3). Bacterial translocation of organisms from the gut in patients learn more with cirrhosis and portal hypertension results in chronic endotoxemia.42 This culminates in a local milieu of proinflammatory cytokines/chemokines, which can up-regulate the adhesion receptor CD11b/CD18 (MAC-1 and complement 3b receptor),

and activate neutrophils through Toll-like receptors (TLR) and chemokine receptors (CXCR1 and CXCR2). Stadlbauer et al.43 demonstrated increased expression of TLR-2, TLR-4, and TLR-9 and decreased expression of CXCR1 and CXCR2 in normal neutrophils incubated with plasma from patients with alcoholic hepatitis. This was associated with phagocytic dysfunction and increased spontaneous OB, endotoxemia, and energy depletion, which was prevented by incubation with albumin, an endotoxin scavenger. Inhibition of TLR-2, TLR-4, and TLR-9 prevented an increase in spontaneous OB and Kinase Inhibitor Library cell line CXCR1/CXR2 expression but did not improve phagocytosis. Ex vivo removal of endotoxin from the plasma of patients with alcoholic hepatitis and cirrhosis decreased neutrophil spontaneous OB and improved phagocytosis.24 In chronic endotoxemia, the adaptive immune system plays a key role in limiting overzealous neutrophil activation by decreasing survival mediated by T regulatory cells.44 Therefore,

the interaction of neutrophils and T regulatory cells in cirrhosis and hyperammonemia warrants further investigation. The rapid recruitment of activated neutrophils to the liver in patients with alcoholic hepatitis/liver injury, and Diflunisal data that supports the development of organ failure in sepsis (both conditions commonly being associated with encephalopathy) results from an inappropriately vigorous response of neutrophils to an inflammatory stimulus.

Therefore, in the context of a patient with cirrhosis, hyperammonemia and chronic endotoxemia, where it has already been shown that neutrophils are pre-primed and have a reduced ability to eliminate bacteria, then it would be logical to suppose that there will be enhanced endothelial–neutrophil interaction within the cerebral microcirculation. This would result in neutrophil adhesion, migration across the blood–brain barrier and the production of chemokines, proinflammatory cytokines, proteases, ROS, and transcription of inflammatory target genes (Fig. 3). It is within this inflammatory milieu that the cerebral effects of ammonia (with or without superimposed infection) will have their greatest impact. Furthermore, astroglial activation promotes neutrophil recruitment by the production of neutrophil-specific chemokines.45 Historically, treatments for HE have been based upon the hypothesis that the colon is the primary source of ammonia and have included dietary protein restriction, the use of nonabsorbable disaccharides and nonabsorbable antibiotics.

“
“This study seeks to identify the delivery method of continuous infusion using a 250 cc this website IV bag via pump, change every 8 h. Additionally, the study will examine the infection risk with the use of 8 h infusions. Ten hemophilia A patients were identified for the study. Each

patient received a bolus factorVIII (FVIII) infusion with a pre FVIII level and 1 h post FVIII level to determine recovery levels for optimal dosing. On the day of 8-h continuous infusion, the pt received a bolus VIII (Kogenate FS ™) for correction to 100% followed by individually calculated continuous infusion (Kogenate FS ™) FVIII. FVIII levels were drawn from the IV bag and peripherally from the patient in the opposite arm at time points: pre infusion, 1, 2, 3, 4, 5, 6 and 8 h. Additionally, blood cultures were drawn from the IV bag and from the IV tubing at time points pre infusion, 4 and 8 h. Fourteen subjects agreed to participate in the study; 4 failed to follow up, hence 10 subjects were included in the analysis of data; 7 severe, 2 moderate, and 1 mild hemophilia A. Age range was 26–62 years. Ethnic breakdown included GS-1101 supplier 5

