Marine macrophytes as a global carbon sink.

Marine macrophyte biomass production, burial, oxidation, calcium carbonate dissolution, and metabolically accelerated diffusion of carbon dioxide across the air-sea interface may combine to sequester at least 10(9) tons of carbon per year in the ocean. This carbon sink may partially account for discrepancies in extant global carbon budgets.

Calcium carbonate production, coral reef growth, and sea level change.

Shallow, seaward portions of modern coral reefs produce about 4 kilograms of calcium carbonate per square meter per year, and protected areas produce about 0.8 kilogram per square meter per year. The difference is probably largely a function of water motion. The more rapid rate, equivalent to a maximum vertical accretion of 3 to 5 millimeters per year, places an upper limit on the potential of modern coral reef communities to create a significant vertical structure on a rising sea.

Calcium carbonate production of the mare incognitum, the upper windward reef slope, at enewetak atoll.

Corals and algal pavement produce calcium carbonate more slowly on the windward reef slope of Enewetak Atoll than on the reef flat despite the high standing crop of reef-building organisms on the slope. The capacity of reefs to remain at or near sea level is therefore not determined primarily by growth on the seaward slope.

Coral chronometers: seasonal growth bands in reef corals.

Autoradiagraphs and x-radiographs have been made of vertical sections through the centers of reef corals from Eniwetok. Radioactivity bands in the coral structure are caused by strontium-90 and are related to specific series of nuclear tests, thus making possible calculation of long-term growth rates. These data indicate that the cyclic variations in radial density revealed by x-radiography are annual.

Strontium-calcium thermometry in coral skeletons.

The strontium to calcium ratio of skeletal aragonite in three genera of reef-building corals varies as a simple function of temperature and the strontium to calcium ratio of the incubation water. The strontiumlcalcium distribution coefficients of coral aragonite apparently differ from the corresponding coefficient of inorganically precipitated aragonite. With some care, coral skeletons can be used as recording thermometers.

Soil erosion and significance for carbon fluxes in a mountainous Mediterranean-climate watershed.

In topographically complex terrains, downslope movement of soil organic carbon (OC) can influence local carbon balance. The primary purpose of the present analysis is to compare the magnitude of OC displacement by erosion with ecosystem metabolism in such a complex terrain. Does erosion matter in this ecosystem carbon balance? We have used the Revised Universal Soil Loss Equation (RUSLE) erosion model to estimate lateral fluxes of OC in a watershed in northwestern Mexico. The watershed (4900 km2) has an average slope of 10 degrees +/- 9 degrees (mean +/- SD); 45% is >10 degrees, and 3% is >30 degrees. Land cover is primarily shrublands (69%) and agricultural lands (22%). Estimated bulk soil erosion averages 1350 Mg x km(-2) x yr(-1). We estimate that there is insignificant erosion on slopes < 2 degrees and that 20% of the area can be considered depositional. Estimated OC erosion rates are 10 Mg x km(-2) x yr(-1) for areas steeper than 2 degrees. Over the entire area, erosion is approximately 50% higher on shrublands than on agricultural lands, but within slope classes, erosion rates are more rapid on agricultural areas. For the whole system, estimated OC erosion is approximately 2% of net primary production (NPP), increasing in high-slope areas to approximately 3% of NPP. Deposition of eroded OC in low-slope areas is approximately 10% of low-slope NPP. Soil OC movement from erosional slopes to alluvial fans alters the mosaic of OC metabolism and storage across the landscape.

Neuro-ophthalmologic manifestations of cholangiocarcinoma: a case series.

PurposeTo describe the neuro-ophthalmologic findings of cholangiocarcinoma.MethodsWe report a retrospective chart review of cholangiocarcinoma patients presenting at two tertiary care centers in the Texas Medical Center.ResultsFive patients with neuro-ophthalmologic symptoms related to cholangiocarcinoma were identified. One patient presented with diplopia due to metastasis to the left medial rectus muscle, two patients had metastasis to the occipital lobe resulting in homonymous hemianopsia, one patient had involvement of the clivus resulting in sixth nerve palsy, and one presented with a hypercoagulable state-related stroke causing a homonymous hemianopsia and visual hallucinations.ConclusionsNeuro-ophthalmic manifestations of cholangiocarcinoma depend upon both mechanism and localization. We report five cases of cholangiocarcinoma with neuro-ophthalmologic findings. To our knowledge, this is the largest such series reported in the English language ophthalmic literature.

GABA expression dominates neuronal lineage progression in the embryonic rat neocortex and facilitates neurite outgrowth via GABA(A) autoreceptor/Cl- channels.

