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The subduction zone in northern Chile is a well‐identified seismic gap that last ruptured in 1877. On 1 April 2014, this region was struck by a large earthquake following a two week long series of foreshocks. This study combines a wide range of observations, including geodetic, tsunami, and seismic data, to produce a reliable kinematic slip model of the Mw=8.1 main shock and a static slip model of the Mw=7.7 aftershock. We use a novel Bayesian modeling approach that accounts for uncertainty in the Green's functions, both static and dynamic, while avoiding nonphysical regularization. The results reveal a sharp slip zone, more compact than previously thought, located downdip of the foreshock sequence and updip of high‐frequency sources inferred by back‐projection analysis. Both the main shock and the Mw=7.7 aftershock did not rupture to the trench and left most of the seismic gap unbroken, leaving the possibility of a future large earthquake in the region. A Bayesian ensemble of kinematic slip models is constructed using geodetic, tsunami and seismic dataThe earthquake involved a sharp slip zone, more compact than previously thoughtThe main asperity is located downdip of the foreshock activity and updip of high‐frequency sources

Interferometric synthetic aperture radar (InSAR) time series methods estimate the spatiotemporal evolution of surface deformation by incorporating information from multiple SAR interferograms. While various models have been developed to describe the interferometric phase and correlation statistics in individual interferograms, efforts to model the generalized covariance matrix that is directly applicable to joint analysis of networks of interferograms have been limited in scope. In this work, we build on existing decorrelation and atmospheric phase screen models and develop a covariance model for interferometric phase noise over space and time. We present arguments to show that the exploitation of the full 3‐D covariance structure within conventional time series inversion techniques is computationally challenging. However, the presented covariance model can aid in designing new inversion techniques that can at least mitigate the impact of spatial correlated nature of InSAR observations. Mode to estimate noise budget and uncertainty in InSAR observationsDetailed covariance model for InSAR observationsChecklist for potential users to consider before using InSAR data

We use high‐resolution Synthetic Aperture Radar‐ and GPS‐derived observations of surface displacements to derive the first probabilistic estimates of fault coupling along the creeping section of the San Andreas Fault, in between the terminations of the 1857 and 1906 magnitude 7.9 earthquakes. Using a fully Bayesian approach enables unequaled resolution and allows us to infer a high probability of significant fault locking along the creeping section. The inferred discreet locked asperities are consistent with evidence for magnitude 6+ earthquakes over the past century in this area and may be associated with the initiation phase of the 1857 earthquake. As creeping segments may be related to the initiation and termination of seismic ruptures, such distribution of locked and creeping asperities highlights the central role of the creeping section on the occurrence of major earthquakes along the San Andreas Fault. Significant strain buildup along the SAF creeping segmentDiscreet asperities in the transition zones on the edges of the creeping segmentCreeping segment may have a role on the initiation of past and future earthquakes

We review recent evidencee supporting the discovery of long-range power-law correlations in DNA sequences that contain non-coding regions. The possible interpretation of this finding is also discussed.

We present a rare case of carotid tear caused by iatrogenic erroneous insertion of a dialysis sheath into the common carotid artery (CCA). This was treated by placement of a covered stent-graft in the CCA over the puncture site. This treatment achieved hemostasis while preserving the carotid artery with good outcome. The technical details are presented and the relevant literature regarding treatment of carotid blowout syndrome is discussed. This case suggests that placement of a covered stent-graft is a good option not only for the “usual” blowout syndrome due to head and neck tumors, but also for treatment of iatrogenic injury to the carotid artery.