African American, 4 Caucasian, 1 Hispanic. With all infusions, the range of FVIII was 65–135% (blood) and 62–200% (bag). After the start of infusion, there were no significant differences noted between the hourly FVIII levels in the subjects and the IV values (P-value range 0.36–0.9). Additionally, given mafosfamide three time points with six cultures per patient, totaling 60

points of cultures drawn for the study, all cultures from the IV bag and patient were negative. The effective delivery method and safety of an 8-h continuous infusion of FVIII (Kogenate FS ™) has been confirmed. This method can be helpful given that many hospitals may not carry the required mini-pumps, allowing a standard safe delivery of FVIII (Kogenate FS ™) continuous infusion by available means. “
“The prelims comprise: Half-Title Page Title Page Copyright Page Table of Contents List of Contributors Introduction Preface “
“Summary.  Assessing response to treatment with bypassing agents presents a substantial challenge in the treatment of patients with haemophilia and inhibitors. Rapid and accurate identification of bleeding episodes that are non-responsive to bypassing therapy with either Factor Eight Inhibitor Bypassing Activity (FEIBA; Baxter AG) or recombinant activated factor VII (rFVIIa; NovoSeven®, Novo Nordisk A/S) is essential to guide treatment decisions and optimize patient outcomes through early intervention. Although both bypassing agents are effective, differential responses to therapy necessitate multiple therapeutic options. This article provides a consensus definition for non–life-threatening joint and muscle bleeds that are non-responsive to bypassing agents.

fda.gov). This warning was put forward by the Food and Drug Administration (FDA) in 2002, based on Phase II trials showing a significantly increased incidence of early posttransplant hepatic artery thrombosis and infection-associate deaths (www.fda.gov). Sirolimus has now passed the test of time in several centers, all reporting no increase in the incidence http://www.selleckchem.com/products/MK-2206.html of these complications.14, 20 Like any potent immunosuppressive drug, sirolimus is linked to a potential for development

of numerous side effects, including dyslipidemia, peripheral edema, anemia, leukopenia, delayed wound healing, and a substantially increased risk of incisional hernia.14, 21, 22 In general, however, we believe that these side effects are relatively minor and easy to manage, and that the data revealed by the present study justify a broader use of protocols including sirolimus after liver transplantation for patients with HCC. It should be clearly emphasized that this study was not designed to look at the effect of specific drugs, but rather reports on protocols containing specific drugs. We had no access to drug doses or trough levels. As such, whereas it sounds logical that the improved survival associated with sirolimus-containing protocols is the result of its anticancer effects, we cannot rule out that lower doses of

calcineurin inhibitors (CNIs) were used in these patients, perhaps reinforcing the effect of sirolimus.6 Of all protocols, sirolimus-based immunosuppression PD-1 antibody inhibitor was the only one associated with an improved posttransplantation survival specific to HCC patients (and not to non-HCC patients), further reinforcing the clinical evidence of its anticancer properties. The use of anti-CD25 antibodies demonstrated similar trends to improved survival in both HCC and non-HCC patients. These observations, together with previous reports combining anti-CD25 antibody induction Tyrosine-protein kinase BLK and delayed introduction of CNIs, speak in favor of the use of this drug after

liver transplantation in general.23 Finally, the present data also support the use of tacrolimus-based rather than cyclosporine-based maintenance immunosuppression after liver transplant. The registry nature of the study is linked to several limitations. We did not have access to data on HCC recurrence, which would have been useful to better define the anticancer impact of the drugs. However, due to the lack of access to effective treatment, most patients with HCC recurrence posttransplant are expected to die from the disease, making the rate of survival a reasonable marker. In addition, most deaths occurring during the first 5 years after transplantation for HCC are related to tumor recurrence (and not other causes like HCV recurrence).

FGF19- human repopulated mice had total bile acid pools 3-fold larger than mouse controls, while the FGF19+ mice had total bile acid pools 1.8-fold larger than controls (p<0.05). RNA sequencing revealed that human hepatocytes had markedly upregulated CYP7a selleck compound (rate-controlling enzyme for bile acid

synthesis) despite the high levels of bile acids in the enterohepatic circulation of FGF19- mice. In contrast, CYP7a was near normal in human hepatocytes in the repopulated FGF19+ mice. Conclusions: Disrupted enterohepatic bile acid signaling in human hepato-cyte repopulated mouse livers leads to abnormal enlargement of the bile acid pool and subsequent enlargement of the liver. This defect can be corrected with introduction of the human FGF19 signal into the mouse model, with resultant reduction toward normal

