EVIDENCE FOR INCREASES IN ANTARCTIC BLUE WHALES BASED ON BAYESIAN MODELLING

Antarctic blue whales ( Balaenoptera musculus intermedia ) are the largest and formerly most abundant blue whale subspecies, but were hunted to near extinction last century. Estimated whaling mortality was unsustainable from 1928 to 1972 (except during 1942–1944), depleting them from 239,000 (95% interval 202,000–311,000) to a low of 360 (150–840) in 1973. Obtaining statistical evidence for subsequent increases has proved difficult due to their scarcity. We fitted Bayesian models to three sighting series (1968–2001), constraining maximum rates of increase to 12% per annum. These models indicated that Antarctic blue whales are increasing at a mean rate of 7.3% per annum (1.4%–11.6%). Informative priors based on blue whale biology (4.3%, SD = 1.9%) and a Bayesian hierarchical meta-analysis of increase rates in other blue whale populations (−3%, SD = 11.6%), suggest plausible increase rates are lower (although the latter has wide intervals), but a meta-analysis of other mysticetes obtains similar rates of increase (6.7%, SD = 4.0%). Possible biases affecting the input abundance estimates are discussed. Although Antarctic blue whales appear to have been increasing since Sovier illegal whaling ended in 1972, they still need to be protected-their estimated 1996 population size, 1,700 (860–2,900), was just 0.7% (0.3%–1.3%) of the pre-exploitation level.     

Temporal and Spatial Occurrence of Female Chinook Salmon Carrying a Male-Specific Genetic Marker in the Columbia River Watershed

Recent declines in many chinook salmon, Oncorhynchus tshawytscha, populations within the Columbia River watershed have prompted an examination of their reproductive biology. In a previous study many female fall chinook salmon collected in 1999 from the Hanford Reach of the Columbia River tested positive for a male-specific DNA marker (OtY1) found on the Y chromosome. The purpose of this study was to determine if females testing positive for the OtY1 marker could be found in other populations of fall chinook salmon from the Columbia River, and to assess the prevalence of OtY1 incidence in different female cohorts. Post-spawned male and female fall chinook salmon from three different naturally spawning populations (Hanford Reach, Yakima River and Ives Island) and one hatchery population (Priest Rapids Hatchery) on the Columbia River were tested in 2000 and 2001 for the OtY1 marker. Among naturally spawning populations, 57.4% of the females tested positive from the Hanford Reach, 33.3% tested positive from the Yakima River, and 32.5% tested positive from Ives Island. Of the Priest Rapids Hatchery fish, 62.5% of the females tested positive, and significant differences were detected between the 1995–1996 and 1997–1998 female cohorts from this population. No significant differences were detected between any of the female cohorts from the naturally spawning populations. All male chinook salmon samples, tested positive for OtY1.     

Cortico-striatal representation of time in animals and humans

Interval timing in the seconds-to-minutes range is crucial to learning, memory, and decision-making. Recent findings argue for the involvement of cortico-striatal circuits that are optimized by the dopaminergic modulation of oscillatory activity and lateral connectivity at the level of cortico-striatal inputs. Striatal medium spiny neurons are proposed to detect the coincident activity of specific beat patterns of cortical oscillations, thereby permitting the discrimination of supra-second durations based upon the reoccurring patterns of subsecond neural firing. This proposal for the cortico-striatal representation of time is consistent with the observed psychophysical properties of interval timing (e.g. linear time scale and scalar variance) as well as much of the available pharmacological, lesion, patient, electrophysiological, and neuroimaging data from animals and humans (e.g. dopamine-related timing deficits in Huntington's and Parkinson's disease as well as related animal models). The conclusion is that although the striatum serves as a 'core timer', it is part of a distributed timing system involving the coordination of large-scale oscillatory networks.     

Structure and denaturation of 4-chlorobenzoyl coenzyme A dehalogenase from <Emphasis Type="Italic">Arthrobacter</Emphasis> sp. strain TM-1

