The ecosystem service of property protection and exposure to environmental stressors in the Gulf of Mexico.

Environmental stressors such as sea-level rise, erosion, and increased storm frequency and intensity are exposing coastal properties to greater amounts of damage. Coastal habitats like beaches, dunes, seagrasses, and wetlands can help reduce exposure and property damage. Using InVEST's Coastal Vulnerability Model, an exposure index value was calculated for every 250 m2 segment along the coastline in Escambia and Santa Rosa counties in Florida, USA. Nineteen sea level-by-habitat management scenarios were evaluated for a suite of shoreline segments across multiple exposures that can be used to inform local decision making as part of larger strategies for coastal management. Overall, a rise in sea level and degradation of coastal habitats could decrease the number of lower exposed shoreline segments and increase the number of higher exposed shoreline segments. These results were used to identify changes in the amount of potential residential property damage among different scenarios. Under high sea levels, additional protection to coastal habitats could reduce the amount of residential property damage resulting from one tropical cyclone event by $50.4 million (2018 US dollars (USD)) (by the year 2050) and by $71.8 million (2018 USD) (by the year 2100) in Escambia and Santa Rosa counties. This research demonstrates the effects that habitat type/abundance and sea-level rise could have on vulnerable coastlines. The results of the modeled scenarios can be incorporated into several recent community resiliency planning initiatives in the region to develop more robust management plans and preparations for a changing environment.

Linking People to Coastal Habitats: A meta-analysis of final ecosystem goods and services on the coast.

Coastal ecosystem goods and services (EGS) have steadily gained traction in the scientific literature over the last few decades, providing a wealth of information about underlying coastal habitat dependencies. This meta-analysis summarizes relationships between coastal habitats and final ecosystem goods and services (FEGS) users. Through a "weight of evidence" approach synthesizing information from published literature, we assessed habitat classes most relevant to coastal users. Approximately 2,800 coastal EGS journal articles were identified by online search engines, of which 16% addressed linkages between specific coastal habitats and FEGS users, and were retained for subsequent analysis. Recreational (83%) and industrial (35%) users were most cited in literature, with experiential-users/hikers and commercial fishermen most prominent in each category, respectively. Recreational users were linked to the widest diversity of coastal habitat subclasses (i.e., 22 of 26). Whereas, mangroves and emergent wetlands were most relevant for property owners. We urge EGS studies to continue surveying local users and identifying habitat dependencies, as these steps are important precursors for developing appropriate coastal FEGS metrics and facilitating local valuation. In addition, understanding how habitats contribute to human well-being may assist communities in prioritizing restoration and evaluating development scenarios in the context of future ecosystem service delivery.

COASTAL HABITAT CHANGE AND MARINE MEGAFAUNA BEHAVIOR: FLORIDA MANATEES ENCOUNTERING REDUCED FOOD PROVISIONS IN A PROMINENT WINTER REFUGE.

A decline in submerged aquatic vegetation (SAV) within Florida's spring-fed, thermal refuges raises questions about how these systems support winter foraging of Florida manatees (Trichechus manatus latirostris). We analyzed telemetry data for 12 manatees over seven years to assess their use of Kings Bay, a winter refuge with diminished SAV. After accounting for the effect of water temperature, we hypothesized that the number of trips out of Kings Bay would increase and the time wintering manatees spent in Kings Bay would decrease. Trips out of and into Kings Bay also were compared to assess potential influences on exiting or entering. There were no detectable differences in the number of trips out of the bay or overall time manatees spent in Kings Bay across winters. The percentage of time water temperatures were below 20°C was the single best predictor of increased time spent in Kings Bay. Trips out of Kings Bay were more likely to occur after 12:00 h and during a high but ebbing tide, compared to trips into the bay. Nine manatees tracked for longer than 75 days in winter spent 7-57% of their time in the Gulf of Mexico, and three of these manatees spent 7-65% of the winter >80 km from the mouth of Kings Bay. Results suggest the low amount of SAV in Kings Bay does not obviate its use by manatees, though there are likely tradeoffs for manatees regularly foraging elsewhere. Accounting for movements of Florida manatees through a network of habitats may improve management strategies and facilitate desirable conservation outcomes.