of the bile acid pool and liver size. Control of liver size (“hepatostat”) may be related to size of the bile acid pool and bile acid signaling. Disclosures: Markus Grompe – Board Membership: Yecuris Corp.; Consulting: Yecuris Corp.; Stock Shareholder: Yecuris Corp. The following people have nothing to selleckchem disclose: Willscott E. Naugler The Hippo pathway has recently emerged as a key regulator of organ size and tumor formation; however, the exact molecular mechanisms leading to enlarged organ size are not well understood. Perturbations of the Hippo pathway are often observed in various human cancers and can initiate tumori-genesis in mice. In order SPTLC1 to examine

how the Hippo pathway regulates liver development and tumor formation, we developed transgenic zebrafish that express an activated form of the transcriptional coactivator Yap (Yap1S87A), the downstream target of the Hippo pathway, under the control of a hepato-cyte-specific promoter (fabp10a). Embryonic liver size was greatly increased in Tg(fabp10a:Yap1S87A) transgenic fish at 120 hours post fertilization. Histological and FACS analyses revealed a duplication of hepatocyte number. Hepatomegaly was maintained in adult Tg(fabp10a:Yap1S87A) fish, which exhibited a 2-fold increase in liver:body weight ratio. The livers of Tg(fabp10a:Yap1S87A) fish exhibited signs of dysplasia, but no frank cancers. Exposure of WT and Tg(fab-p10a:Yap1S87A) juveniles to the chemical carcinogen dimeth-ylbenzanthracene (DMBA) provoked liver tumor development, and Tg(fabp10a:Yap1S87A) fish demonstrated dramatically accelerated tumor formation. In order to identify genes that may contribute to the substantial pro-proliferative properties of Yap prior to tumor formation, we performed transcriptomic analysis (RNA-seq) in WT and transgenic adult livers. Interestingly, expression of genes involved in nitrogen metabolism were significantly altered. Particularly striking was a >10-fold increase in glutamine synthase, a central regulator of nitrogen metabolism in the liver.

Prognosis is excellent with spontaneous resolution in most cases. Mortality of HEV is greater than that of HAV, especially in pregnant patients, who have a mortality of 25-30%. No specific antiviral treatment is available for HAV or HEV. Effective immunoprophylaxis

for hepatitis A is widely accessible, while a safe and PF-02341066 purchase effective recombinant HEV vaccine has recently been tested in volunteers. Non-hepatotropic viruses such as herpesviruses, adenoviruses, enteroviruses and parvovirus B-19, among others, can cause acute hepatitis and have significant consequences in immunocompromised individuals. “
“Magnifying endoscopy with flexible spectral imaging color enhancement (FICE) is clinically useful in diagnosing gastric cancer and determining treatment options; however, there is a learning curve. Accurate FICE-based diagnosis requires training and experience. In addition, objectivity is necessary. Thus, a software program that can identify gastric cancer quantitatively was developed. A bag-of-features framework with densely sampled scale-invariant feature transform descriptors to magnifying endoscopy images of 46 mucosal gastric cancers was applied. Computer-based findings were compared with histologic findings. The probability of gastric cancer was calculated by means of logistic regression, and sensitivity and specificity of the system were determined. The average probability was 0.78 ± 0.25 for the images of cancer and 0.31 ± 0.25

for the Quizartinib nmr images of noncancer tissue, with a significant difference between the two groups. An optimal cut-off point of 0.59 was determined on the basis of the receiver operating characteristic curves. The computer-aided diagnosis system yielded a detection accuracy of 85.9% (79/92), sensitivity for a diagnosis of cancer of 84.8% (39/46), and specificity of 87.0% (40/46).

Further development of this system will allow for quantitative evaluation of mucosal gastric cancers on magnifying gastrointestinal endoscopy images obtained with FICE. “
“The reporting of three independent genome-wide association Immune system studies has heralded a burst of excitement for the use of interleukin-28B (IL-28B) polymorphisms in the prediction of spontaneous or treatment-induced hepatitis C virus (HCV) clearance. In the year following the initial reports,1-3 there were more than 20 publications on the subject. Several studies,4-6 including a recent publication in Hepatology,7 argue that IL-28B genotyping will be of central importance for the management of patients. Although we agree that this discovery holds promise for understanding the variable host responses to interferon-α–based regimens, we believe that there may be some confusion with respect to the difference between odds ratio (OR) and the predictive value of the IL-28B genotype as a standalone biomarker. OR describes the strength of association between an IL-28 single-nucleotide polymorphism and virological response. Tanaka et al.

