Predation on Moose Calves by European Brown Bears

Abstract: In North America, brown bears (Ursus arctos) can be a significant predator on moose (Alces alces) calves. Our study in Sweden is the first in which brown bears are the only predator on moose calves. Bears and moose occurred at densities of about 30/1,000 km² and 920/1,000 km², respectively, and bears killed about 26% of the calves. Ninety-two percent of the predation took place when calves were <1 month old. Bear predation was probably additive to other natural mortality, which was about 10% in areas both with and without bears. Females that lost their calves in spring produced more calves the following year (1.54 calves/F) than females that kept their calves (1.11 calves/F), which reduced the net loss of calves due to predation to about 22%.     

Butyrylcholinesterase and the control of synaptic responses in acetylcholinesterase knockout mice

At the neuromuscular junction (NMJ) acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) can hydrolyze acetylcholine (ACh). Released ACh quanta are known to diffuse rapidly across the narrow synaptic cleft and pairs of ACh molecules cooperate to open endplate channels. During their diffusion through the cleft, or after being released from muscle nicotinic ACh receptors (nAChRs), most ACh molecules are hydrolyzed by AChE highly concentrated at the NMJ. Advances in mouse genomics offered new approaches to assess the role of specific cholinesterases involved in synaptic transmission. AChE knockout mice (AChE-KO) provide a valuable tool for examining the complete abolition of AChE activity and the role of BChE. AChE-KO mice live to adulthood, and exhibit an increased sensitivity to BChE inhibitors, suggesting that BChE activity facilitated their survival and compensated for AChE function. Our results show that BChE is present at the endplate region of wild-type and AChE-KO mature muscles. The decay time constant of focally recorded miniature endplate currents was 1.04 +/- 0.06 ms in wild-type junctions and 5.4 ms +/- 0.3 ms in AChE-KO junctions, and remained unaffected by BChE-specific inhibitors, indicating that BChE is not limiting ACh duration on endplate nAChRs. Inhibition of BChE decreased evoked quantal ACh release in AChE-KO NMJs. This reduction in ACh release can explain the greatest sensitivity of AChE-KO mice to BChE inhibitors. BChE is known to be localized in perisynaptic Schwann cells, and our results strongly suggest that BChE's role at the NMJ is to protect nerve terminals from an excess of ACh.     

Effect of testosterone on oxidative stress and cell damage induced by 3-nitropropionic acid in striatum of ovariectomized rats

This paper evaluates the effects of testosterone (0.5 mg/kg subcutaneously (s.c.) for 8 days) on oxidative stress and cell damage induced by 3-nitropropionic acid (20 mg/kg intraperitoneally (i.p.) for 4 days) in ovariectomized rats. Gonadectomy triggered oxidative damage and cell loss, evaluated by the detection of caspase-3, whereas 3-nitropropionic acid increased the levels of oxidative stress induced by ovariectomy and prompted cell damage characterized by enhanced levels of lactate dehydrogenase. These changes were blocked by testosterone administration. Our results support the following conclusions: i) ovariectomy triggers oxidative and cell damage via caspase-3 in the striatum; ii) 3-nitropropionic acid exacerbates oxidative stress induced by ovariectomy and leads to cell damage characterized by increased levels of lactate dehydrogenase; iii) testosterone administration decreases oxidative stress and cell damage. Additionally, these data support the hypothesis that testosterone might play an important role in the onset and development of neurodegenerative diseases.     

Hypomorphic mutations in the gene encoding a key Fanconi anemia protein, FANCD2, sustain a significant group of FA-D2 patients with severe phenotype

FANCD2 is an evolutionarily conserved Fanconi anemia (FA) gene that plays a key role in DNA double-strand-type damage responses. Using complementation assays and immunoblotting, a consortium of American and European groups assigned 29 patients with FA from 23 families and 4 additional unrelated patients to complementation group FA-D2. This amounts to 3%-6% of FA-affected patients registered in various data sets. Malformations are frequent in FA-D2 patients, and hematological manifestations appear earlier and progress more rapidly when compared with all other patients combined (FA-non-D2) in the International Fanconi Anemia Registry. FANCD2 is flanked by two pseudogenes. Mutation analysis revealed the expected total of 66 mutated alleles, 34 of which result in aberrant splicing patterns. Many mutations are recurrent and have ethnic associations and shared allelic haplotypes. There were no biallelic null mutations; residual FANCD2 protein of both isotypes was observed in all available patient cell lines. These analyses suggest that, unlike the knockout mouse model, total absence of FANCD2 does not exist in FA-D2 patients, because of constraints on viable combinations of FANCD2 mutations. Although hypomorphic mutations arie involved, clinically, these patients have a relatively severe form of FA.     

A library of linear undecapeptides with bactericidal activity against phytopathogenic bacteria

A 125-member library of synthetic linear undecapeptides was prepared based on a previously described peptide H-K¹KLFKKILKF¹⁰L-NH₂ (BP76) that inhibited in vitro growth of the plant pathogenic bacteria Erwinia amylovora, Xanthomonas axonopodis pv. vesicatoria, and Pseudomonas syringae pv. syringae at low micromolar concentrations. Peptides were designed using a combinatorial chemistry approach by incorporating amino acids possessing various degrees of hydrophobicity and hydrophilicity at positions 1 and 10 and by varying the N-terminus. Library screening for in vitro growth inhibition identified 27, 40 and 113 sequences with MIC values below 7.5 μM against E. amylovora, P. syringae and X. axonopodis, respectively. Cytotoxicity, bactericidal activity and stability towards protease degradation of the most active peptides were also determined. Seven peptides with a good balance between antibacterial and hemolytic activities were identified. Several analogues displayed a bactericidal effect and low susceptibility to protease degradation. The most promising peptides were tested in vivo by evaluating their preventive effect of inhibition of E. amylovora infection in detached apple and pear flowers. The peptide H-KKLFKKILKYL-NH₂ (BP100) showed efficacies in flowers of 63–76% at 100 μM, being more potent than BP76 and only less effective than streptomycin, currently used for fire blight control.     