Objective: While coronary artery disease (CAD) is associated with disturbances of the plasma fibrinolytic system, the nature of these disturbances is not fully defined. Fibrinolysis is regulated by plasmin, whose production is mediated by plasminogen activator conversion of plasminogen (Plg) to plasmin. The cascade is modulated by feedback loops that include Plg activator inhibitor 1 (PAI‐1). Molecular interactions with Plg kringle domains play an important role in regulating plasmin production and its modulation of fibrinolysis. We hypothesized that interactions of tissue plasminogen activator (tPA) with Plg kringle domains regulates plasmin levels in patients with stable CAD. Methods: Plasma was collected from patients (n = 33) with an angiographically significant CAD and controls (n = 18) with angiographically established normal or minimally diseased arteries. Plasmin activity, tPA activity, and plasma levels of Plg, PAI‐1, uPA, and tPA were determined. Results: CAD patients had 1.7‐fold greater plasmin activity (P = 0.02) that correlated with 1.5‐fold higher tPA activity when compared to controls. Epitope mapping of Plg domains showed Plg differences in epitope exposure between the two groups. Plasma from CAD patients had 50% less (P < 0.001) detectable kringle 4 and 48% less (P = 0.007) detectable kringles 1–3. Conclusions: Based on detectable differences in Plg, we conclude that in patients with stable CAD, Plg complexed with tPA exists in a conformation that enables increased tPA activity and Plg conversion to plasmin.

Clinical practice guidelines are a tool to assist with clinical decision making. They provide information about the care for a condition and make recommendations based on research evidence, which can be adapted locally. A focus group within the Allied Health Interest Group of the Australian and New Zealand Burn Association has compiled the “Occupational Therapy and Physiotherapy for the Patient with Burns—Principles and Management Guidelines.” These guidelines are designed as a practical guide to the relevant clinical knowledge and therapy intervention techniques required for effective patient management. Content areas include respiratory management, edema management, splinting and positioning, physical function (mobility, function, exercise), scar management, and psychosocial and mutual elements. The document has undergone extensive review by members of the Australian and New Zealand Burn Association to ensure clarity, internal consistency, and acceptability. The guidelines have been endorsed by the Australian and New Zealand Burn Association. An abridged version of the guidelines is included in this article, with the full document available from www.anzba.org.au.

Spermine is a low molecular weight polyamine involved in the postnatal maturation of the gut. When it is administered orally to suckling rats, it induces maturation of the intestinal tract (liver, pancreas and small intestine). Here we show that this polyamine is able to induce precocious intestinal and splenic development in suckling mice. In fact, in 15-day-old mice which had received spermine orally twice daily for 3 days we observed an increase in the ratio of white pulp surface to total spleen surface in comparison with untreated mice. The two macrophage subsets of the marginal zone and the B-cell population were more developed and reached the development level of 5- or 10-week-old mice. The proliferation rate of B-cells was increased by spermine administration to pups. These observations suggest that spermine might play a role in immune system development; further investigation of its effects are intended, namely the evaluation of its capacity to enhance defence during the neonatal period. Experimental Physiology (2002) 87.1, 69-75.

