Meta-analysis of New Zealand's nitrous oxide emission factors for ruminant excreta supports disaggregation based on excreta form, livestock type and slope class.

Globally, animal excreta (dung and urine) deposition onto grazed pastures represents more than half of anthropogenic nitrous oxide (N2O) emissions. To account for these emissions, New Zealand currently employs urine and dung emission factor (EF3) values of 1.0% and 0.25%, respectively, for all livestock. These values are primarily based on field studies conducted on fertile, flatland pastures predominantly used for dairy cattle production but do not consider emissions from hill land pastures primarily used for sheep, deer and non-dairy cattle. The objective of this study was to determine the most suitable urine and dung EF3 values for dairy cattle, non-dairy cattle, and sheep grazing pastures on different slopes based on a meta-analysis of New Zealand EF3 studies. As none of the studies included deer excreta, deer EF3 values were estimated from cattle and sheep values. The analysis revealed that a single dung EF3 value should be maintained, although the value should be reduced from 0.25% to 0.12%. Furthermore, urine EF3 should be disaggregated by livestock type (cattle > sheep) and topography (flatland and low sloping hill country > medium and steep sloping hill country), with EF3 values ranging from 0.08% (sheep urine on medium and steep slopes) to 0.98% (dairy cattle on flatland and low slopes). While the mechanism(s) causing differences in urine EF3 values for sheep and cattle are unknown, the 'slope effect' on urine EF3 is partly due to differences in soil chemical and physical characteristics, which influence soil microbial processes on the different slope classes. The revised EF3 values were used in an updated New Zealand inventory approach, resulting in 30% lower national N2O emissions for 2017 compared to using the current EF3 values. We recommend using the revised EF3 values in New Zealand's national greenhouse gas inventory to more accurately capture N2O emissions from livestock grazing.

Impact of urease inhibitor on ammonia and nitrous oxide emissions from temperate pasture soil cores receiving urea fertilizer and cattle urine.

New Zealand's intensively grazed pastures receive the majority of nitrogen (N) input in the form of urea, which is the major constituent of animal urine and the most common form of mineral N in inorganic N fertilizers. In soil, urea is rapidly hydrolyzed to ammonium (NH4(+)) ions, a part of which may be lost as ammonia (NH3) and subsequently as nitrous oxide (N2O), which is a greenhouse gas. Two glasshouse experiments were conducted to study the effect of a urease inhibitor (UI), N-(n-butyl) thiophosphoric triamide (NBPT), commercially named Agrotain, applied with urine and urea on urea hydrolysis and NH3 and N2O emissions. Treatments included the commercially available products Sustain Yellow (urea+Agrotain+4% sulfur coating), Sustain Green (urea+Agrotain) and urea, and cattle urine (476 kg N ha(-1)) with and without Agrotain applied to intact soil cores of a fine sandy loam soil. The addition of Agrotain to urine and urea (i.e. Sustain Green) reduced NH3 emission by 22% to 47%, respectively. Agrotain was also effective in reducing N2O emissions from urine and Sustain Green by 62% and 48%, respectively. The reduction in N2O emissions varied with the type and amount of N applied and plant N uptake. Plant N uptake was significantly higher in the soil cores receiving Agrotain with urea than urea alone, but the slight increase in dry matter yield was non-significant. Hence, urease inhibitor reduced N losses through NH3 and N2O emissions, thereby increasing plant uptake of N.

CYLD mutations in familial skin appendage tumours.

BACKGROUND: Germ-line mutations in CYLD are found in patients with familial skin appendage tumours. The protein product functions as a deubiquitinase enzyme, which negatively regulates NF-kappaB and c-Jun N-terminal kinase signalling. Brooke-Spiegler syndrome (BSS) is characterised by cylindromas, trichoepitheliomas and spiradenomas, whereas in familial cylindromatosis (FC) patients present with cylindromas and in multiple familial trichoepitheliomas (MFT) with trichoepitheliomas as the only skin tumour type. Although described as distinct entities, recent studies suggest that they are within the spectrum of a single entity. OBJECTIVE: To investigate the mutation spectrum of CYLD and possible genotype-phenotype correlations. METHODS: 25 families including 13 BSS, 3 FC, and 9 MFT families were examined and evaluated for mutations in the CYLD gene. RESULTS: In total, 18 mutations in CYLD, including 6 novel mutations, were identified in 25 probands (72%). The mutation frequencies among distinct phenotypes were 85% for BSS, 100% for FC, and 44% for MFT. The majority of the mutations were insertions, deletions or nonsense mutations leading to formation of truncated proteins. All mutations were located between exons 9 to 20, encoding the NEMO binding site and the catalytic domain. Genotype-phenotype analysis failed to reveal a correlation between the types of mutations and their location within the gene and the patients' phenotypes and disease severity. CONCLUSIONS: This study provides further evidence on the role of CYLD in the pathogenesis of skin appendage tumours characterised by cylindromas, trichoepitheliomas and/or spiradenomas, but the molecular mechanisms of CYLD in skin tumorigenesis and the reasons for phenotypic variability remain to be explored.