Intravenous miconazole therapy of mycotic infections.

The efficacy and safety of intravenously administered miconazole nitrate was examined in eight patients with the following infections: cutaneous North American blastomycosis (one), extensive dermatophytosis(one), and chronic mucocutaneous candidiasis (six). Mycologic assessment included direct examination for fungal elements, fungal culture, and histopathology. Laboratory evaluations were performed before and at regular intervals during the study. The total miconazole nitrate dosage, which was administered over a seven- to 32-day period, ranged from 4.0 to 46.8 g. Follow-up examinations extended from two to 15 months. Excellent results were obtained in five patients and fair results in three. No renal, cardiac, hepatic, or hematopoietic toxicity was observed. Other side effects, however, necessitated premature cessation of therapy in four patients. Overall, intravenously administered miconazole is an effective antifungal agent for these cutaneous infections.

New-generation valved conduit: an experimental study.

OBJECTIVE: An ideal valved conduit to repair complex congenital heart defects is yet to be developed. In this study we have evaluated the merits of our newly developed calcification-free biologic valve incorporated in a compatible conduit of biologic origin in an animal model. METHODS: Porcine aortic valves and main pulmonary arteries were cross-linked in glutaraldehyde, followed by coupling to partially degraded heparin through an intermediate surface-bound substrate containing amino groups. Because commercially available valves are treated only with glutaraldehyde, control aortic valves and main pulmonary arteries were cross-linked in 0.625% glutaraldehyde. Valved conduits were fabricated from main pulmonary arteries, which were sewn to the aortic and ventricular ends of aortic valves. Valved conduits were examined for calcification and other pathologic changes after being implanted in the descending thoracic aorta in juvenile sheep for 5 months. RESULTS: Severe calcification was noticed in all layers of cusps (calcium, 231.86 +/- 17.90 mg/gm) and aortic wall (calcium, 123.24 +/- 24.72 mg/gm) of aortic valves and main pulmonary arteries (calcium, 135.43 +/- 26.63 mg/gm) of valved conduits treated with 0.625% glutaraldehyde. Cusps (calcium, 1.28 +/- 0.22 mg/gm) of the aortic valve of heparin-bonded conduits did not calcify at all. Only sparse calcific deposits were noticed in the medial layer of the aortic wall (calcium, 25.90 +/- 22.79 mg/gm) of aortic valves and main pulmonary arteries (calcium, 9.64 +/- 10.79 mg/gm) of the valved conduits coupled to heparin. CONCLUSION: Heparin coupling is effective in preventing calcification of glutaraldehyde cross-linked valved conduits implanted in the systemic circulation of juvenile sheep.

Anticalcification treatment of pericardial prostheses.

The aim of the present study was to develop a chemical treatment to eliminate highly antigenic substances, to standardize the glutaraldehyde fixation procedure, to determine the dominant factors contributing to the calcification process and to understand the role of macromolecules like chitosan in the prevention of calcification of bioprosthetic heart valves. Bovine pericardium treated with 5% sodium chloride-trypsin-glutaraldehyde (GA)-chitosan did not calcify at 12 wk in the rat (calcium, 1.1 +/- 0.27 mg/g; von Kossa, 0). Slow release of residual GA from the bioprosthesis and free aldehyde groups on that are still considered the dominant factors for enhancing calcification of GA-treated bioprostheses.

Use of the glutaraldehyde-chitosan-treated porcine pericardium as a pericardial substitute.

The efficacy of chitosan post-treatment of glutaraldehyde-treated porcine pericardial substitute for the prevention of postoperative epicardial reaction and adhesion formation in mongrel dogs has been assessed. Glutaraldehyde (0.625%)-treated porcine pericardium showed moderate to dense adhesions to the heart and other underlying organs with moderate to severe epicardial reaction. None to minimal epicardial reaction without adhesion was observed in glutaraldehyde-treated porcine pericardium post-treated with chitosan at 5 months. Presumably, chitosan post-treatment prevents the slow release of residual glutaraldehyde and reduces the toxicity of the glutaraldehyde-treated implants, minimizing the chance of adhesion formation and epicardial reaction.

Heparin in calcification prevention of porcine pericardial bioprostheses.

