Efficacy of Hypoxia Against Tribolium castaneum (Coleoptera: Tenebrionidae) Throughout Ontogeny.

Hermetic grain storage technology offers a viable chemical-free approach to control storage insects. However, there is limited knowledge on how hypoxia affects the survival of insect life stages during grain storage in hermetic bags. We exposed Tribolium castaneum (Herbst) (Coleoptera: Tenebrionidae) eggs (2 d), young larvae (7 d), old larvae (21 d), pupae (28 d), and adults (2 d after emergence) to 2, 4, 8, and 20.9% oxygen levels for 1, 3, 5, 10, and 15 d and assessed subsequent mortality. At 2% oxygen, complete mortality was achieved in 3 d for eggs and young larvae, 10 d for old larvae and pupae, and 15 d for adults. At 4% oxygen, 15 d were required to kill all eggs and old larvae but not the other insect life stages. At 8% oxygen after 15 d, complete mortality of any insect life stage was not observed; but even a relatively short exposure (1-3 d) caused significant developmental delays in immature insects. Our study shows potential utility of hermetic technology for control of T. castaneum, but internal oxygen should be maintained below 2% level for at least 15 d for complete control. Increased oxygen levels improved the development of all insect life stages leading to increased adult emergence. There is a need to explore exposure time required to achieve complete mortality of all insect life stage above the 2% oxygen level.

Economics of integrated insect management in stored corn.

Insects can cause substantial damage to stored grain. In addition, consumers and therefore food processors are increasingly interested in chemical-free products. Integrated pest management (IPM) may increase farmers' profits while reducing their use of pesticides. This study uses a stochastic dynamic programming framework to model the economics of optimal insect control in corn, Zea mays L., stored on-farm with multiple controls conditional on the biophysical conditions of the grain in the bin. We find that for farmers who have a contract with a food processor, where there are quality premiums, the optimal management strategy depends on monitoring the biophysical conditions of the grain and the time period under consideration. For farmers who deliver to the commodity market, their current practices are optimal.

Antiphospholipid antibodies are associated with enhanced oxidative stress, decreased plasma nitric oxide and paraoxonase activity in an experimental mouse model.

OBJECTIVE: Oxidative stress contributes to atherosclerosis, and evidence of enhanced oxidative stress exists in antiphospholipid syndrome (APS). In a non-lupus murine model, we evaluated whether anticardiolipin (aCL) antibodies could affect the oxidant/antioxidant balance as an early biochemical step of APS. METHODS: Hybridomas producing human and murine aCL and anti-beta(2)-glycoprotein I (abeta2-GPI) monoclonal antibodies were injected into three groups of five female BALB/c severe combined immunodeficiency (SCID) mice. Corresponding hybridomas secreting non-antiphospholipid antibodies of the same isotype were employed as controls. Sera and organs were collected after 30 days. Paraoxonase (PON) activity, peroxynitrite, superoxide, nitric oxide (NO) and nitrotyrosine were measured in plasma. Expression of endothelial nitric oxide synthase and inducible nitric oxide synthase (iNOS) was assessed by western blot and immunohistochemistry. RESULTS: PON activity and NO (sum of nitrate and nitrite) levels were reduced in the human aCL IgG group (P<0.002 and P<0.04, respectively), whilst peroxynitrite and superoxide and expression of total antioxidant capacity of plasma were increased (P<0.01). PON and NO were decreased in the murine abeta2-GPI IgG and IgM aCL groups (P<0.03 and P<0.05, respectively). Nitrotyrosine was elevated in the human aCL IgG group (P<0.03). Western blotting showed reduced iNOS expression in the hearts of the IgG aCL group, confirmed by immunostaining. PON inversely correlated with IgG aCL titres (P<0.001), superoxide (P<0.008) and peroxynitrite levels (P<0.0009). Peroxynitrite and total IgG aCL were independent predictors of PON (P<0.0009 and P<0.02, respectively). Superoxide was the only independent predictor of NO (P<0.008) and of nitrotyrosine (P<0.002). CONCLUSION: aCL antibodies are associated with the decreased PON activity and reduced NO that may occur in the preclinical phase of APS.

