Plant functional types and elevated CO2: A method of scanning for causes of community alteration

In this paper, a general method for an a posteriori plant functional type (PFT) analysis of global change effects on community composition is developed. We apply the method to a case study, specifically the Giessen-FACE experiment. This experiment involves a Central European meadow that has been exposed to moderate CO2-enrichment since May 1998.The method for an a posteriori PFT-analysis: The method consists of four working steps and uses a combination of standard gradient analysis and Random Forests (RF). (1) The trait composition of the species is studied using Principal Components Analysis. Species trait information is gathered from databases. Natural PFT, i.e. groups of species with similar trait-sets, are identified specifically for the community under study. (2) A ranking of the species according to standardized/absolute CO2 abundance response is obtained from Redundancy Analysis. Initially, species with a response above or below the median are grouped into three response groups (RG) each having similar behaviour, i.e. positive/negative or no-response. (3) The outlyingness measure of RF is used to shift RG boundaries until satisfactory RG homogeneity is achieved. RF is utilized to find the best traits for the RG classification. The behaviour of species representative of the RG is derived from RF class centers. (4) From knowledge gained in steps 1-3, hypotheses about the causes underlying the community alteration are built. Strengths/weaknesses of the method are discussed.Application of the method to the case study: The community consists of three natural PFT. Five species are summer-green forbs of varying competitiveness. Four species are evergreen ruderal forbs characterized as (semi-) basal rosette plants. The third natural PFT contains evergreen, more or less competitive species, mostly grasses, but also a few forbs.Negative standardized CO2-response was practically restricted to two natural PFT, i.e. the summer-greens, irrespective of their competitiveness, and the evergreen ruderals. Standard positive response covered part of the evergreen competitive natural PFT. Among them was Glechoma hederacea, one of the forbs with the greatest similarity to grasses. Two hypotheses were formulated to explain the response pattern: (1) Summer-greens lost in competition with evergreens, because the annual time-integral they can use for enhanced growth was more limited with year-round CO2-enrichment. (2) As rosette plants, ruderal evergreens lagged behind evergreen competitors because periods with full sunlight, which enabled them to gain additional carbon, were shorter for them.Absolute responses were additionally dependent on dominance patterns. The most striking difference to standard responses was the restriction of positive response to (sub-)dominant grasses

Excluding random walks in the foraging behaviour of the portunid crab Thalamita crenata: modelisation and simulation based on real data

Présentation avec posterinfo:eu-repo/semantics/publishedHexennial International Conference ‘Meeting on Mangrove ecology, functioning and Management – MMM3’, 2-6 juillet, Galle, Sri Lank

Hypothalamic and gonadal components of hypogonadism in boys with Prader-Labhart-Willi syndrome

CONTEXT: The specific form of hypogonadism in Prader-Labhart-Willi syndrome (PWS), central or peripheral, remains unexplained. OBJECTIVES: The objectives of this study were to investigate the cause of hypogonadism in PWS and determine whether human chorionic gonadotropin (hCG) treatment can restore pubertal development. DESIGN: This was a clinical follow-up study, divided into two samples, over a duration of 1.5 and 4.5 yr. PATIENTS: Eight male infants and six peripubertal boys (age at start of observation, 0.06-0.93 and 8.1-10.8 yr, respectively) with genetically confirmed PWS were studied. INTERVENTION: hCG (500-1500 U twice weekly) was given from age 13.5 yr to the present. MAIN OUTCOME MEASURES: Serum FSH, LH, inhibin B, and testosterone levels and pubertal development were the main outcome measures. RESULTS: Infants with PWS presented normal LH (2.3 +/- 0.7 U/liter) and testosterone (2.5 +/- 0.9 nmol/liter) levels (mean +/- sem at 5 months) compared with the reference range. However, two thirds of the boys displayed cryptorchidism. Inhibin B levels were at the lowest level of the normal range and decreased significantly between infancy and puberty (at 13 yr, 72 +/- 17 pg/ml), whereas FSH secretion increased (9.9 +/- 2.6 U/liter). Pubertal maturation stopped at an average bone age of 13.9 yr. hCG therapy increased testosterone (11 +/- 2 nmol/liter) and reduced FSH (at 16 yr, 1.1 +/- 0.9 U/liter) levels. Testicular volume (5.6 +/- 1 ml) and inhibin B (26.5 +/- 11.9 pg/ml) remained low. CONCLUSION: Children with PWS display a specific form of combined hypothalamic (low LH) and peripheral (low inhibin B and high FSH) hypogonadism, suggesting a primary defect in Sertoli and/or germ cell maturation or an early germ cell loss. hCG therapy stimulates testosterone production and virilization

Monocarboxylate transporter 8 deficiency: Altered thyroid morphology and persistent high triiodothyronine/thyroxine ratio after thyroidectomy.

