Function of marshes in reducing eutrophication of estuaries of the Middle Atlantic Region

Annual nitrogen, phosphorus and carbon budgets for two Virginia salt marshes were determined by monthly measurements of water discharge and constituent concentrations over tidal cycles. Considering all three forms of phosphorus measured (total, dissolved organic and orthophosphate) there was a net loss from the estuary to the marshes. The data reveal a loss of particulate μhosphorus of estuarine origin to marsh sediments and mineralization of this phosphorus in the marshes with subsequent export of dissolved inorganic and organic phosphorus back to the estuary. Nitrogen flux data show a loss of nitrate and nitrite to the marshes. Particulate nitrogen is imported to the marshes where it is mineralized and returned to the estuary as ammonia and dissolved organic nitrogen. The magnitude of nitrogen export suggests significant fixation of atmospheric nitrogen by marsh flora with subsequent export as dissolved species. Carbon flux data show significant contributions of both particulate and dissolved organic carbon to the estuary from the marshes. Estimates of export, based on marsh grass productivity, suggest a loss of 36 and 49% of a years primary production on the marshes as detritus for Ware and Carter Creeks respectively

Public health implications of 1990 air toxics concentrations across the United States.

Occupational and toxicological studies have demonstrated adverse health effects from exposure to toxic air contaminants. Data on outdoor levels of toxic air contaminants have not been available for most communities in the United States, making it difficult to assess the potential for adverse human health effects from general population exposures. Emissions data from stationary and mobile sources are used in an atmospheric dispersion model to estimate outdoor concentrations of 148 toxic air contaminants for each of the 60,803 census tracts in the contiguous United States for 1990. Outdoor concentrations of air toxics were compared to previously defined benchmark concentrations for cancer and noncancer health effects. Benchmark concentrations are based on standard toxicological references and represent air toxic levels above which health risks may occur. The number of benchmark concentrations exceeded by modeled concentrations ranged from 8 to 32 per census tract, with a mean of 14. Estimated concentrations of benzene, formaldehyde, and 1,3-butadiene were greater than cancer benchmark concentrations in over 90% of the census tracts. Approximately 10% of all census tracts had estimated concentrations of one or more carcinogenic HAPs greater than a 1-in-10,000 risk level. Twenty-two pollutants with chronic toxicity benchmark concentrations had modeled concentrations in excess of these benchmarks, and approximately 200 census tracts had a modeled concentration 100 times the benchmark for at least one of these pollutants. This comprehensive assessment of air toxics concentrations across the United States indicates hazardous air pollutants may pose a potential public health problem

CLASSIFICATION OF THYMUS-DERIVED AND MARROW-DERIVED LYMPHOCYTES BY DEMONSTRATION OF THEIR ANTIGEN-BINDING CHARACTERISTICS

Antigen-binding cells of T and B origin can readily be determined by quantitating the number of sheep erythrocytes per rosette after glutaraldehyde fixation. The T1 and T2 populations have low antigen-binding properties and are very unstable without fixation. The B1 and B2 populations are stable and correlate with precursor and secretory cells. Fixation of rosettes permits a sensitive test for studying differentiation of T and B cells

Eigen-transitions in cantilever cylindrical shells subjected to vertical edge loads

A thin cantilever cylindrical shell subjected to a transverse shear force at the free end can experience two distinct modes of buckling, depending on its relative thickness and length. If the former parameter is fixed then a short cylinder buckles in a diffuse manner, while the eigenmodal deformation of a moderately long shell is localised, both axially and circumferentially, near its fixed end. Donnelltype buckling equations for cylindrical shells are here coupled with a non-symmetric membrane basic state to produce a linear boundary-value problem that is shown to capture the transition between the aforementioned instability modes. The main interest lies in exploring the approximate asymptotic separation of the independent variables in the corresponding stability equations, when the eigen-deformation is doubly localised. Comparisons with direct numerical simulations of the full buckling problem provide further insight into the accuracy and limitations of our approximations

On the Possibility of Measuring the Gravitomagnetic Clock Effect in an Earth Space-Based Experiment

In this paper the effect of the post-Newtonian gravitomagnetic force on the mean longitudes $l$ of a pair of counter-rotating Earth artificial satellites following almost identical circular equatorial orbits is investigated. The possibility of measuring it is examined. The observable is the difference of the times required to $l$ in passing from 0 to 2$\pi$ for both senses of motion. Such gravitomagnetic time shift, which is independent of the orbital parameters of the satellites, amounts to 5$\times 10^{-7}$ s for Earth; it is cumulative and should be measured after a sufficiently high number of revolutions. The major limiting factors are the unavoidable imperfect cancellation of the Keplerian periods, which yields a constraint of 10$^{-2}$ cm in knowing the difference between the semimajor axes $a$ of the satellites, and the difference $I$ of the inclinations $i$ of the orbital planes which, for $i\sim 0.01^\circ$, should be less than $0.006^\circ$. A pair of spacecrafts endowed with a sophisticated intersatellite tracking apparatus and drag-free control down to 10$^{-9}$ cm s$^{-2}$ Hz$^{-{1/2}}$ level might allow to meet the stringent requirements posed by such a mission.Comment: LaTex2e, 22 pages, no tables, 1 figure, 38 references. Final version accepted for publication in Classical and Quantum Gravit

Local Application of BMP-2 Specific Plasmids in Fibrin Glue does not Promote Implant Fixation