A human anti-dsDNA monoclonal antibody caused hyaline thrombi formation in kidneys of 'leaky' SCID mice.

There are few studies assessing the pathogenicity of human monoclonal anti-DNA antibodies. The use of SCID mice avoids the problem of rejection of the human hybridoma cells thus allowing in vivo assessment of human immunoglobulins. Using electron microscopy we have shown that the human IgG anti-dsDNA monoclonal antibody, RH14, is nephritogenic in SCID mice, causing morphological changes in the kidney due to immunoglobulin deposition. The problem with using SCID mice is that they have an abnormal immune system; normally they are used at about 2 months of age, at which time they have virtually no functional T or B cells. It is known that older SCID mice become increasingly 'leaky', that is they develop some mature lymphocyte clones. Our aim was to assess if implanting anti-DNA antibodies into older 'leaky' SCID mice would result in pathology which was observable by light microscopy. Eight-month-old SCID mice were implanted with human hybridoma cells secreting either RH14 an anti-dsDNA IgG, CL24, an antiphospholipid antibody or an irrelevant human IgG control. As previously, RH14 deposited in the kidney and caused proteinuria but unexpectedly we also observed hyaline thrombi in the kidney glomeruli and peritubular capillaries. These thrombi occurred only in the case of RH14 implanted mice and were found to stain positively for human IgG and fibrin. However, apart from the interesting thrombi, we did not observe any greater pathological damage resulting from the anti-dsDNA antibody deposition than we had seen in the younger mice; indeed, the electron microscopic findings were more limited.

Pediatric cardiac emergencies.

Successful management of pediatric cardiac emergencies requires an accurate diagnosis to institute an appropriate plan of therapy. The diagnosis, however, is not always straightforward, as evidenced by the nonspecific clinical picture that can be presented by congenital heart defects. Entertaining the possibility of a cardiac problem in neonates with pulmonary symptoms unresponsive to standard therapies is crucial for successful management of patients with congenital heart disease. In addition to ventilatory support, prostaglandin E1 infusions or emergency interventional cardiac catheterization is often a life-saving initial measure in patients with acutely decompensated congenital cardiac lesions that require a patent ductus arteriosus for survival. Pericardial tamponade is associated with various acquired and iatrogenic causes. Emergent pericardiocentesis is mandatory when cardiovascular compromise occurs. The goal of anesthetic management is to maintain cardiac output. With the increasing use of central venous catheters in neonatal ICUs and the high mortality rate for central venous catheter-related cardiac tamponade, the diagnosis must be considered in any patient with a central venous catheter in situ who acutely develops unexplained hypotension, bradycardia, and diminished pulses. Arrhythmias also can cause hemodynamic instability in infants and children. Supraventricular tachycardia is by far the most common emergently presenting arrhythmia in the pediatric population. Unstable patients require immediate intravenous adenosine or synchronized cardioversion. Complete heart block is rare, but it can lead to congestive heart failure and occasionally to cardiovascular collapse and sudden death. Emergency treatment of complete heart block includes pharmacologic support and temporary or permanent pacemaker placement as indicated. In infants, congestive heart failure usually is related to congenital heart disease, whereas in older children, it tends to be secondary to an acquired cause. Supportive measures, fluid restriction, and inotropic support are the principles of initial treatment. Prompt recognition and initiation of appropriate therapy in pediatric cardiac emergencies are essential for favorable outcomes.

Efficacy and fumigation characteristics of ozone in stored maize.

