Is Eriocnemis luciani meridae (Aves: Trochilidae) a diagnosable taxon and does it come from Venezuela, with remarks on the collectors Salomn Briceo and Walther Frederick Henninger.

Eriocnemis luciani meridae was originally described from a single specimen collected in the late 19th century in western Venezuela. Subsequently a second specimen of E. luciani, also labelled Venezuela, has been taken as additional proof for a highly disjunct population of this hummingbird, which otherwise ranges from southwest Colombia to southern Peru (taxonomy-dependent). Eriocnemis l. meridae has been accepted by all of the global checklists of birds, but has been routinely ignored by Venezuelan sources. In an effort to resolve this dichotomy of treatment, we re-examined the specimens plumage in comparison with relevant material in two major European bird collections. We found that the characters used to erect E. l. meridae are only doubtfully or weakly expressed in the holotype and appear invisible in the Ohio specimen, but both are clearly referrable to the species E. luciani. Evidence that the second specimen was definitely collected in Venezuela is weak and its overall provenance is unclear. In contrast, an extensive historical investigation of the relevant collectors indicates that the holotype does appear to have been taken in Venezuela, although perhaps not in the precise locality indicated for it. This leaves an unusual situation whereby we consider the case for a separate Venezuelan endemic taxon to be unproven, but there is no incontrovertible reason to exclude the species from the countrys avifauna; according to recent niche modelling data it is best searched for in the Sierra Nevada of Mrida state. In contrast, a second subspecies of E. luciani, E. l. baptistae, described by the same authors as endemic to part of western Ecuador is, according to our reappraisal, clearly diagnosable and is upheld.

Cerebral venous thrombosis during pregnancy in the setting of type I antithrombin deficiency: case report and literature review.

Inherited antithrombin deficiency is estimated to carry a 50% risk of a venous thrombotic complication during each pregnancy and puerperium. We present a case of a female with heterozygous type I antithrombin deficiency who presented with a central nervous system transverse sinus thrombosis in the third trimester of pregnancy despite the use of therapeutic doses of low molecular weight heparin, as venous thromboembolic prophylaxis, since conception. A successful pregnancy outcome was achieved with the combined use of therapeutic anticoagulation and regular plasma-derived antithrombin concentrate infusions to normalize her antithrombin levels. This case lends further debate to the issue of whether antithrombin concentrate, in addition to anticoagulation, should be routinely administered for venous thromboembolic prophylaxis during pregnancy and the puerperium to women with inherited antithrombin deficiency. This point may become more relevant as further experience is gained with the use of recombinant human antithrombin.

Calcitonin plays a critical role in regulating skeletal mineral metabolism during lactation.

The maternal skeleton rapidly demineralizes during lactation to provide calcium to milk, responding to the stimuli of estrogen deficiency and mammary-secreted PTH-related protein. We used calcitonin/calcitonin gene-related peptide-alpha (Ctcgrp) null mice to determine whether calcitonin also modulates lactational mineral metabolism. During 21 d of lactation, spine bone mineral content dropped 53.6% in Ctcgrp nulls vs. 23.6% in wild-type (WT) siblings (P < 0.0002). After weaning, bone mineral content returned fully to baseline in 18.1 d in Ctcgrp null vs. 13.1 d in WT (P < 0.01) mice. Daily treatment with salmon calcitonin from the onset of lactation normalized the losses in Ctcgrp null mice, whereas calcitonin gene-related peptide-alpha or vehicle was without effect. Compared with WT, Ctcgrp null mice had increased circulating levels of PTH and up-regulation of mammary gland PTH-related protein mRNA. In addition, lactation caused the Ctcgrp null skeleton to undergo more trabecular thinning and increased trabecular separation compared with WT. Our studies confirm that an important physiological role of calcitonin is to protect the maternal skeleton against excessive resorption and attendant fragility during lactation and reveal that the postweaning skeleton has the remarkable ability to rapidly recover even from losses of over 50% of skeletal mineral content.