Imaging subsurface fault slip from surface observations is essential to improving our understanding of the physics of earthquakes and tsunamis. As the estimation of subsurface fault slip is inherently ill‐posed, common inversion methods usually require a regularization term to counteract instabilities. Such regularization introduces biases in inferred slip estimates. Here, we discuss the effects that prior information, implied by a given regularization scheme, can have on fault slip estimates. We propose a novel Equal Posterior Information Condition (EPIC)—based Tikhonov regularization that generalizes the concept of prior information. The EPIC determines variances of prior information based on a chosen form of the structure of the posterior covariance matrix. In the context of subduction zone earthquakes, use of the EPIC counterbalances the spatial heterogeneity of observational constraints on fault slip, improving stability, quality and interpretability of fault slip estimates. We investigate the efficiency of the EPIC in the context of various synthetic fault slip distributions. We also demonstrate the methodology by inferring co‐seismic slip from geodetic data for the 2011 (Mw9.0) Tohoku‐Oki, Japan, earthquake, obtaining robust slip estimates that are similar to those inferred using a unregularized fully Bayesian approach. Inferring the distribution of relative motion across earthquake faults in Earth's subsurface using observations of motion at the surface is an essential component of improving our knowledge of the physics of earthquakes and tsunamis. However, surface observations only provide limited resolution and thus the estimation problem is non‐unique and may be unstable in the presence of noise. Therefore, prior information or regularization is commonly used to control the solutions. We analyze the influence that different regularization schemes have on inferred images of fault motion. In addition, we propose a novel Equal Posterior Information Condition (EPIC) ‐based Tikhonov regularization, that selects a spatially variable strength of regularization to obtain images with spatially uniform precision. In synthetic tests, this new approach shows an improvement of the quality, interpretability and stability of fault motion estimates in the presence of different noise realizations. We investigate the quality of the EPIC‐based regularization on simulated earthquake scenarios and demonstrate the methodology by inferring images of fault slip for the March 11, 2011, (Mw9.0) great Tohoku‐Oki, Japan, earthquake. Common approaches to spatial regularization are susceptible to unstable biases in estimates of subsurface fault slipWe introduce a novel spatially variable regularization scheme called Equal Posterior Information Condition (EPIC) TikhonovUse of EPIC Tikhonov results in robust estimates of fault slip, in terms of stability, bias, and ease of uncertainty analysis Common approaches to spatial regularization are susceptible to unstable biases in estimates of subsurface fault slip We introduce a novel spatially variable regularization scheme called Equal Posterior Information Condition (EPIC) Tikhonov Use of EPIC Tikhonov results in robust estimates of fault slip, in terms of stability, bias, and ease of uncertainty analysis

Syndecan-4 is a unique member of the syndecan gene family that has the ability to bind and activate protein kinase C-alpha. Whereas increased syndecan-4 levels have been noted in ischemic hearts, little is known regarding the regulation of its expression. To investigate the role of cardiac myocytes in induction of syndecan-4 expression, human endothelial cells (ECV304) were exposed to a medium conditioned by primary mouse cardiac myocytes or H9c2 cells. The medium conditioned by hypoxic but not normal myocytes was able to induce syndecan-4 expression in ECV cells. Western analysis of the conditioned medium demonstrated an increased presence of tumor necrosis factor-alpha (TNF-alpha) in the medium conditioned by hypoxic but not normal myoblasts. Primary cardiac myocytes collected from the wild type C57/129 but not the homozygous TNF-alpha-/- knockout mice were able to induce syndecan-4 expression in ECV cells when cultured under hypoxic conditions. In vitro studies demonstrated that TNF-alpha induced endothelial cell syndecan-4 expression by both increasing syndecan-4 gene expression in an NF-kappaB-dependent manner and by prolonging syndecan-4 mRNA half-life. We conclude that TNF-alpha is the principal factor produced by the ischemic myocytes that is responsible for induction of endothelial cell syndecan-4 expression and that this requires both transcriptional and posttranscriptional mechanisms.

To determine the role played by syndecan-4 cytoplasmic domain in the mediation of basic fibroblast growth factor (bFGF) signaling, immortalized human cells (ECV) were used to generate cell lines expressing constructs encoding full-length sequences for syndecan-4 (S4), syndecan-1 (S1), glypican-1 (G1), or chimeric proteins consisting of the ectoplasmic domain of glypican-1 linked to the transmembrane/cytoplasmic domain of syndecan-4 (G1-S4c) and the ectoplasmic domain of syndecan-4 linked to the glypican-1 glycosylphosphatidylinositol (GPI) anchor sequence (S4-GPI). Vector-transduced cells (VC) were used as controls. Expression of all these proteoglycans (except for the vector control) significantly increased cell-associated heparan sulfate mass and the number of low affinity bFGF-binding sites. However, in low serum medium, the addition of bFGF stimulated growth and migration of cells expressing S4 and G1-S4c constructs but not G1, S1, S4-GPI, or VC cells. Similar results were obtained using Matrigel growth assays. Mutations of heparan sulfate attachment sites on S4 construct abolished syndecan-4-dependent augmentation of bFGF responses. We conclude that cytoplasmic tail of syndecan-4 plays an important role in bFGF-mediated signal transduction.