44 Liver abnormalities include (1) asymptomatic

elevation of serum ALT, alkaline phosphatase, and gamma glutamyl transferase as isolated laboratory abnormalities; (2) slowly progressive cholestatic jaundice; and (3) acute hepatocellular injury (hepatitic GVHD).37 Immunosuppressive therapy is not usually indicated when stable, minor elevation of serum enzymes is the only finding. In contrast, patients with jaundice may have histological findings of cholestatic GVHD—lymphocytic infiltration of bile ducts, extensive damage to, and click here loss of, small bile duct epithelial cells, cholestasis, portal fibrosis and piecemeal necrosis.36, 44 Iron overload has been reported to mimic GVHD.15 Patients with steeply rising serum ALT with or without jaundice present a differential diagnosis

of viral infection, drug-injury, and hepatitic GVHD. Hepatitic GVHD is characterized by lobular hepatitis, portal inflammation, and damage to small bile ducts.37, 44 Cytochrome P450 1A2 appears to be a target antigen in GVHD. Acyclovir should be started pending results of viral tests, and if negative, treatment for GVHD started with a calcineurin inhibitor, prednisone 1-2 mg/kg/day, and ursodiol.37 Immunosuppressive drug treatment of cGVHD is successful in only half of patients: 50% are able to discontinue therapy after 5 years, 10% require treatment for longer, and 40% die without resolution of cGVHD.44 The ABT-263 molecular weight only liver-specific therapy is ursodeoxycholic acid (12-15 mg/kg/day), which results in normalization or improvement in liver enzymes.2, 45 Ductopenic GVHD is potentially reversible if ongoing immunologic destruction of epithelium ceases, but this process may take months

before resolution of jaundice.37 Liver transplantation, including living-donor Celastrol transplantation from the original hematopoietic cell donor,46 has been performed for patients with intractable hepatic GVHD. Hepatitis C virus infection in transplant survivors almost always results in chronic hepatitis.7, 47 In the first 10 years posttransplant, there is little liver-related morbidity.7 However, cirrhosis and end-stage liver disease are now prevalent among patients transplanted before the 1990s. Survivors of allogeneic transplant often have suboptimal platelet and granulocyte counts; the long half-life of pegylated interferon may be associated with rapid falls in these counts. Interferon-based therapy may also activate chronic GVHD. The serologic pattern of HBV infection may be atypical in HCT survivors, probably as a consequence of immunosuppression. Clearance of surface antigenemia is particularly likely if the donor was naturally anti-HBs-positive.1 Because HCT survivors are at increased risk of second malignancy or recurrent malignancy, HBV viral status should be reassessed prior to any chemotherapy (particularly rituximab and alemtuzumab) for these cancers.

griseus (Takano et al., 2003). This makes us speculate that BldG serves as a hub in the complex network and connects various environmental and physiological signal inputs to developmental and stress-responsive output processes. Detailed biochemical characterization with respect to the association

learn more of BldG with its binding targets will provide useful information regarding the mechanism of signal switching. This study was supported by the High-tech Research Center Project of MEXT, Japan. Fig. S1. Native polyacrylamide gel electrophoresis (PAGE) analysis of RshA and BldG-6xHis proteins. Table S1. Oligonucleotide primers used in this study. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Radiological Protection Research and Instrumentation

KU-60019 purchase Branch, Atomic energy of Canada Limited, Chalk River, ON K0J 1J0, Canada Trichothecenes are an important family of mycotoxins produced by several species of the genus Fusarium. These fungi cause serious disease on infected plants and postharvest storage of crops, and the toxins can cause health problems for humans and animals. Unfortunately, there are few methods for controlling mycotoxin production by fungal pathogens, and most rely on chemicals, creating therefore subsequent problems of chemical resistance. We tested the impact of the symbiotic arbuscular mycorrhizal fungus Glomus irregulare on a trichothecene-producing strain of Fusarium sambucinum isolated from naturally infected potato plants. Using dual in vitro cultures, we showed that G. irregulare inhibited the growth of F. sambucinum Cell press and significantly reduced the production of the trichothecene 4, 15-diacetoxyscirpenol (DAS). Furthermore, using G. irregulare-colonized potato plants infected with F. sambucinum, we found that the G. irregulare treatment inhibited the production