The secondary structure of the trimeric protein 4-chlorobenzoyl coenzyme A dehalogenase from Arthrobacter sp. strain TM-1, the second of three enzymes involved in the dechlorination of 4-chlorobenzoate to form 4-hydroxybenzoate, has been examined. E_mM for the enzyme was 12.59. Analysis by circular dichroism spectrometry in the far uv indicated that 4-chlorobenzoyl coenzyme A dehalogenase was composed mostly of α-helix (56%) with lesser amounts of random coil (21%), β-turn (13%) and β-sheet (9%). These data are in close agreement with a computational prediction of secondary structure from the primary amino acid sequence, which indicated 55.8% α-helix, 33.7% random coil and 10.5% β-sheet; the enzyme is, therefore, similar to the 4-chlorobenzoyl coenzyme A dehalogenase from Pseudomonas sp. CBS-3. The three-dimensional structure, including that of the presumed active site, predicted by computational analysis, is also closely similar to that of the Pseudomonas dehalogenase. Study of the stability and physicochemical properties revealed that at room temperature, the enzyme was stable for 24 h but was completely inactivated by heating to 60°C for 5 min; thereafter by cooling at 1°C min⁻¹ to 45°C, 20.6% of the activity could be recovered. Mildly acidic (pH 5.2) or alkaline (pH 10.1) conditions caused complete inactivation, but activity was fully recovered on returning the enzyme to pH 7.4. Circular dichroism studies also indicated that secondary structure was little altered by heating to 60°C, or by changing the pH from 7.4 to 6.0 or 9.2. Complete, irreversible destruction of, and maximal decrease in the fluorescence yield of the protein at 330–350 nm were brought about by 4.5 M urea or 1.1 M guanidinium chloride. Evidence was obtained to support the hypothetical three-dimensional model, that residues W140 and W167 are buried in a non-polar environment, whereas W182 appears at or close to the surface of the protein. At least one of the enzymes of the dehalogenase system (the combined 4-chlorobenzoate:CoA ligase, the dehalogenase and 4-hydroxybenzoyl coenzyme A thioesterase) appears to be capable of association with the cell membrane.

An intracellular motif of GLUT4 regulates fusion of GLUT4-containing vesicles

Background  

Insulin stimulates glucose uptake by adipocytes through increasing translocation of the glucose transporter GLUT4 from an intracellular compartment to the plasma membrane. Fusion of GLUT4-containing vesicles at the cell surface is thought to involve phospholipase D activity, generating the signalling lipid phosphatidic acid, although the mechanism of action is not yet clear.     

Induction of apoptosis by Drosophila Myc

Myc proteins are essential regulators of cellular growth and proliferation during normal development. Activating mutations in myc genes result in excessive growth and are frequently associated with human cancers. At the same time, forced expression of Myc sensitizes vertebrate cells towards different pro-apoptotic stimuli. Recently, the ability of overexpressed Myc to induce cell-autonomous apoptosis has been shown to be evolutionarily conserved in Drosophila Myc (dMyc). Here, we show that dMyc induced apoptosis is accompanied by the induction of Drosophila p53 mRNA, but that dp53 activity is not essential for dMyc's ability to induce apoptosis. Conversely, larvae carrying a hypomorphic dmyc mutation are more resistant to the apoptosis-promoting effects of X-irradiation. These data suggest that the control of apoptosis is a physiological function of Myc and that dMyc might play a role in the response to DNA damage.     

The twists and turns of Maurer's cleft trafficking in P. falciparum-infected erythrocytes

The malaria parasite, Plasmodium falciparum, invades the red blood cells (RBCs) of its human host and initiates a series of morphological rearrangements within the host cell cytoplasm. The mature RBC has no endogenous trafficking machinery; therefore, the parasite generates novel structures to mediate protein transport. These include compartments called the Maurer's clefts (MC), which play an important role in the trafficking of parasite proteins to the surface of the host cell. Recent electron tomography studies have revealed MC as convoluted flotillas of flattened discs that are tethered to the RBC membrane, prompting speculation that the MC could, in one respect, represent an extracellular equivalent of the Golgi apparatus. Visualization of both resident and cargo proteins has helped decipher the signals and routes for trafficking of parasite proteins to the MC and beyond.     

Trichloroethylene and Human Cancer

Evidence to suggest that trichloroethylene may be a human carcinogen comes mainly from two small epidemiological studies with supporting evidence from human toxicity and genotoxicity studies and from rodent cancer bioassays. Careful analysis of these data reveal marked inconsistencies between the data, differences in the conclusions drawn by various authorities reviewing the same data and, for certain key human studies, a complete absence of exposure data. Much of the rodent cancer data may be dismissed as not indicative of a human hazard because the tumors result from either peroxisome proliferation, or as a consequence of exceptionally high metabolic rates that are found uniquely in mouse tissues, or because the tumors only occur in the presence of overt toxicity. A common mechanism invoked to account for the development of renal tumors in both rats and humans is unproven, there is contrary evidence to suggest that this mechanism does not result in renal cancer, and alternative mechanisms have been proposed. Overall, the uncertainty and lack of consistency throughout the trichloroethylene studies, whether they are in humans, in animals, or in tests in vitro, lead to the conclusion that it would be wholly inappropriate to classify trichloroethylene as a human carcinogen.