Objective: Because C5a induces tissue injury by activating polymorphonuclear leukocytes, the hypothesis was that inhibition of C5a activity would reduce cardioplegia-related injury. Methods: Pigs were placed on cardiopulmonary bypass. The hearts were arrested for 1 hour with hyperkalemic cardioplegia. Pigs were then separated from bypass, and the hearts were reperfused for 2 hours. Anti-porcine C5a monoclonal antibody (1.6 mg/kg, intravenously; n = 6) was administered 20 minutes before the onset of cardiopulmonary bypass. Six pigs received saline solution vehicle. Reactivity of coronary arterioles was studied in vitro with videomicroscopy. Microvessels from uninstrumented pigs served as controls for vascular studies. Results: Endothelium-dependent relaxation to adenosine diphosphate (percent relaxation of precontraction) was reduced after cardioplegic reperfusion (63% +/- 14% vs 77% +/- 10% in control at 10 @mmol/L; P = .01). This impairment in endothelium-dependent relaxation was improved with anti-porcine C5a monoclonal antibody (80% +/- 22%; P = .01 vs saline solution), as was the impaired endothelium-dependent relaxation to clonidine (64% +/- 12% control; 26% +/- 17% saline solution; 55% +/- 24% anti-porcine C5a monoclonal antibody at 10 @mmol/L; P = .01 saline solution vs control or anti-porcine C5a monoclonal antibody). Myeloperoxidase activity was significantly decreased (0.2 +/- 0.2 units/g protein; P = .04) in the anti-porcine C5a monoclonal antibody group compared with 5.2 +/- 2.7 in the saline solution group. CH"5"0 2 hours after bypass was not statistically different (0.57 +/- 0.41 unit and 0.65 +/- 0.41 unit, respectively) between the anti-porcine C5a monoclonal antibody and saline solution groups. Despite less myocardial polymorphonuclear leukocyte infiltration after C5a inhibition, maximum rate of rise of left ventricular pressure, percent segmental shortening, and blood flow through the left anterior descending coronary artery were similar in the anti-porcine C5a monoclonal antibody and saline solution groups. Conclusions: Inhibition of C5a limits neutrophil-mediated impairment of endothelium-dependent relaxation after cardiopulmonary bypass and cardioplegic reperfusion, but it has no effect on short-term myocardial functional preservation. (J Thorac Cardiovasc Surg 1998;116:1060-8)

Objectives:The present study was designed to study the effects of a single intrapericardial injection of basic fibroblast growth factor on myocardial vascular resistance and endothelium-dependent microvascular dilatation in a porcine model of chronic myocardial ischemia and to investigate the mechanism of ischemia-induced impairment of endothelium-dependent vasodilatation. Methods: Yorkshire pigs underwent ameroid constrictor placement on the left circumflex coronary artery. At 3 weeks, animals were randomized to a single intrapericardial injection of saline solution (n = 10), 30 @mg basic fibroblast growth factor (n = 10), or 2 mg basic fibroblast growth factor (n = 10). Myocardial vascular resistance in the normal (left anterior descending) and ischemic collateral-dependent (left circumflex artery) territories (using colored microspheres) and microvascular reactivity to adenosine diphosphate and sodium nitroprusside were measured before treatment and 4 weeks after treatment. The expression of inducible and endothelial nitric oxide synthase was determined in normal and ischemic myocardium by means of reverse transcriptase-polymerase chain reaction and Western analysis, and the effect of nitric oxide on endothelium-dependent vasodilatation was determined. Results: Compared with results in the control group, treatment with basic fibroblast growth factor resulted in significant improvement in left circumflex artery resistance and endothelium-dependent vasodilatation, reflecting increased collaterals. Myocardial ischemia was associated with increased expression of inducible nitric oxide synthase with no change in endothelial nitric oxide synthase. However, the nitric oxide donor sodium nitroprusside did not affect endothelium-dependent vasodilatation to adenosine diphosphate. Conclusions: A single intrapericardial bolus of basic fibroblast growth factor may be a useful therapeutic strategy for the treatment of myocardial ischemia in patients with coronary artery disease. Although chronic myocardial ischemia is associated with increased expression of inducible nitric oxide synthase, it does not appear to be the cause of altered endothelial function. (J Thorac Cardiovasc Surg 1998;116:1022-8)