of DAS in roots and tubers. Thus, in addition to the known beneficial effect of mycorrhizal symbiosis on plant growth, we found that G. irregulare controlled the growth of a virulent fungal pathogen and reduced production of a mycotoxin. This previously undescribed, biological control of Fusarium mycotoxin production by G. irregulare has potential implications for improved potato crop production and food safety. “
“Escherichia coli transformation is an essential step in many molecular biology experiments. Despite earlier advances in the field, many studies including shotgun cloning still require more efficient transformation protocols. Chemical transformation has been the most popular method, in which competent cells are transformed following a brief period of heat shock. Here, we report a novel protocol with higher efficiency, in which competent E.

griseus (Takano et al., 2003). This makes us speculate that BldG serves as a hub in the complex network and connects various environmental and physiological signal inputs to developmental and stress-responsive output processes. Detailed biochemical characterization with respect to the association

Selleckchem PD-1 inhibitor of BldG with its binding targets will provide useful information regarding the mechanism of signal switching. This study was supported by the High-tech Research Center Project of MEXT, Japan. Fig. S1. Native polyacrylamide gel electrophoresis (PAGE) analysis of RshA and BldG-6xHis proteins. Table S1. Oligonucleotide primers used in this study. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Radiological Protection Research and Instrumentation

selleck inhibitor Branch, Atomic energy of Canada Limited, Chalk River, ON K0J 1J0, Canada Trichothecenes are an important family of mycotoxins produced by several species of the genus Fusarium. These fungi cause serious disease on infected plants and postharvest storage of crops, and the toxins can cause health problems for humans and animals. Unfortunately, there are few methods for controlling mycotoxin production by fungal pathogens, and most rely on chemicals, creating therefore subsequent problems of chemical resistance. We tested the impact of the symbiotic arbuscular mycorrhizal fungus Glomus irregulare on a trichothecene-producing strain of Fusarium sambucinum isolated from naturally infected potato plants. Using dual in vitro cultures, we showed that G. irregulare inhibited the growth of F. sambucinum mafosfamide and significantly reduced the production of the trichothecene 4, 15-diacetoxyscirpenol (DAS). Furthermore, using G. irregulare-colonized potato plants infected with F. sambucinum, we found that the G. irregulare treatment inhibited the production

of DAS in roots and tubers. Thus, in addition to the known beneficial effect of mycorrhizal symbiosis on plant growth, we found that G. irregulare controlled the growth of a virulent fungal pathogen and reduced production of a mycotoxin. This previously undescribed, biological control of Fusarium mycotoxin production by G. irregulare has potential implications for improved potato crop production and food safety. “
“Escherichia coli transformation is an essential step in many molecular biology experiments. Despite earlier advances in the field, many studies including shotgun cloning still require more efficient transformation protocols. Chemical transformation has been the most popular method, in which competent cells are transformed following a brief period of heat shock. Here, we report a novel protocol with higher efficiency, in which competent E.

1a); however, under these conditions, we were not able to detect NspC in cells that did not overexpress this protein. To detect wild-type levels of NspC, we had to use a more sensitive detection system, which allowed us to visualize the NspC protein in cells that did not contain the pnspC plasmid. This result ensured that NspC was being expressed from its chromosomal location under our experimental conditions (Supporting Information, Fig. S1). We then assayed the effect of elevated NspC levels on various aspects of V. cholerae physiology. The presence of pnspC altered growth characteristics of the cells such that the lag time was much shorter, the growth rate 1.5-fold higher, and the cell density

at stationary phase also higher (Fig. S2). Proteasome inhibitor Thus, the presence of pnspC appears to impart a growth advantage to V. cholerae Lumacaftor molecular weight under the conditions of our

experiment. Biofilm assays showed that increased production of NspC resulted in an approximately fivefold increase in biofilm cell density (Fig. 1b). This result is in contrast to a previous study which reported an inhibitory effect of ectopic expression of nspC on biofilms formed by V. cholerae O1 El Tor (Lee et al., 2009). The reasons for this disagreement are not known but can potentially be a result of different genetic backgrounds or plasmid systems used in these experiments. Planktonic cell density showed a very small but statistically significant reduction in the strain containing the pnspC plasmid. In most cases, strains that have a high propensity to form biofilms show reduced densities of planktonic cells. The fact that we did not see a large Cyclooxygenase (COX) reduction in planktonic cells overexpressing nspC may be accounted