Calcific degeneration is the main cause of failure of glutaraldehyde-treated xenograft heart valve substitutes implanted in humans. Coupling of heparin through an intermediate surface-bound substrate containing amino groups showed complete prevention of calcification of glutaraldehyde-treated porcine pericardium implanted subdermally in weanling rats for 5 months (heparin bonded pericardium: calcium, 0.625 +/- 0.24 mg g(-1); glutaraldehyde-only-treated pericardium: calcium, 228.32 +/- 37.39 mg g(-1); P < 0.0001). Conceivably, inactivation of unpaired aldehyde moieties present in bioprostheses after exposure to glutaraldehyde by amino compounds followed by blocking the potential binding sites of the graft with a surface modifying agent like heparin would be the key steps in the prevention of calcification and degeneration of glutaraldehyde-treated biological tissue grafts.

Valved conduit in the descending thoracic aorta in juvenile sheep: a useful, cost-effective model for accelerated calcification study in systemic circulation.

To evaluate the efficacy of any new anticalcificant in bioprostheses, a cost-effective and easy circulatory model is proposed. Calcification of 0.625% glutaraldehyde-treated porcine aortic valved conduits implanted in the descending thoracic aorta in 11 juvenile sheep for 5 months was compared with that of leaflets of glutaraldehyde-treated porcine aortic valve implanted subcutaneously in 3-week-old male Wistar rats for the same period. Cusps of valved conduits (Ca, 205.41 +/- 16.24 mg g(-1)) in sheep and aortic valve leaflets in rats (Ca, 235.21 +/- 45.25 mg g(-1)) (P = 0.0299) were severely calcified. Morphological characteristics of calcification of all explants were virtually identical. This model provides a model for testing calcification that lies between the subcutaneous weanling rat model and orthotopic whole valve replacement on the left side of the heart. It is less costly and easier to perform than the latter, but does provide exposure to the bloodstream under pressure, which the rat model does not.

Heparin coupling in inhibition of calcification of vascular bioprostheses.

Inhibitory effect of heparin coupling on calcification of bioprosthetic vascular grafts of different origin was studied. Heparin-bonded (Hep) and 0.625% glutaraldehyde-cross-linked (GA) segments of porcine thoracic aorta (AO), pulmonary artery (PA), jugular vein (JV) and rabbit aorta (RA) were implanted subcutaneously in weanling rats for 5 months. Heparin bonding is ineffective in prevention of calcification of JV (Hep: Ca, 159 +/- 32.26 mg g-1; GA: Ca, 193.55 +/- 17.81; p = 0.075) and RA (Hep: Ca, 150.17 +/- 14.78; GA: Ca, 192.12 +/- 26.61; p = 0.015). Calcium content of heparin-coupled PA and AO was significantly less when compared with their GA-treated counterparts. Calcification inhibition was achieved to a greater extent in heparin-bonded PA (Hep: Ca = 22.62 +/- 5.72, GA: Ca = 115.99 +/- 21.91, p < 0.0001) than in the AO coupled to heparin (Hep: Ca = 63.77 +/- 22.75, GA: Ca = 150.40 +/- 35.21, p < 0.0001). Elastin fibers were the predominant site of calcification in all explanted vascular grafts. Heparin-bonded porcine pulmonary artery is seemed to be the best among all vascular bioprostheses in this study.

In vitro and in vivo calcification of vascular bioprostheses.

Efficacy of different chemical treatments on calcification of vascular graft in vitro and in vivo was studied. Culture medium-filled rat aortas were separately treated in 0.2% glutaraldehyde and epoxy compound, and photooxidized in 0.01% methylene blue for a shorter period (group 1). Another group of rat aortas were separately treated in the same chemicals for a longer period (group 2). All fresh and treated aortas of both groups were cultured for 21 days in an organ culture medium and implanted (except for group 1) in weanling rats for five months. Histology and immunohistochemistry revealed that differently treated aortas of group 1 grow and calcify, and the smooth muscle cells between elastin fibers are the primary site of calcium deposition. In contrast, differently treated aortas of group 2 neither grew, nor did calcify in the medium except the epoxy compound cross-linked aorta of group 2 which did not grow but did calcify. Untreated aorta did not calcify. All fresh and differently treated aortic homografts calcified severely in rats. Our whole arterial segment-calcification system would be useful for analyzing the molecular and cellular mechanisms of both bioprosthetic and atherosclerotic calcification of vascular graft. New anticalcification technique is the only hope for better outcome of future vascular bioprostheses.