GABA emerges as a trophic signal during rat neocortical development in which it modulates proliferation of neuronal progenitors in the ventricular/subventricular zone (VZ/SVZ) and mediates radial migration of neurons from the VZ/SVZ to the cortical plate/subplate (CP/SP) region. In this study we investigated the role of GABA in the earliest phases of neuronal differentiation in the CP/SP. GABAergic-signaling components emerging during neuronal lineage progression were comprehensively characterized using flow cytometry and immunophenotyping together with physiological indicator dyes. During migration from the VZ/SVZ to the CP/SP, differentiating cortical neurons became predominantly GABAergic, and their dominant GABA(A) receptor subunit expression pattern changed from alpha4beta1gamma1 to alpha3beta3gamma2gamma3 coincident with an increasing potency of GABA on GABA(A) receptor-mediated depolarization. GABA(A) autoreceptor/Cl(-) channel activity in cultured CP/SP neurons dominated their baseline potential and indirectly their cytosolic Ca(2+) (Ca(2+)c) levels via Ca(2+) entry through L-type Ca(2+) channels. Block of this autocrine circuit at the level of GABA synthesis, GABA(A) receptor activation, intracellular Cl(-) ion homeostasis, or L-type Ca(2+) channels attenuated neurite outgrowth in most GABAergic CP/SP neurons. In the absence of autocrine GABAergic signaling, neuritogenesis could be preserved by depolarizing cells and elevating Ca(2+)c. These results reveal a morphogenic role for GABA during embryonic neocortical neuron development that involves GABA(A) autoreceptors and L-type Ca(2+) channels.

Glutamate acting at NMDA receptors stimulates embryonic cortical neuronal migration.

During cortical development, embryonic neurons migrate from germinal zones near the ventricle into the cortical plate, where they organize into layers. Mechanisms that direct neuronal migration may include molecules that act as chemoattractants. In rats, GABA, which localizes near the target destination for migrating cortical neurons, stimulates embryonic neuronal migration in vitro. In mice, glutamate is highly localized near the target destinations for migrating cortical neurons. Glutamate-induced migration of murine embryonic cortical cells was evaluated in cell dissociates and cortical slice cultures. In dissociates, the chemotropic effects of glutamate were 10-fold greater than the effects of GABA, demonstrating that for murine cortical cells, glutamate is a more potent chemoattractant than GABA. Thus, cortical chemoattractants appear to differ between species. Micromolar glutamate stimulated neuronal chemotaxis that was mimicked by microM NMDA but not by other ionotropic glutamate receptor agonists (AMPA, kainate, quisqualate). Responding cells were primarily derived from immature cortical regions [ventricular zone (vz)/subventricular zone (svz)]. Bromodeoxyuridine (BrdU) pulse labeling of cortical slices cultured in NMDA antagonists (microM MK801 or APV) revealed that antagonist exposure blocked the migration of BrdU-positive cells from the vz/svz into the cortical plate. PCR confirmed the presence of NMDA receptor expression in vz/svz cells, whereas electrophysiology and Ca2+ imaging demonstrated that vz/svz cells exhibited physiological responses to NMDA. These studies indicate that, in mice, glutamate may serve as a chemoattractant for neurons in the developing cortex, signaling cells to migrate into the cortical plate via NMDA receptor activation.

Disulfide bonds in a recombinant protein modeled after a core repeat in an aquatic insect's silk protein.

We constructed a gene encoding rCAS, recombinant constant and subrepeat protein, modeled after tandem repeats found in the major silk proteins synthesized by aquatic larvae of the midge, Chironomus tentans. Bacterially synthesized rCAS was purified to near homogeneity and characterized by several biochemical and biophysical methods including amino-terminal sequencing, amino acid compositional analysis, sedimentation equilibrium ultracentrifugation, and mass spectrometry. Complementing these techniques with quantitative sulfhydryl assays, we discovered that the four cysteines present in rCAS form two intramolecular disulfide bonds. Mapping studies revealed that the disulfide bonds are heterogeneous. When reduced and denatured rCAS was allowed to refold and its disulfide bonding state monitored, it again adopted a conformation with two intramolecular disulfide bonds. The inherent ability of rCAS to quantitatively form two intramolecular disulfide bonds may reflect a previously unknown feature of the in vivo silk proteins from which it is derived.

Effects of bromocriptine and occlusion of nipples on prolactin receptor and lactose synthetase activity in the mammary gland of the lactating rat.

The response of prolactin receptor and lactose synthetase to suppression of plasma concentrations of prolactin was examined in normal and occluded (teat-sealed) mammary glands of Sprague-Dawley rats, Rats, with mammary glands unilaterally occluded, were given bromocriptine (2.5 mg/kg per 12 h) between 5 and 8 post partum. Bromocriptine reduced plasma prolactin concentrations from 460.4 +/- 120.8 (mean +/- s.e.m.) to 2.56 +/- 0.89 ng/ml within 12h whilst concentrations in control rats were 553.4 +/- 110.25 ng/ml. Lactose synthetase activity declined rapidly, within 24h, in occluded glands of both groups but was maintained for 24 h in normal glands of bromocriptine-treated rats and decreased thereafter. Prolactin receptors also declined significantly within 24h in occluded glands. Desaturation of the prolactin receptor by bromocriptine treatment in vivo was compared with desaturation by exposure of membranes to MgCl2 in vitro. Both treatments enhanced prolactin binding but the increase after treatment with MgCl2 may have been partly artefactual since there was a selective loss of protein from the membranes. These results indicate that the prolactin receptor in rat mammary gland may be maintained after acute suppression of prolactin secretion.