<p>Abstract</p> <p>Background</p> <p>BMP-2 is known to accelerate fracture healing and might also enhance osseointegration and implant fixation. Application of recombinant BMP-2 has a time-limited effect. Therefore, a gene transfer approach with a steady production of BMP-2 appears to be attractive. The aim of this study was to examine the effect of locally applied BMP-2 plasmids on the bone-implant integration in a non-weight bearing rabbit tibia model using a comparatively new non-viral copolymer-protected gene vector (COPROG).</p> <p>Methods</p> <p>Sixty rabbits were divided into 4 groups. All of them received nailing of both tibiae. The verum group had the nails inserted with the COPROG vector and BMP-2 plasmids using fibrin glue as a carrier. Controls were a group with fibrin glue only and a blank group. After 28 and 56 days, these three groups were sacrificed and one tibia was randomly chosen for biomechanical testing, while the other tibia underwent histomorphometrical examination. In a fourth group, a reporter-gene was incorporated in the fibrin glue instead of the BMP-2 formula to prove that transfection was successful.</p> <p>Results</p> <p>Implant fixation strength was significantly lower after 28 and 56 days in the verum group. Histomorphometry supported the findings after 28 days, showing less bone-implant contact.</p> <p>In the fourth group, successful transfection could be confirmed by detection of the reporter-gene in 20 of 22 tibiae. But, also systemic reporter-gene expression was found in heterotopic locations, showing an undesired spreading of the locally applied gene formula.</p> <p>Conclusion</p> <p>Our results underline the transfecting capability of this vector and support the idea that BMP-2 might diminish osseointegration. Further studies are necessary to specify the exact mechanisms and the systemic effects.</p

AA-Amyloidosis Can Be Transferred by Peripheral Blood Monocytes

Spongiform encephalopathies have been reported to be transmitted by blood transfusion even prior to the clinical onset. Experimental AA-amyloidosis shows similarities with prion disease and amyloid-containing organ-extracts can prime a recipient for the disease. In this systemic form of amyloidosis N-terminal fragments of the acute-phase reactant apolipoprotein serum amyloid A are the main amyloid protein. Initial amyloid deposits appear in the perifollicular region of the spleen, followed by deposits in the liver. We used the established murine model and induced AA-amyloidosis in NMRI mice by intravenous injections of purified amyloid fibrils (‘amyloid enhancing factor’) combined with inflammatory challenge (silver nitrate subcutaneously). Blood plasma and peripheral blood monocytes were isolated, sonicated and re-injected into new recipients followed by an inflammatory challenge during a three week period. When the animals were sacrificed presence of amyloid was analyzed in spleen sections after Congo red staining. Our result shows that some of the peripheral blood monocytes, isolated from animals with detectable amyloid, contained amyloid-seed that primed for AA-amyloid. The seeding material seems to have been phagocytosed by the cells since the AA-precursor (SAA1) was found not be expressed by the monocytes. Plasma recovered from mice with AA amyloidosis lacked seeding capacity. Amyloid enhancing activity can reside in monocytes recovered from mice with AA-amyloidosis and in a prion-like way trigger amyloid formation in conjunction with an inflammatory disorder. Human AA-amyloidosis resembles the murine form and every individual is expected to be exposed to conditions that initiate production of the acute-phase reactant. The monocyte-transfer mechanism should be eligible for the human disease and we point out blood transfusion as a putative route for transfer of amyloidosis

Meeting Report: Moving Upstream—Evaluating Adverse Upstream End Points for Improved Risk Assessment and Decision-Making

Background Assessing adverse effects from environmental chemical exposure is integral to public health policies. Toxicology assays identifying early biological changes from chemical exposure are increasing our ability to evaluate links between early biological disturbances and subsequent overt downstream effects. A workshop was held to consider how the resulting data inform consideration of an “adverse effect” in the context of hazard identification and risk assessment. Objectives Our objective here is to review what is known about the relationships between chemical exposure, early biological effects (upstream events), and later overt effects (downstream events) through three case studies (thyroid hormone disruption, antiandrogen effects, immune system disruption) and to consider how to evaluate hazard and risk when early biological effect data are available. Discussion Each case study presents data on the toxicity pathways linking early biological perturbations with downstream overt effects. Case studies also emphasize several factors that can influence risk of overt disease as a result from early biological perturbations, including background chemical exposures, underlying individual biological processes, and disease susceptibility. Certain effects resulting from exposure during periods of sensitivity may be irreversible. A chemical can act through multiple modes of action, resulting in similar or different overt effects. Conclusions For certain classes of early perturbations, sufficient information on the disease process is known, so hazard and quantitative risk assessment can proceed using information on upstream biological perturbations. Upstream data will support improved approaches for considering developmental stage, background exposures, disease status, and other factors important to assessing hazard and risk for the whole population

ILC3 function as a double-edged sword in inflammatory bowel diseases

Inflammatory bowel diseases (IBD), composed mainly of Crohn’s disease (CD) and ulcerative colitis (UC), are strongly implicated in the development of intestinal inflammation lesions. Its exact etiology and pathogenesis are still undetermined. Recently accumulating evidence supports that group 3 innate lymphoid cells (ILC3) are responsible for gastrointestinal mucosal homeostasis through moderate generation of IL-22, IL-17, and GM-CSF in the physiological state. ILC3 contribute to the progression and aggravation of IBD while both IL-22 and IL-17, along with IFN-γ, are overexpressed by the dysregulation of NCR− ILC3 or NCR+ ILC3 function and the bias of NCR+ ILC3 towards ILC1 as well as regulatory ILC dysfunction in the pathological state. Herein, we feature the group 3 innate lymphoid cells’ development, biological function, maintenance of gut homeostasis, mediation of IBD occurrence, and potential application to IBD therapy