A distinguishing feature of Alzheimer's disease (AD) is the deposition of amyloid plaques in brain parenchyma. These plaques arise by the abnormal accumulation of beta A4, a proteolytic fragment of amyloid precursor protein (APP). Despite the fact that neurons are dramatically affected in the course of the disease, little is known about the neuronal processing of APP. To address this question we have expressed in fully mature, synaptically active rat hippocampal neurons, the neuronal form of human APP (APP695), two mutant forms of human APP associated with AD, and the mouse form of APP (a species known not to develop amyloid plaques). Protein expression was achieved via the Semliki Forest Virus system. Expression of wild type human APP695 resulted in the secretion of beta A4‐amyloid peptide and the intracellular accumulation of potential amyloidogenic and non‐amyloidogenic fragments. The relative amount of amyloid‐containing fragments increased dramatically during expression of the clinical mutants, while it decreased strongly when the mouse form of APP was expressed. ‘Humanizing’ the rodent APP sequence by introducing three mutations in the beta A4‐region also led to increased production of amyloid peptide to levels similar to those obtained with human APP. The single Gly601 to Arg substitution alone was sufficient to triple the ratio of beta A4‐peptide to non‐amyloidogenic p3‐peptide. Due to the capacity of these cells to secrete and accumulate intracellular amyloid fragments, we hypothesize that in the pathogenesis of AD there is a positive feed‐back loop where neurons are both producers and victims of amyloid, leading to neuronal degeneration and dementia.(ABSTRACT TRUNCATED AT 250 WORDS)

We have analysed the axonal sorting signals of amyloid precursor protein (APP). Wild‐type and mutant versions of human APP were expressed in hippocampal neurons using the Semliki forest virus system. We show that wild‐type APP and mutations implicated in Alzheimer's disease and another brain beta‐amyloidosis are sorted to the axon. By analysis of deletion mutants we found that the membrane‐inserted APP ectodomain but not the cytoplasmic tail is required for axonal sorting. Systematic deletions of the APP ectodomain identified two regions required for axonal delivery: one encoded by exons 11–15 in the carbohydrate domain, the other encoded by exons 16–17 in the juxtamembraneous beta‐amyloid domain. Treatment of the cells with the N‐glycosylation inhibitor tunicamycin induced missorting of wild‐type APP, supporting the importance of glycosylation in axonal sorting of APP. The data revealed a hierarchy of sorting signals on APP: the beta‐amyloid‐dependent membrane proximal signal was the major contributor to axonal sorting, while N‐glycosylation had a weaker effect. Furthermore, recessive somatodendritic signals, most likely in the cytoplasmic tail, directed the protein to the dendrites when the ectodomain was deleted. Analysis of detergent solubility of APP and another axonally delivered protein, hemagglutinin, demonstrated that only hemagglutinin formed CHAPS‐insoluble complexes, suggesting distinct mechanisms of axonal sorting for these two proteins. This study is the first delineation of sorting requirements of an axonally targeted protein in polarized neurons and indicates that the beta‐amyloid domain plays a major role in axonal delivery of APP.

