position), followed by magnetic resonance imaging at 0° of abduction. The CT and magnetic resonance images were then imported into a customized software program to undergo 3-dimensional reconstruction followed by finite element modeling of the bone and soft tissue including the upper part of the rotator cuff and glenohumeral labral complex. Glenohumeral motion from 0° to the ABER position was simulated by CT images in 2 different humeral positions. On the basis of simulated humeral motion with respect to the scapula, we measured the stress value on the biceps-labral complex and upper part of the rotator cuff as a consequence of their structural deformation. In addition, we intended to design 2 types of labra--a normal stable labrum and an unstable posterosuperior labrum--to evaluate the geometric alteration and resulting stress change on the posterosuperior labrum against a compressive force from the humeral head and rotator cuff. RESULTS: In the ABER position, the posterosuperior labrum was deformed by the humeral head and interposed posterior part of the rotator cuff. When viewed from the rotator cuff, the posterior part of the rotator cuff came into contact with the posterosuperior labrum as external rotation increased. The measured peak contact stress values were 19.7 MPa and 23.5 MPa for the posterosuperior labrum and the upper rotator cuff, respectively. The stress values for both structures decreased to 5.8 MPa and 18.1 MPa, respectively, in the simulated SLAP model. The root of the long head of the biceps became compressed halfway through the range of motion by the humeral head, especially from the part involving horizontal extension and external rotation, resulting in a high stress of 22.4 MPa. CONCLUSIONS: In this simulated SLAP model, the posterosuperior labrum was medially displaced by the humeral head and upper rotator cuff in the ABER position, causing a functional loss of the spacer effect. CLINICAL RELEVANCE: In SLAP lesions, the posterosuperior labrum loses its ability to function as a spacer in certain positions (especially ABER) and may decrease the important spacer effect between the humerus and the rotator cuff; this may lead to posterosuperior subluxation of the humeral head or rotator cuff abnormalities and tears during repetitive ABER tasks.

Ethyl pyruvate rescues nigrostriatal dopaminergic neurons by regulating glial activation in a mouse model of Parkinson's disease.

This study examined whether ethyl pyruvate (EP) promotes the survival of nigrostriatal dopaminergic (DA) neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. MPTP induced degeneration of nigrostriatal DA neurons and glial activation as visualized by tyrosine hydroxylase, macrophage Ag complex-1, and/or glial fibrillary acidic protein immunoreactivity. Western blotting and immunohistochemistry showed activation of microglial NADPH oxidase and astroglial myeloperoxidase (MPO) and subsequent reactive oxygen species/reactive nitrogen species production and oxidative DNA damage in the MPTP-treated substantia nigra. Treatment with EP prevented degeneration of nigrostriatal DA neurons, increased striatal dopamine levels, and improved motor function. This neuroprotection afforded by EP was associated with the suppression of astroglial MPO expression, NADPH oxidase-, and/or inducible NO synthase-derived reactive oxygen species/reactive nitrogen species production by activated microglia. Interestingly, EP was found to protect DA neurons from 1-methyl-4-phenyl-pyridinium neurotoxicity in cocultures of mesencephalic neurons and microglia but not in neuron-enriched mesencephalic cultures devoid of microglia. The present findings show that EP may inhibit glial-mediated oxidative stress, suggesting that EP may have therapeutic value in the treatment of aspects of Parkinson's disease related to glia-derived oxidative damage.

The vasodilatory effect of ketamine is independent of the N-methyl-D-aspartate receptor: lack of functional N-methyl-D-aspartate receptors in rat mesenteric artery smooth muscle.