Los mamíferos insulares del Mioceno medio y superior de Menorca (islas Baleares, Mediterráneo occidental)

The insular mammals from the karstic deposits of Punta Nati-2 and the marine beds of es Cul de sa Ferrada, placed in the northwest coast of Minorca (Balearic islands, Spain, western Mediterranean) are described in this work. One of the mammals (only present in Punta Nati-2) is a new glirid species, Margaritamys adroveri, closely related with Margaritamys llulli Mein and Adrover, 1982 and Pseudodryomys granatensis Agustí, 1993, from the middle Miocene of Santa Margalida and Sant Llorenç (Mallorca) and Murchas (Granada), respectively. M. adroveri shows more derived characters than P. granatensis and is more archaic than M. llulli, the size being similar to P. granatensis. The ochotonid present in Minorca is very similar to Gymnesicolagus gelaberti Mein and Adrover, 1982 from Mallorca. In the two minorcan deposits were recovered the first mandibles of this ochotonid, characterized by their big size. The medium weight (estimated from the length of the lower row) for G. aff. gelaberti is 5.4 kg, very similar to that some extant leporids like Lepus alleni Mearns, 1890 or Lepus arcticus Ross, 1819 and higher than any other living ochotonid. Doubtless, the big size of G. aff. gelaberti is a consequence of insular evolution, but not the short diastema, a primitive character shared with continental ochotonids and insular leporids. The discovery of a mandible in the marine beds of es Cul de sa Ferrada permits to place G. aff. gelaberti in the lower Tortonian, which represents the youngest record for this species with respect the faunal associations of Mallorca and Granada, Langhian-Serravalian in age (middle-upper Miocene). The fauna from Punta Nati-2 may represent an endemic association or a faunal group closely related to the fauna of Mallorca and Granada, but in an older context. The age of Gymnesicolagus and the presence of a similar fauna in Mallorca and Minorca suggest a connection between both islands during the Serravalian and the existence of an emerged area in Minorca after the Tortonian transgression.     

S-Nitrosation of proteins during D-galactosamine-induced cell death in human hepatocytes

Nitric oxide (NO) participates in the cell death induced by d-Galactosamine (d-GalN) in hepatocytes, and NO-derived reactive oxygen intermediates are critical contributors to protein modification and hepatocellular injury. It is anticipated that S-nitrosation of proteins will participate in the mechanisms leading to cell death in d-GalN-treated human hepatocytes. In the present study, d-GalN-induced cell death was related to augmented levels of NO production and S-nitrosothiol (SNO) content. The biotin switch assay confirmed that d-GalN increased the levels of S-nitrosated proteins in human hepatocytes. S-nitrosocysteine (CSNO) enhanced protein S-nitrosation and altered cell death parameters that were related to S-nitrosation of the executioner caspase-3. Fifteen S-nitrosated proteins participating in metabolism, antioxidative defense and cellular homeostasis were identified in human hepatocytes treated with CSNO. Among them, seven were also identified in d-GalN-treated hepatocytes. The results here reported underline the importance of the alteration of SNO homeostasis during d-GalN-induced cell death in human hepatocytes.     

Relationships between heterozygosity and fitness in the Iberian threatened larkspur Delphinium bolosii (Ranunculaceae)

The relationship between individual heretozygosity and fitness was explored in the perennial larkspur Delphinium bolosii (Ranunculaceae), an endangered species endemic to Catalonia (North-Eastern Spain), as a part of several studies prior to designing a programme for the reintroduction of this species in a locality where it has been extinct for approximately one century. Allozyme electrophoresis was used to quantify the levels of heterozygosity at nearly to one hundred surveyed individuals in two extant populations. At the same time, eight parameters of vegetative and reproductive fitness were measured. A principal component analysis reduced the original fitness variables to three uncorrelated principal components, two associated with the maternal plant and the other one with the offspring. However, none of the components were significantly correlated with heterozygosity. The low number of variable allozyme markers and the likely influence of ecological factors could be responsible for the lack of correlation between individual heterozygosity and fitness.     

Mapping the binding site of arginine vasopressin to V1a and V1b vasopressin receptors

Starting from the 2.8-A resolution x-ray structure of bovine rhodopsin, three-dimensional molecular models of the complexes between arginine vasopressin and two receptor subtypes (V1a, V1b) have been built. Amino acid sequence alignment and docking studies suggest that four key residues (1.35, 2.65, 4.61, and 5.35) fine tune the binding of vasopressin and related peptide agonists to both receptor subtypes. To validate these predictions, a series of single or double mutants were engineered at V1a and V1b receptor subtypes and tested for their binding and functional properties. Two negatively charged amino acids at positions 1.35 and 2.65 are key anchoring residues to the Arg8 residue of arginine vasopressin. Moreover, two amino acids (V(4.61) and P(5.35)) delineating a hydrophobic subsite at the human V1b receptor are responsible for the recognition of V1b selective peptide agonists. Last, one of the latter positions (5.35) is hypothesized to explain the pharmacological species differences between rat and human vasopressin receptors for a V1b peptide agonist. Altogether these refined three-dimensional models of V1a and V1b human receptors should enable the identification of further new selective V1a and V1b agonists as pharmacological but also therapeutic tools.