We performed a prospective study to determine whether 99Tcm-DTPA differential renal function (DRF) in the case of acute obstruction in a unipapillary kidney rat model shows a similar pattern of results as 99Tcm-DMSA in a multipapillary kidney model [1], and to exclude recirculation or a block of tubular transport of DMSA which might explain the discrepancy reported by Kelleher et al.[1]. In 15 male and 4 female Wistar rats (weight 300–350 g), 99Tcm-DMSA renal uptake was measured 24 h before complete obstruction of the right ureter, which served as reference values. Twenty-four hours after obstruction, 99Tcm-DTPA (18.5 MBq) renography and 99Tcm-DMSA (111 MBq) non-depth-corrected renal uptake measurements were performed in the 15 male rats; in the 4 female rats, 740 MBq of 99Tcm-DMSA were injected and absolute, non-depth-corrected renal uptake measured at 24, 48 and 72 h. 99Tcm-DMSA DRF of the right kidney ranged from 48 to 55 (μU: 51; σ: 2) before obstruction and from 14 to 35 (μU: 24; σ: 6) after obstruction, whereas 99Tcm-DTPA DRF ranged from 16 to 30 (μU: 25; σ; 4). No significant differences were found between DRF measured by 99Tcm-DMSA and 99Tcm-DTPA (P= 0.18), or between DRF of the obstructed kidney as measured by 99Tcm-DMSA at 24, 48 and 72 h (P>0.2). Hypothetically, the discrepancy between our findings and those of Kelleher et al.[1] may be due to intratubular pressure. In conclusion, the present findings and those of Kelleher et al.suggest the differences in DRF following complete unilateral renal obstruction, as determined by DTPA and DMSA, are probably species-specific. Furthermore, recirculation and block of tubular transport are unlikely to contribute significantly to differences in DRF as measured by the two radiopharmaceuticals.

Lines of oats (Arena sativaL.) in breeding nurseries at Madison, Wis. ranged from highly resistant to highly susceptible to infection by crown rust (Puccinia coronataCda.). The correlation between crown rust severity (as percentage of leaf area affected) and the protein percentage of the grain averaged −0.470 over a 3‐year period. Forty oat lines at Ames, Iowa ranged from moderate to high in susceptibility, as measured by the relative reduction in yield and seed weight caused by crown rust. With extremely high levels of infection, these strains showed significant variation in response of protein and groat percentages to infection. A significant reduction in protein percentage occurred in one strain and significant increases in protein percentages occurred in five other strains. Overall, the effect of crown rust on protein percentage was negatively correlated with its effects on yield (r=−0.362) and seed weight (r=−0.421). The effects crown rust on protein and groat percentages of the different lines, as measured in diseased plots, were not significantly correlated with either the inherent yields or the inherent protein percentages of the lines in unrusted control plots. This suggests that selection in breeding programs for high yield and high protein percentage could be carried out readily in conjunction with selection for crown rust resistance. The heritabilities of the effects of crown rust on protein and groat percentages were 81 and 91%, respectively.

This paper proposes a novel nonlinear controller that exactly linearizes the dynamics of the A/F-ratio loop in SI-engines. Using nonlinear models of all relevant parts and ideas taken from the feedback linearization approach, a nonlinear state feedback is derived that both performs the usual fuel-film compensation and removes the inherent nonlinearity of A/F-ratio loops. It is shown that the proposed controller has certain similarities with known pragmatic solutions. Some questions connected to the realization (state observation, disturbance decoupling, etc.) are also discussed.

Zooplankton of the Avon-Heathcote Estuary (43°33'S, 172°44'E), Christchurch, was studied at approximately 2-weekly intervals for 6 months over the autumn-winter period. Samples were collected at high tide during the day at 5 stations distributed from the northern head to the estuary mouth. During the sampling period, water temperature varied between 8.0 and 20.5°C, salinity between S = 2.0 and S = 33.5, and suspended matter between 2.9 and 36.8 mg L-1. Ninety-three taxa were identified; most were coastal, marine plankters. Estuarine species included the copepods Gladioferens pectinatus and Halicyclops neglectus, and the ostracods Leptocythere spp. and Propontocypris sp. Two species of rotifer and 6 cladocerans of freshwater origin were found also. Marine species were generally most abundant towards the mouth of the estuary, and estuarine and freshwater species were commonest towards the estuary head. Zooplankton composition at any position within the estuary was not influenced by turbidity, but reflected the degree of mixing of coastal water, fresh water, and residual estuarine water. Some organisms showed evidence of seasonality, but for most, numbers fluctuated markedly between fortnightly samples with no indication of any seasonal patterns. The data confirm the variable nature of estuarine plankton reported elsewhere.