BACKGROUND AND OBJECTIVE: Ketamine, which is a general anaesthetic that induces a dissociative anaesthesia, acts by blocking the N-methyl-D-aspartate receptor (NMDAr) in the brain. Although ketamine elevates blood pressure under the clinical setting, the in-vitro effect of ketamine is vasodilatory. However, it is not clear yet whether the vasodilation by ketamine involves functions of the NMDAr. Therefore, we examined whether the NMDAr is functional in vascular smooth muscle and whether the vasodilatory effect of ketamine is associated with the NMDAr. METHODS: We measured isometric tension of endothelium-denuded arterial rings from rat mesentery. The relaxing effects of ketamine, after rings were precontracted with noradrenaline (10 mumol l) or high KCl (70 mmol l), were examined. The effects of DL-2-amino-5-phosphonopentanoic acid (AP-5), a competitive NMDAr blocker that is structurally distinct from ketamine, were also examined. The relaxing effects of ketamine in the presence of AP-5 were compared with those in the absence of AP-5. The effects of NMDAr agonists N-methyl-D-aspartate and glutamate were analysed in order to examine the existence of a functional NMDAr. RESULTS: Both S(+)-ketamine and racemic(+/-)-ketamine, with similar potencies and efficacies and in a concentration-dependent manner, relaxed the precontracted arterial rings. However, AP-5 neither relaxed the arteries nor affected the vasodilatory actions of ketamine. N-methyl-D-aspartate and glutamate (0.01-1 mmol l) had negligible effects on isometric tension under the resting or precontracted condition. CONCLUSION: These results suggest that the NMDAr is not functional in vascular smooth muscle, and the vasodilatory action of ketamine is independent of the NMDAr in the rat mesenteric artery.

Delta neutrophil index as an early predictive marker of severe acute pancreatitis in the emergency department.

Background: Predicting severe acute pancreatitis (AP) in the early clinical stage is important for low morbidity and mortality. Delta neutrophil index (DNI) is used to detect infection and inflammation, but no previous studies have evaluated the usefulness of DNI as an early predictor of progression to severe AP (SAP). Methods: The medical records of patients who were diagnosed with AP at the emergency department (ED) of Wonju Severance Christian Hospital from January 2012 to August 2016 were retrospectively reviewed. The initial DNI obtained in the ED was compared with other inflammatory markers to predict SAP. Multivariate logistic regression was used for statistical analysis. Results: Of the 209 cases included in the analysis, 13 were classified as SAP. Compared to the DNI of the mild to moderately SAP group, that in the SAP group was considerably higher. The DNI showed a positive correlation with the Atlanta classification and bedside index of severity in AP. Using multivariate logistic regression analysis, DNI was an independent predictor of early SAP detection (odds ratio 1.122, 95% CI 1.045-1.205, p = 0.001). Among the biomarkers, DNI had the highest predictive value for SAP. Conclusions: The DNI measured in the ED at presentation is a potentially useful adjunctive marker to predict SAP.

Axotomy-induced dopaminergic neurodegeneration is accompanied with c-Jun phosphorylation and activation transcription factor 3 expression.

Accumulating evidence has shown that both phosphorylated c-Jun (pc-Jun) and activating transcription factor 3 (ATF3) were upregulated in a variety of tissue injuries and proposed to play an important role in cell death/survival. To elucidate the significance and functional role of these immediate-early genes during neuronal damage in the central nervous system, we examined temporal and spatial profiles of pc-Jun and ATF3 in dopaminergic neurons of the substantia nigra (SN) following transection of the medial forebrain bundle (MFB) in adult rats. Morphological characteristics of pc-Jun-positive dopaminergic neurons as well as microglial reaction in response to the axotomy-induced neurodegeneration were also investigated. Following MFB transection, both c-Jun phosphorylation and ATF3 were found in the nuclei of tyrosine hydroxylase-immunoreactive (TH-ir) neurons of the ipsilateral SN, but not in those of the contralateral SN. In the ipsilateral SN, the number of pc-Jun- and ATF3-positive nuclei was increased by 5-7 days post-lesion, and then progressively decreased probably due to the loss of neurons. Retrograde tracing with FluoroGold (FG) in hemi-axotomized rat brain demonstrated that none of the intact, unaxotomized (FG-ir) neurons was pc-Jun-positive, indicating phosphorylation of c-Jun occurs only in axotomized neurons. Concomitant co-localization of pc-Jun and ATF3 in the same TH-ir neuron was also demonstrated by triple immunofluorescence labeling. Many TH-ir neurons that underwent various steps of consecutive neurodegenerative changes retained pc-Jun in the condensed or fragmented nuclei. Moreover, numerous activated microglia, identified by both phagocytic (ED1) and MHC II (OX6) markers, closely apposed to these neurons throughout the entire neurodegenerative process, suggesting that they are actively phagocytosing dying neurons. Taken together, these results support the idea that pc-Jun and its putative dimeric partner ATF3 may be closely participating in axotomy-induced neurodegeneration.