Study of prolactin levels in the ferret.

A radioimmunoassay for canine prolactin has been used to measure prolactin in the ferret. Serial dilutions of extracts of ferret pituitary glands and of ferret plasma yielded curves that were parallel with the canine prolactin standard curve. The sensitivity, accuracy, reproducibility and precision of the assay were within acceptable limits. Plasma prolactin levels increased after the administration of thyrotrophin releasing hormone (TRH) or chlorpromazine, but not after giving luteinizing hormone releasing hormone. Female ferrets, which were anoestrous, oestrous or spayed, and male ferrets had similar basal prolactin levels when sampled under sodium pentobarbitone anaesthesia. These basal levels were higher than in conscious males and the latter also showed a lesser response to TRH. Hypophysectomy significantly reduced basal prolactin levels in female ferrets by 2 h postoperatively and abolished the response to TRH.

Effects of continuous intravenous infusion of an ovine placental extract enriched in placental lactogen on plasma hormones, metabolites and metabolite biokinetics in non-pregnant sheep.

Continuous intravenous infusions of saline or of a placental extract containing ovine placental lactogen were given to three non-pregnant, non-lactating ewes over periods of 36 h, 1 week apart. During saline infusion no placental lactogen was detected in jugular vein plasma. but infusion of the placental extract raised the placental lactogen concentration from undetectable to 40-50 micrograms/l, similar to concentrations in ewes with one fetus on day 90 of pregnancy. By comparison with the saline control period, infusion of the placental extract consistently increased both plasma concentrations and irreversible loss of nonesterified fatty acids. Plasma concentrations of glucose and urea, but not irreversible loss of these metabolites, were consistently increased. Although the placental extract was not subjected to extensive purification, it was enriched in placental lactogen and contained no detectable contamination with insulin, prolactin or growth hormone. The results are suggestive of a role for placental lactogen in modifying metabolism and acting during pregnancy to provide nutrients for fetal metabolism.

Placental lactogen in the goat in relation to stage of gestation, number of fetuses, metabolites, progesterone and time of day.

Placental lactogen has been measured in goats throughout pregnancy by radioreceptor assay of prolactin-like activity. Lactogenic activity, which is not prolactin, increased from less than 5 nmol/l in week 8 to 27 nmol/l by week 16. There was no further change until term. Plateau concentrations (week 16 to term) were highest in animals carrying triplets, 49.5 nmol/l. There were marked functuations in placental lactogen over a 24 h period. These short-term fluctuations were not related to changes in glucose, non-esterified fatty acids or, in two animals, progesterone. However, there was a negative correlation between mean concentrations of placental lactogen and glucose in plasma of 20 goats sampled over a 24 h period between weeks 15 and 20 of gestation. There was no difference in placental lactogen concentration from week 16 to term between goats in their first and second pregnancies although the normal period of increase in placental lactogen was delayed by some 3 weeks in goats in their second pregnancy. In hemimastectomized goats, hypophysectomy on day 60 did not affect placental lactogen but daily treatment with bromocriptine (5 mg/day) from day 60 to day 120 blocked the normal rise in concentration.

SGN-10. Seattle Genetics.

Seattle Genetics is developing SGN-10 (BR96-SCIT), a single-chain immunotoxin (SCIT) under license from Bristol-Myers Squibb (BMS), as both a monotherapy and in combination with Taxotere (Rhône-Poulenc Rorer) for the potential treatment for cancer [308773]. SGN-10 is currently in phase I clinical trials [308773], [369809], [382807], [408963], [410348]. The compound is a follow-up to SGN-15 (BR96-DOX; BMS) and is potentially more effective and cheaper to manufacture. It delivers a bacterial toxin which is 250-times more potent than BR96-DOX and is one third the size, hence enabling tumor penetration more easily. BMS submitted an IND for SGN-10 in the first quarter of 1996 [200849], [204704]. BMS licensed the SCA-protein (single-chain antigen-binding protein) technology from Enzon in 1993 [352743]. In April 1998, Seattle Genetics completed a licensing agreement with BMS to take over development of SGN-10 [308773].

Nitrate esters as nitric oxide donors: SS-nitrates.

[structure: see text]. The important biological secondary messenger NO can be generated from exogenous nitrovasodilators and NO donors. Nitrate esters are nitrovasodilators and NO mimetics, believed to be biotransformed to NO in vivo. On the basis of a mechanistic hypothesis, nitrates have been synthesized that release NO at significant rates in neutral aqueous solution in the presence only of added thiol. The novel masked beta-mercaptonitrates reported (SS-nitrates), provide information on possible sulfhydryl-dependent biotransformation mechanisms for nitrates in clinical use.