Modelling organic matter dynamics in New Zealand soils.

To ensure the sustainability of land systems in terms of nutrient cycling and maintenance of soil physical conditions, there is a need to understand soil organic matter (SOM) and its dynamics. It has been suggested that soil-carbon (C) models developed internationally do not perform well under New Zealand's unique climatic and soil mineralogical conditions. To test this hypothesis, we conducted 14C-labelled ryegrass decomposition studies and assessed the influence of abiotic factors on decomposition rates. These factors were characterized by estimating system mean residence times (MRTs) from estimates of first-order rate coefficients in a simple, three-compartment model. A range of MRTs obtained for decomposition was related to climatic conditions and soil properties. We summarise this work and extend this study to apply the Rothamsted soil-C turnover model, a five-compartment model, to our data with the view of testing both the model projections and the decomposability factors assumed in the model.

New Ultraviolet spectrophotometric method for the estimation of nimesulide.

Two simple and accurate ultraviolet (UV) spectrophotometric methods with better detection range for estimation of nimesulide in pure form and in solid dosage form were developed in the present studies using 50% v/v and 100% v/v acetonitrile as the solvent system. The linearity range of nimesulide in both the methods was found to be 10-50 micrograms/ml at a lambda max of 300 nm. The linear regression equations obtained by the least-square regression method are Abs = 1.33 x 10(-1).Conc + 1.89 x 10(-1) in 50% v/v acetonitrile and Abs = 1.05 x 10(-1).Conc + 1.14 x 10(-1) in 100% v/v acetonitrile. The detection limit as per the error propagation theory was found to be 0.46 microgram/ml and 1.04 micrograms/ml, respectively, in 50% v/v and 100% v/v acetonitrile. The developed methods were employed with high degree of precision and accuracy for the estimation of total drug content in three commercial tablet formulations of nimesulide. The results of the analysis were validated statistically and by recovery studies.

Multiple endocrine neoplasia type 1: clinical and genetic features of the hereditary endocrine neoplasias.

MEN1 is a syndrome of parathyroid adenomas, gastrinomas, prolactinomas, and other endocrine tumors. Collagenomas and facial angiofibromas are newly recognized but common skin expressions. Many tumors in MEN1 are benign; however, many entero-pancreatic neuroendocrine tumors and foregut carcinoid tumors are malignant. MEN1 is thus the expression of a cancer gene but without available prevention or cure for malignancy. Hereditary (as compared to sporadic) endocrine tumors show early onset age and multiplicity, because each cell of the body has "one hit" by inheritance. Multiple neoplasia syndromes with endocrine tumor(s) all include nonendocrine components; their known defective genes seem mainly to disturb cell accumulation. Hereditary neoplasia/hyperplasia of one endocrine tissue reflects a defect that is tissue selective and directed at cell secretion. Though the hereditary endocrine neoplasias are rare, most of their identified genes also contribute to common sporadic endocrine neoplasms. Hereditary tumors may be caused by activation of an oncogene (e.g., RET) or, more often, by inactivation of a tumor suppressor gene (e.g., P53, MEN1). Recently, MEN1 was identified by positional cloning. This strategy included narrowing the gene candidate interval, identifying many or all genes in that interval, and testing the newly identified candidate genes for mutation in MEN1 cases. MEN1 was identified because it showed mutation in 14 of 15 MEN1 cases. NIH testing showed germline MEN1 mutations in 47 of 50 MEN1 index cases and in seven of eight cases with sporadic MEN1. Despite proven capacity to find germline MEN1 mutation, NIH testing found no MEN1 mutation among five families with isolated hyperparathyroidism, suggesting that this often arises from mutation of other gene(s). Analogous studies in Japan found that familial isolated pituitary tumors also did not show MEN1 germline mutation. MEN1 mutation testing can now be considered for cases of MEN1 and its phenocopies and for asymptomatic members of families with known MEN1 mutation. Germline MEN1 testing does not have the urgency of RET testing in MEN2a and 2b, as MEN1 testing does not commonly lead to an important intervention. Somatic MEN1 mutation was found in sporadic tumors: parathyroid adenoma (21%), gastrinoma (33%), insulinoma (17%), and bronchial carcinoid (36%). For each of these, MEN1 was the known gene most frequently mutated. MEN1 has a widely expressed mRNA that encodes a protein (menin) of 610 amino acids. The protein sequence is not informative about domains or functions. The protein was mainly nuclear. Menin binds to JunD, an AP-1 transcription factor, inhibiting JunD's activation of transcription. Most of the germline and somatic MEN1 mutations predict truncation of menin, a likely destructive change. Inactivating MEN1 mutations in germline and in sporadic neoplasms support prior predictions that MEN1 is a tumor suppressor gene. Germline MEN1 mutation underlies all or most cases of MEN1 (familial or sporadic). Somatic MEN1 mutation is the most common gene mutation in many sporadic endocrine tumor types.

Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription.

MEN1 is a tumor suppressor gene that encodes a 610 amino acid nuclear protein (menin) of previously unknown function. Using a yeast two-hybrid screen with menin as the bait, we have identified the transcription factor JunD as a direct menin-interacting partner. Menin did not interact directly with other Jun and Fos family members. The menin-JunD interaction was confirmed in vitro and in vivo. Menin repressed transcriptional activation mediated by JunD fused to the Gal4 DNA-binding domain from a Gal4 responsive reporter, or by JunD from an AP1-responsive reporter. Several naturally occurring and clustered MEN1 missense mutations disrupted menin interaction with JunD. These observations suggest that menin's tumor suppressor function involves direct binding to JunD and inhibition of JunD activated transcription.

Somatic mutation of the MEN1 gene in parathyroid tumours.

Primary hyperparathyroidism is a common disorder with an annual incidence of approximately 0.5 in 1,000 (ref. 1). In more than 95% of cases, the disease is caused by sporadic parathyroid adenoma or sporadic hyperplasia. Some cases are caused by inherited syndromes, such as multiple endocrine neoplasia type 1 (MEN1; ref. 2). In most cases, the molecular basis of parathyroid neoplasia is unknown. Parathyroid adenomas are usually monoclonal, suggesting that one important step in tumour development is a mutation in a progenitor cell. Approximately 30% of sporadic parathyroid tumours show loss of heterozygosity (LOH) for polymorphic markers on 11q13, the site of the MEN1 tumour suppressor gene. This raises the question of whether such sporadic parathyroid tumours are caused by sequential inactivation of both alleles of the MEN1 gene. We recently cloned the MEN1 gene and identified MEN1 germline mutations in fourteen of fifteen kindreds with familial MEN1 (ref. 10). We have studied parathyroid tumours not associated with MEN1 to determine whether somatic mutations in the MEN1 gene are present. Among 33 tumours we found somatic MEN1 gene mutation in 7, while the corresponding MEN1 germline sequence was normal in each patient. All tumours with MEN1 gene mutation showed LOH on 11q13, making the tumour cells hemi- or homozygous for the mutant allele. Thus, somatic MEN1 gene mutation for the mutant allele. Thus, somatic MEN1 gene mutation contributes to tumorigenesis in a substantial number of parathyroid tumours not associated with the MEN1 syndrome.

Regulation of male fertility by pyrimethamine in adult mice.

Studies were carried out to determine the antifertility and reversibility effect of pyrimethamine (PYR) in adult male mice. The parameters mainly included sperm count and motility, fertility, histoarchitecture of testis and testicular cell kinetics quantitatively following oral administration of PYR (50 mg/kg body weight per day) for 30 days. The same parameters were also studied in PYR-treated animals which were allowed to recover for 45 days (recovery group). The results suggest that sperm motility as well as counts were significantly decreased in PYR-treated animals, and the fertility rate fell to zero. Testicular histology as well as germ cell kinetics were altered. However, in the animals of the recovery group, all the parameters studied were more or less similar to those of control animals. The study demonstrates the antifertility as well as reversible efficacy of PYR.