Use of glutaraldehyde-gentamicin-treated bovine pericardium as a wound dressing.

Glutaraldehyde (GA)-pretreated gentamicin post-fixed bovine pericardium has been evaluated as a wound dressing in this study. Two excisions approximately 7 x 4 cm, each of full thickness skin, from the upper and lower parts down to, but not including, the panniculus carnosus were made from the back of the guinea pig. The skin excised from the upper part was placed on the wound bed of the lower part as an autograft, whereas the upper wound was closed using 5% sodium chloride-trypsin-0.1% GA-0.048% gentamicin-treated bovine pericardium and sutured for comparative study. The wounds were inspected every 3-6 d for infection and exudation. Histopathological studies were performed at weekly intervals in the post-operative period. At the fifth week, a very thin linear scar on the epidermal aspect without remarkable contracture was observed and histopathology showed the completion of epithelization across the wounds in all cases. This study demonstrates that GA-pretreated, gentamicin-post-fixed bovine pericardium may be used as an alternative biological dressing in the case of large wounds.

Prevention of calcification of heart valve bioprostheses: an experimental study in rat.

To eliminate highly antigenic substances, bovine pericardium was washed in 5% sodium chloride (NaCl) for 24 hours, followed by incubation in trypsin for 40 minutes. To achieve adequate fixation, NaCl-trypsin-treated pericardium was preserved in glutaraldehyde (GA) solution with gradually increasing concentrations from 0.1% to 0.25%. To inactivate the free aldehyde groups and residual GA on the surface of the implant, NaCl-trypsin-GA-treated pericardial samples were posttreated separately with 1% lysine, 8% monosodium glutamate, and 4% chitosan. Fresh (untreated) and 0.1%, 0.2%, and 0.625% GA-treated and NaCl-trypsin-GA-treated pericardial specimens were prepared for comparative study. All samples were implanted subdermally in rats for 2, 4, 8, and 12 weeks for calcification studies. Morphologic and chemical analyses showed mild calcification in fresh pericardia (Ca, 10.5 +/- 1.25 micrograms/mg, von Kossa +) and in glutamate-posttreated pericardia (Ca, 11.5 +/- 3.45 micrograms/mg, von Kossa +). Calcium was practically undetectable in chitosan-posttreated implants (Ca, 1.1 +/- 0.27 micrograms/mg, von Kossa 0), whereas severe calcification was noticed in the rest of the samples (mean Ca greater than 200.0 micrograms/mg, von Kossa ) at 12 weeks. This study suggests that posttreatment with an amino compound such as chitosan would prevent the calcification of GA-treated bioprostheses at an early implantation stage, but elimination of antigenic factors and adequate GA fixation would prevent tissue degeneration, thus enabling the prosthesis to function over a long period.

Prevention of calcification in glutaraldehyde-treated porcine aortic and pulmonary valves.

BACKGROUND: The problem of calcification in porcine aortic (AVs) and pulmonary (PVs) valves and its relationship to glutaraldehyde (GA) is of current interest. We proposed an anticalcification treatment to develop noncalcifying porcine AVs and PVs. METHODS: Porcine AVs and PVs were cross-linked in GA. Partially degraded heparin was coupled to the GA-treated AVs and PVs through intermediate surface-bound substrate containing amino groups. Control AVs and PVs were cross-linked in 0.625% GA but had no heparin coupling. All specimens were implanted subdermally in 3-week-old rats for 5 months for calcification studies. RESULTS: Control AVs (Ca, 233.69 +/- 42.61 mg/g) and PVs (Ca, 181.48 +/- 4.06 mg/g) were severely calcified. Coupling of partially degraded heparin revealed complete prevention of calcification in GA-treated AVs (Ca, 0.73 +/- 0.27) and PVs (Ca, 1.125 +/- 0.22 mg/g) implanted subcutaneously in weanling rats for 5 months. CONCLUSIONS: The proposed anticalcification treatment is effective in preventing calcification of GA-treated AVs and PVs implanted subcutaneously in weanling rats for 5 months.