Levamisole has been shown to augment the in vitroresponsiveness of lymphocytes to PHA stimulation. The response of lymphocytes of 14 (42%) of 33 patients with pulmonary tuberculosis was augmented by levamisole. Augmentation was observed in 9 (64%) of 14 PHA hyporesponsives lymphocytes and in 5 (26%) of 19 normo-responsive lymphocytes.

Monthly samples of the burrowing mud crab, Macrophthalmus hirtipes (Jacquinot 1853) were collected from February 1978 to April 1979 from a marine inlet, Governors Bay (43°38'S, 172°39'E) and from the Avon-Heathcote Estuary (43°33'S, 172°44'E), New Zealand. The estuarine population was generally unimodal and had an annual cycle of population change sustained by a concentrated summer recruitment. In contrast, the bay population was unimodal and bimodal at different times, and recruitment occurred thoughout the year with no clear peak. Both populations had equal sex ratios and were dominated by immature individuals (crabs≤10·0 mm carapace width). Estuarine crabs were generally smaller than marine crabs.At both sites, ovigerous females were found from late May to early March; the smallest egg-bearing female measured CW 10·0 mm at the estuary and CW 10·5 mm at the bay. Cycles of ovarian and embryological development were similar at the two localities. Three peaks of egg oviposition occurred within one breeding season and mature females were capable of producing successive broods. Fecundity was related exponentially to female carapace width and did not alter during the breeding season. Estuarine females carried more eggs than marine females of similar size. Egg volume was related to time of oviposition and eggs laid at the start of the breeding season were significantly larger than those deposited during the second half; however, estuarine eggs showed less reduction in size at this time than did marine eggs.Estuarine sediments had higher levels of chlorophyll 'a', ATP, and microorganism activity and productivity than marine sediments. As M. hirtipes is a detritus feeder, the differences in food resources are believed to account for the elevated fecundity of estuarine crabs. At the bay, salinities were high with little tidal and seasonal variation, whereas in the estuary sea water was diluted significantly both daily and seasonally. The differences in salinity characteristics between the sites may be affecting larval distribution; recruitment in the estuary was concentrated to the summer and in the bay it was almost continuous.

Recent studies suggest that some of the heparan sulfate-carrying proteoglycans may directly participate in signaling via their cytoplasmic tail. The present investigation addresses the potential involvement of syndecan-4, a widely expressed transmembrane proteoglycan, in this process. We found that the cytoplasmic tail of syndecan-4 is phosphorylated on a single serine residue (Ser183) in growth-arrested NIH 3T3 fibroblasts, with a stoichiometry of 0.3 mol Pi/mol syndecan-4. Treatment of the cells with a protein kinase C (PKC)-activating phorbol ester lead to a 2.5-fold increase in Ser183 phosphorylation. This increase was inhibited by a generic PKC inhibitor but not by an inhibitor specific to the calcium-dependent conventional PKCs, suggesting that the cytoplasmic tail of syndecan-4 is phosphorylated by a calcium-independent novel PKC isozyme. Application of 10-30 ng/ml basic fibroblast growth factor (bFGF) produced a 2-3-fold reduction in the phosphorylation of syndecan-4. Because treatment with the phosphatase inhibitor calyculin prevented the bFGF-induced decrease in syndecan-4 phosphorylation, the effect of bFGF appears to be mediated by a protein serine/threonine phosphatase type 1 or 2A. We conclude that the cytoplasmic tail of syndecan-4 is subject to in vivo phosphorylation on Ser183, which is regulated by the activities of a novel PKC isozyme and a bFGF-dependent serine/threonine phosphatase.