for by the fact that this strain can grow slightly faster and to higher cell densities. Formation of biofilms usually requires the presence of an exopolysaccharide in the biofilm matrix whose synthesis and export is achieved by proteins encoded by the vps genes (Watnick & Kolter, 1999; Yildiz & Schoolnik, 1999). Under most conditions, increases in biofilm formation are accompanied by increases in vps gene transcription. These genes are found on the V. cholerae large chromosome in two operons: vpsA-K and vpsL-Q (Watnick & Kolter, 1999; Yildiz & Schoolnik, 1999). To test whether increased nspC gene expression also leads to an increase in vps gene transcription, we assayed the activity of the vpsL promoter, making use of a chromosomal vpsLp-lacZ fusion in our strains (Haugo & Watnick, 2002). This insertion does not change the physiological characteristics of the wild-type bacteria such as growth, motility, and biofilm formation under the conditions of our experiments. Increased levels of the NspC protein resulted in a threefold and an eightfold increase in β-galactosidase activity in exponential and stationary-phase cells, respectively (Fig. 1c).

Sample-specific inhibition and in vitro transcription efficiency were determined by quantification of spiked external RNA standard to each RNA extract and its quantification by a specific qPCR assay (Wieczorek et al., 2011). Cellulose and cellobiose were degraded under both oxic and anoxic conditions (Figs 1 and 2; Fig. S1). Products of cellulose hydrolysis (cellobiose or glucose) were not detected (≤ 0.5 μmol gsoil

DW−1) suggesting an efficient assimilation of hydrolysis products. Small amounts of acetate, propionate, and butyrate accumulated in anoxic cellulose-supplemented microcosms (< 5 μmol gsoilDW−1), and ferrous iron formation was stimulated, i.e. ferric iron reducers were active (Fig. 1). Similar product Torin 1 profiles have been observed previously in other aerated soils (Küsel & Drake, 1995; Küsel et al., 2002). Hydrolysis of supplemental cellobiose led to a transient accumulation of glucose (Fig. 2; Fig. S2; Table S2) and could have been caused by β–glucosidases that were released by cellulolytic aerobes (Lynd et al., 2002) under the preceding oxic conditions. Traces of molecular hydrogen were detected in cellobiose-supplemented

microcosms (Fig. 2; Fig. S1), and pH ranged from 4.7 to 6.2 (data not shown). Cellulose degradation was analysed only at high herbicide concentrations (Fig. 1) and revealed that both pesticides have the potential to impair cellulose degradation at oxic and anoxic conditions. The toxic effect of Bentazon and MCPA on cellobiose degradation under oxic conditions was only apparent at concentrations above values that are typical Selleckchem SCH772984 of crop field soils. At typical in situ herbicide concentrations, inhibition of aerobic cellobiose degradation

was not apparent (Fig. 2; Table S3). Under anoxic conditions, Bentazon and MCPA impaired consumption of glucose in cellobiose-supplemented soil microcosms (Figs 1 and 2). Cellobiose consumption rates were not affected (Table S3). This toxic Histone demethylase effect was observed at high and low herbicide concentrations (Figs 1 and 2; Fig. S1). Concentrations of formed organic acids (i.e. acetate, propionate, butyrate) were below the quantification limit (i.e. < 1.5 μmol gsoil DW−1 in total) (data not shown). The production of carbon dioxide and molecular hydrogen was decreased up to 85% and 100%, respectively, and ferrous iron production was negligible (Table S3). Thus, anaerobic cellulose-degradation was highly sensitive to the toxicity of both herbicides. The findings on the toxic effects of the tested two herbicides agree with observations (1) that MCPA that was applied at the recommended dose did not affect either carbon dioxide production, or oxygen uptake or N-mineralization in an cropland soil and (2) that aerobic cellulose degradation was only slightly decreased even when MCPA was spread directly on cellulose sheets (Grossbard, 1971; Schröder, 1979). Nonetheless, reduction of nitrogen mineralization and soil respiration (i.e.