Milrinone for long-term pharmacologic support of the status 1 heart transplant candidates.

BACKGROUND: We determined the efficacy of long-term therapy with milrinone alone or in combination with inotropic agents in status 1 heart transplant candidates as a pharmacological support until heart transplantation. METHODS: Hemodynamic and biochemical variables were recorded in 29 status 1 men with symptoms of severe congestive heart failure, who received continuous intravenous milrinone alone (group 1, n = 21) or in combination with inotropic agents (group 2, n = 8) while awaiting heart transplantation. RESULTS: Symptomatic relief was noted in all patients of both groups without any preoperative deaths. One patient (4.8%) of group 1 died on the second day and 1 patient of group 2 died 16.4 months after transplantation. Although pulmonary capillary wedge pressure (group 1, p = 0.021; group 2, p = 0.0002), mean pulmonary artery pressure (group 1, p = 0.051; group 2, p = 0.004), and pulmonary vascular resistance (group 1, p = 0.0026; group 2, p = 0.056) were reduced by 1 hour after the onset of treatment and maintained unchanged until transplantation, the changes in mean pulmonary artery pressure in group 1 and pulmonary vascular resistance in group 2 were statistically insignificant except in the posttransplantation period. CONCLUSIONS: Long-term therapy with milrinone in combination with inotropic agents is safe and effective when only milrinone infusion is inadequate for pharmacologic support in status 1 candidates.

Reversal of preexisting vasospasm in coronary artery conduits.

BACKGROUND: To reverse preexisting coronary graft spasm, we investigated the vasodilative effect of the average therapeutic plasma concentration of nitroglycerin (NTG) alone and various calcium antagonists in combination with NTG in human arterial and venous conduits. METHODS: Vasodilative effects of 2 x 10(-8) mol/L NTG alone and 10(-8) mol/L NTG in combination with 2.2 x 10(-7) mol/L diltiazem, 2.8 x 10(-7) mol/L nifedipine, 10(-7) mol/L verapamil, or 5.6 x 10(-8) mol/L nicardipine were assessed in human radial artery, internal thoracic artery, and saphenous vein segments precontracted with a mixture of ten times the maximum plasma concentrations of endothelin-1 (8.6 x 10(-13) mol/L), angiotensin II (36 x 10(-11) mol/L), 5-hydroxytryptamine (3.4 x 10(-7) mol/L), and norepinephrine (1.7 x 10(-8) mol/L). The studies were done in organ baths. RESULTS: The therapeutic concentration of NTG alone or nifedipine, verapamil, diltiazem, or nicardipine in combination with NTG caused equal relaxation in a particular group of vascular segments (average vasodilation: radial artery, 83% to 95% [p = 0.7608 by analysis of variancel; saphenous vein, 47% to 70% [p = 0.3142]; internal thoracic artery, 54% to 79% [p = 0.27831). These combinations were not equally effective when compared between different groups of vascular segments (vasodilation; radial artery > internal thoracic artery > saphenous vein [p < 0.0001 by analysis of variance]). Although not significant, in comparison with NTG alone, NTG in combination with a calcium antagonist caused less vasodilation in any group of vascular segments. CONCLUSIONS: Nitroglycerin alone or in combination with nifedipine, verapamil, diltiazem, or nicardipine effectively reverses preexisting vasospasm in coronary artery conduits.

Prevention of radial artery graft vasospasm after coronary bypass.