Context Thyroid hormone transport across the plasma membrane depends on transmembrane transport proteins, including monocarboxylate transporter 8 (MCT8). Mutations in MCT8 (or SLC16A2) lead to a severe form of X-linked psychomotor retardation, which is characterised by elevated plasma triiodothyronine (T(3)) and low/normal thyroxine (T(4)). MCT8 contributes to hormone release from the thyroid gland. Objective To characterise the potential impact of MCT8-deficiency on thyroid morphology in a patient and in Mct8-deficient mice. Design Thyroid morphology in a patient carrying the A224V mutation was followed by ultrasound imaging for over 10 years. After thyroidectomy, a histopathological analysis was carried out. The findings were compared with histological analyses of mouse thyroids from the Mct8(-/y) model. Results We show that an inactivating mutation in MCT8 leads to a unique, progressive thyroid follicular pathology in a patient. After thyroidectomy, histological analysis revealed gross morphological changes, including several hyperplastic nodules, microfollicular areas with stromal fibrosis and a small focus of microfollicular structures with nuclear features reminiscent of papillary thyroid carcinoma (PTC). These findings are supported by an Mct8-null mouse model in which we found massive papillary hyperplasia in 6- to 12-month-old mice and nuclear features consistent with PTC in almost 2-year-old animals. After complete thyroidectomy and substitution with levothyroxine (l-T(4)), the preoperative, inadequately low T(4) and free T(4) remained, while increasing the l-T(4) dosage led to T(3) serum concentrations above the normal range. Conclusions Our results implicate peripheral deiodination in the peculiar hormonal constellation of MCT8-deficient patients. Other MCT8-deficient patients should be closely monitored for potential thyroid abnormalities

Neuronal 3',3,5-triiodothyronine (T₃) uptake and behavioral phenotype of mice deficient in Mct8, the neuronal T₃ transporter mutated in Allan-Herndon-Dudley syndrome.

Thyroid hormone transport into cells requires plasma membrane transport proteins. Mutations in one of these, monocarboxylate transporter 8 (MCT8), have been identified as underlying cause for the Allan-Herndon-Dudley syndrome, an X-linked mental retardation in which the patients also present with abnormally high 3 ',3,5-triiodothyronine (T-3) plasma levels. Mice deficient in Mct8 replicate the thyroid hormone abnormalities observed in the human condition. However, no neurological deficits have been described in mice lacking Mct8. Therefore, we subjected Mct8-deficient mice to a comprehensive immunohistochemical, neurological, and behavioral screen. Several behavioral abnormalities were found in the mutants. Interestingly, some of these behavioral changes are compatible with hypothyroidism, whereas others rather indicate hyperthyroidism. We thus hypothesized that neurons exclusively dependent on Mct8 are in a hypothyroid state, whereas neurons expressing other T-3 transporters become hyperthyroid, if they are exposed directly to the high plasma T-3. The majority of T-3 uptake in primary cortical neurons is mediated by Mct8, but pharmacological inhibition suggested functional expression of additional T-3 transporter classes. mRNAs encoding six T-3 transporters, including L-type amino acid transporters (LATs), were coexpressed with Mct8 in isolated neurons. We then demonstrated Lat2 expression in cultured neurons and throughout murine brain development. In contrast, LAT2 is expressed in microglia in the developing human brain during gestation, but not in neurons. We suggest that lack of functional complementation by alternative thyroid hormone transporters in developing human neurons precipitates the devastating neurodevelopmental phenotype in MCT8-deficient patients, whereas Mct8-deficient mouse neurons are functionally complemented by other transporters, for possibly Lat2