A phylogenetic analysis of <Emphasis Type="Italic">Leucothoe</Emphasis> s.l. (Ericaceae; tribe Gaultherieae) based on phenotypic characters

Phylogenetic relationships within the genus Leucothoe s.l. (including all eight species) and related taxa of the Gaultherieae, Andromedeae, and Vaccinieae were investigated by a cladistic analysis based on phenotypic (external morphology, anatomy, chromosome number, and secondary chemistry) characters. The parsimony analysis resulted in two most parsimonious trees, both very similar, which show Leucothoe s.l. to be polyphyletic, with its species distributed among three distinct clades. Our results indicate that L. racemosa and L. recurva form a strongly supported clade, which is sister to Chamaedaphne calyculata, and these three species are probably the sister-group of the wintergreen clade (consisting of Gaultheria and Diplycosia). Leucothoe axillaris, L. fontanesiana, L. davisiae, L. griffithiana, and L. keiskei, consistently form a monophyletic group corresponding to Leucothoe s.s., which is probably sister to the remaining members of the tribe Gaultherieae. Leucothoe grayana, the final species traditionally placed in the genus, belongs to neither of these clades and may be sister to Andromeda. Phenotypic characters provide no support for the monophyly of Leucothoe, instead suggesting that it is polyphyletic, in agreement with preliminary DNA-based analyses. Thus, we redefine the genus Leucothoe, placing its species into three genera: 1) Eubotrys (the E. racemosa + E. recurva clade), 2) Leucothoe s.s. (the L. axillaris + L. fontanesiana + L. davisiae + L. griffithiana + L. keiskei clade), and 3) Eubotryoides (containing only E. grayana).     

Investigating health at Kerma: sacrificial versus nonsacrificial individuals

This analysis examines heterogeneity in risks by assessing the health status of individuals in two distinct burial contexts from the Nubian site of Kerma: sacrificial (n = 100) and nonsacrificial (n = 190) burial areas dated to the classic Kerma period ( approximately 1750-1500 BC). Indicators of physiological stress that were examined include cribra orbitalia, dental enamel hypoplasia, tibial osteoperiostitis, and femur length. The analysis presented here shows that the people interred in the sacrificial and nonsacrificial burial contexts at Kerma in Upper Nubia had similar health profiles that were comparable with other contemporaneous samples from the region. If sacrificial individuals did not experience the same risk of death as nonsacrificial individuals, it was not evident in the frequencies of nonspecific stress indicators. However, this differential risk of death may be blurred by our inability to examine nonadults for childhood disease. This research demonstrates the complexities involved in understanding the multiple factors that result in heterogeneity in skeletal samples.     

Mitochondrial DNA deletion mutations: a causal role in sarcopenia.

Mitochondrial DNA (mtDNA) deletion mutations accumulate with age in tissues of a variety of species. Although the relatively low calculated abundance of these deletion mutations in whole tissue homogenates led some investigators to suggest that these mutations do not have any physiological impact, their focal and segmental accumulation suggests that they can, and do, accumulate to levels sufficient to affect the metabolism of a tissue. This phenomenon is most clearly demonstrated in skeletal muscle, where the accumulation of mtDNA deletion mutations remove critical subunits that encode for the electron transport system (ETS). In this review, we detail and provide evidence for a molecular basis of muscle fiber loss with age. Our data suggest that the mtDNA deletion mutations, which are generated in tissues with age, cause muscle fiber loss. Within a fiber, the process begins with a mtDNA replication error, an error that results in a loss of 25-80% of the mitochondrial genome. This smaller genome is replicated and, through a process not well understood, eventually comprises the majority of mtDNA within the small affected region of the muscle fiber. The preponderance of the smaller genomes results in a dysfunctional ETS in the affected area. As a consequence of both the decline in energy production and the increase in oxidative damage in the region, the fiber is no longer capable of self-maintenance, resulting in the observed intrafiber atrophy and fiber breakage. We are therefore proposing that a process contained within a very small region of a muscle fiber can result in breakage and loss of muscle fiber from the tissue.     

Dynamics and regulation of TSH secretion by superfused anterior pituitary cells

Superfused dispersed cells respond rapidly to 2- to 10-min pulses of TRH (10(-10) to 10(-7) M) in a dose-dependent manner. The effects of decreasing the stimulus duration can be overcome by a proportional increase in concentration of TRH. A TRH stimulus of 10 min or greater duration results in a sharp peak in TSH secretion followed by a lower plateau. Somatostatin (10(-8) M inhibits the response to TRH (t X 10(-9) M). T3 (2.0 microgram/dl) inhibits TRH-induced TSH secretion by superfused pituitary fragments, but not by dispersed cells. Corticosterone (50 microgram/dl), however, inhibits crude CRF-induced ACTH secretion by such cells.     

Prostatic Alpha-Linolenic Acid (ALA) Is Positively Associated with Aggressive Prostate Cancer: A Relationship Which May Depend on Genetic Variation in ALA Metabolism

Previous observational studies have reported associations between prostate cancer and alpha-linolenic acid (ALA). However, few investigations have been able to study this relationship prospectively and in well-controlled settings. Moreover, no studies have determined whether single nucleotide polymorphisms (SNPs) that influence ALA metabolism are associated with this common cancer. The purpose of this study was to explore associations between prostatic levels of ALA, SNPs and prostate cancer-specific biomarkers in samples collected from a previous randomized clinical trial conducted using a presurgical model and which tested the effects of flaxseed supplementation, a rich source of ALA, prior to prostatectomy (n = 134). Serum prostate-specific antigen (PSA) was determined and immunohistochemistry was used to assess tumor proliferation rate (Ki67). Prostatic ALA was determined with gas chromatography. Seven previously identified SNPs associated with delta-6 desaturase activity (rs99780, rs174537, rs174545, rs174572, rs498793, rs3834458 and rs968567) were tested for associations with prostatic ALA, PSA and Ki67. Despite consuming seven times more ALA per day, men in the flaxseed arm had similar amounts of prostatic ALA relative to men not consuming flaxseed. In unadjusted analysis, there were significant positive associations between prostatic ALA and PSA (ρ = 0.191, p = 0.028) and Ki67 (ρ = 0.186, p = 0.037). After adjusting for covariates (flaxseed, age, race, BMI and statin-use) the association between ALA and PSA remained (p = 0.004) but was slightly attenuated for Ki67 (p = 0.051). We did not observe associations between any of the SNPs studied and prostatic ALA; however, in models for PSA there was a significant interaction between rs498793 and ALA and for Ki67 there were significant interactions with ALA and rs99780 and rs174545. Independent and inverse associations were observed between rs174572 and Ki67. This study provides evidence that prostatic ALA, independent of the amount of ALA consumed, is positively associated with biomarkers of aggressive prostate cancer and that genetic variation may modify this relationship.