BACKGROUND: Pharmacologic prophylaxis for prevention of notorious radial artery (RA) spasm is critical because of the increasingly routine use of the RA conduit during coronary bypass. Therefore, we investigated the vasodilatory effect of calcium antagonist in combination with nitroglycerin (NTG) RA segments. METHODS: We evaluated the vasodilatory effect of nifedipine alone, verapamil alone, diltiazem alone, NTG alone, and calcium antagonist in combination with in endothelin-1 (ET-1)-, angiotensin II (AII)-, 5-hydroxytryptamine (5-HT)-, and norepinephrine (NE)-precontracted human RA rings mounted in organ baths. RESULTS: Nifedipine (10(-5) M) alone, diltiazem (10(-5) M) alone, verapamil (10(-5) M) alone, and NTG (10(-5) M) alone showed maximum vasodilatory effect in either 10(-7) M ET-1-, 10(-7) M AII-, 10(-5) M NE-, or 10(-4) M 5-HT-precontracted RA segments. The 10(-5) M NTG alone-induced vasodilation (88.5% +/- 7.7%) in ET-1-precontracted segments was the highest vasodilation (ANOVA, p = 0.0008) among NTG alone-induced vasodilatory effects in RA. The relaxing effect of any of the calcium antagonists alone varied from 32.7% +/- 13.2% to 76.5% +/- 20.5% in RA precontracted with different vasoconstrictors. Nearly 200% vasodilation was observed with calcium antagonist in combination with NTG in AII-precontracted vessels. Nonetheless, the vasodilatory effect of calcium antagonist in combination with NTG in RA segments precontracted with different vasoconstrictors other than AII was nearly 100%. CONCLUSIONS: A calcium antagonist in combination with NTG is more potent than calcium antagonist alone or NTG alone in prevention of human RA vasospasm after coronary bypass.

Inhibitory effect of photooxidation on intimal and medial thickening of saphenous vein.

BACKGROUND: The inhibitory effect of short-term photooxidation on medial and neointimal proliferation of human saphenous vein was investigated. METHODS: Culture medium-filled surgically prepared saphenous vein segments were photooxidized in 0.01% methylene blue solution for 5 minutes. Photooxidized and nonphotooxidized saphenous veins were checked for viability of endothelial cells by culturing vein segments for 21 days followed by histologic and immunohistochemical studies. RESULTS: Endothelial cells of saphenous vein segments remained unaffected after photooxidation. Both the intima and media of nonphotooxidized veins became highly cellular and thickened because of the proliferation and migration of smooth muscle cells. Like precultured fresh saphenous vein, intimal (0.031+/-0.017 mm; p=0.0067) and medial thicknesses (0.702+/-0.123 mm; p < 0.0001) and proliferating cell nuclear antigen-positive cell count (14+/-8/mm2; p=0.0005) of cultured photooxidized veins were significantly less than those of cultured nonphotooxidized veins (intimal thickness, 0.059+/-0.041 mm; medial thickness, 0.997+/-0.228 mm; proliferating cell nuclear antigen positive cell count, 34+/-16/mm2. CONCLUSIONS: Methylene blue-induced short-term photooxidation is effective in inhibition of intimal and medial thickening of saphenous vein.

Possible relationship between degenerative cardiac valvular pathology and lyme disease.

We report an unusual clinical presentation of Lyme carditis in a previously healthy 20-year-old black woman without any epidemiologic history of Lyme disease, fulminant in nature, involving a heart valve necessitating emergent mitral valve replacement, and requiring further surgical intervention because of the development of pericardial effusion and tamponade. A dilated right ventricle with normal contractility and severe tricuspid regurgitation with increase in the right atrial size diagnosed later remains under close surveillance.

Surgical treatment of isolated secundum atrial septal defect in patients more than 50 years old.

BACKGROUND: Arrhythmia-related thromboembolic accidents continue to occur in patients even after closure of secundum atrial septal defect. Older age is usually not a contraindication to the repair of an atrial septal defect. To assess the importance of the type of management in elderly patients with atrial septal defect our clinical experience is reviewed. METHODS: Between 1974 and 1994, 49 patients 50 years of age or older (average, 57.4 years) underwent surgical closure of secundum atrial septal defect. All patients have been followed up for 2 to 21 years (mean, 9.7 years). RESULTS: There were no operative deaths. Functional classes in most of the patients were improved after operation. There were two cerebrovascular thromboembolic accidents with one permanent neurologic dysfunction, hemiparesis, and one septal dehiscence in the early postoperative period. One patient (2%) died of renal failure 6 years after operation, late arrhythmias developed in 3 patients (6%), 3 patients had a late stroke (6%), and 1 patient was not available for follow-up. CONCLUSIONS: Long-term operative results are satisfactory and beneficial to the quality of life in elderly patients. Because there is no safe and effective nonsurgical alternative to surgical closure, atrial septal defect repair in elderly patients without severe pulmonary vascular disease should not be delayed once the diagnosis had been made.