Monitoring of aerial pollutants emitted from Swine houses in Korea.

This on-site survey study was performed to determine the concentrations and emissions of aerial contaminants in the different types of swine houses in Korea and then to present beneficial information available for Korean pig producers to manage optimal air quality in swine house. The swine houses investigated in this research were selected based on three criteria; manure removal system, ventilation mode and growth stage of swine. Mean concentrations of aerial pollutants in swine houses were 8 ppm for ammonia, 300 ppb for hydrogen sulfide, 2 mg m(-3) for total dust, 0.6 mg m(-3) for respirable dust, 4 log(cfu m(-3)) for total airborne bacteria and 3 log(cfu m(-3)) for total airborne fungi, respectively. Mean emissions based on pig (liveweight; 75 kg) and area (m(2)) were 250 and 340 mg h(-1) for ammonia, 40 and 50 mg h(-1) for hydrogen sulfide, 40 and 50 mg h(-1) for total dust, 10 and 15 mg h(-1) for respirable dust, 1.0 and 1.3 log(cfu) h(-1) for total airborne bacteria and 0.7 and 1.0 log(cfu) h(-1) for total airborne fungi, respectively. In general concentrations and emissions of gases were relatively higher in the swine houses managed with deep-pit manure system with slats and mechanical ventilation mode than the different swine housing types whereas those of particulates and bioaerosol were highest in the naturally ventilated swine houses with deep-litter bed system.

Pathological dynamics of activated microglia following medial forebrain bundle transection.

To elucidate the role and pathological dynamics of activated microglia, this study assessed the phagocytic, immunophenotypic, morphological, and migratory properties of activated microglia in the medial forebrain bundle (MFB) axotomized rat brain. Activated microglia were identified using two different monoclonal antibodies: ED1 for phagocytic activity and OX6 for major histocompatibility complex (MHC) class II. Phagocytic microglia, characterized by ED1-immunoreactivity or ED1- and OX6-immunoreactivity, appeared in the MFB and substantia nigra (SN) as early as 1-3 days post-lesion (dpl), when there was no apparent loss of SN dopamine (DA) neurons. Thereafter, a great number of activated microglia selectively adhered to degenerating axons, dendrites and DA neuronal somas of the SN. This was followed by significant loss of these fibers and nigral DA neurons. Activation of microglia into phagocytic stage was most pronounced between 14 approximately 28 dpl and gradually subsided, but phagocytic microglia persisted until 70 dpl, the last time point examined. ED1 expression preceded MHC II expression in phagocytic microglia. All phagocytic microglia sticking to DA neurons showed activated but ramified form with enlarged somas and thickened processes. They were recruited to the SNc from cranial, dorsal and ventral aspects along various structures and finally stuck to DA neurons of the SNc. Characteristic rod-shaped microglia in the white matter were thought to migrate a long distance. The present study strongly suggests that neurons undergoing delayed neurodegeneration may be phagocytosed by numerous phagocytic, ramified microglia at various sites where specific surface signals are exposed or diffusible molecules are released.

PKCdelta-dependent cleavage and nuclear translocation of annexin A1 by phorbol 12-myristate 13-acetate.

Annexin A1 (ANX-1), a calcium-dependent, phospholipid binding protein, is known to be involved in diverse cellular processes, including regulation of cell growth and differentiation, apoptosis, and inflammation. The mitogen phorbol 12-myristate 13-acetate (PMA) induces expression and phosphorylation of ANX-1. However, the roles of ANX-1 in PMA-induced signal transduction is unknown. Here, we study the cellular localization of ANX-1 in the PMA-induced signal transduction process. We have found that PMA induces the cleavage of ANX-1 in human embryonic kidney (HEK) 293 cells, and that the cleaved form of ANX-1 translocates to the nucleus. The PMA-induced nuclear translocation of ANX-1 was inhibited by the protein kinase C (PKC)delta-specific inhibitor rottlerin, indicating that PKCdelta plays a role in nuclear translocation of the cleaved ANX-1. We propose a novel mechanism of PMA-induced translocation of ANX-1 to the nucleus that may participate in the regulation of cell proliferation and differentiation.