This study evaluated the efficacy of ozone as a fumigant to disinfest stored maize. Treatment of 8.9tonnes (350bu) of maize with 50ppm ozone for 3d resulted in 92-100% mortality of adult red flour beetle, Tribolium castaneum (Herbst), adult maize weevil, Sitophilus zeamais (Motsch.), and larval Indian meal moth, Plodia interpunctella (Hübner) and reduced by 63% the contamination level of the fungus Aspergillus parasiticus Speare on the kernel surface. Ozone fumigation of maize had two distinct phases. Phase 1 was characterized by rapid degradation of the ozone and slow movement through the grain. In Phase 2, the ozone flowed freely through the grain with little degradation and occurred once the molecular sites responsible for ozone degradation became saturated. The rate of saturation depended on the velocity of the ozone/air stream. The optimum apparent velocity for deep penetration of ozone into the grain mass was 0.03m/s, a velocity that is achievable in typical storage structures with current fans and motors. At this velocity 85% of the ozone penetrated 2.7m into the column of grain in 0.8d during Phase 1 and within 5d a stable degradation rate of 1ppm/0.3m was achieved. Optimum velocity for Phase 2 was 0.02m/s. At this velocity, 90% of the ozone dose penetrated 2.7m in less than 0.5d. These data demonstrate the potential usefulness of using ozone in managing stored maize and possibly other grains.

A comparative study into the mechanisms of action of anti-tumor necrosis factor alpha, anti-CD4, and combined anti-tumor necrosis factor alpha/anti-CD4 treatment in early collagen-induced arthritis.

OBJECTIVE: Anti-tumor necrosis factor alpha (anti-TNFalpha) therapy is very effective in rheumatoid arthritis (RA), whereas depleting anti-CD4 therapy is relatively ineffective. To explain the differences in efficacy between these 2 therapies, we used an animal model of RA to compare their effects on different aspects of the disease process. METHODS: Mice with collagen-induced arthritis were treated with depleting anti-CD4 monoclonal antibodies (mAb), anti-TNFalpha mAb, or phosphate buffered saline. Another group was given a combination of anti-TNFalpha plus anti-CD4. The treatments were compared for their ability to down-regulate the expression of proinflammatory cytokines and adhesion molecules, reduce the cellularity of the joint, and inhibit Th1 activity. RESULTS: Anti-TNFalpha significantly reduced the numbers of cells expressing TNFalpha, interleukin-1beta (IL-1beta), very late activation antigen 4 (VLA-4), vascular cell adhesion molecule 1 (VCAM-1), and numbers of CD4+ T cells and macrophages in the joint. Anti-CD4 treatment led to a small reduction in the expression of TNFalpha, IL-1beta, VLA-4, and VCAM-1, but this did not reach statistical significance. Depleting anti-CD4 was also surprisingly ineffective in eliminating CD4+ T cells from the joint. Anti-TNFalpha therapy was also more effective than anti-CD4 in reducing Thl activity, as assessed by the production of interferon-gamma in lymph node cell cultures. There was a synergistic relationship between anti-TNFalpha and anti-CD4 in the reduction of histologic score and inhibition of TNFalpha/IL-1beta expression in the joints. CONCLUSION: The efficacy of the 3 treatments correlated with their ability to modulate the expression of inflammatory cytokines and adhesion molecules in the joint, reduce the cellularity of the joint, and inhibit Th1 activity. This kind of analysis may prove useful in the testing of novel therapies for RA.

Immunization with a peptide of Sm B/B' results in limited epitope spreading but not autoimmune disease.

An experimental model of systemic lupus erythematosus has recently been described in normal animals. We sought to confirm and extend this model, which involved immunization of normal rabbits and mice with a peptide of Sm B/B', PPPGMRPP. This peptide is an early target of the immune response in anti-Sm-positive patients with lupus. The peptide was used in a multiple Ag peptide format, with multiple copies of PPPGMRPP bound to an inert lysine backbone. New Zealand White rabbits and A/J and C57BL/10ScSn mouse strains were immunized with PPPGMRPP-MAP. Pepscan assays were used to determine the epitope spreading of the anti-PPPGMRPP-MAP response to other octamers of SmB/B' following immunization. We obtained high titer anti-PPPGMRPP-MAP IgG responses in the New Zealand White rabbits and A/J mice. The rabbits immunized with PPPGMRPP-MAP showed varying degrees of epitope spreading, while the A/J mice showed no spreading. We observed no autoantibodies to dsDNA or other anti-nuclear autoantibodies in our animals by ELISA or immunofluorescence, although anti-nuclear autoantibodies were found by Western blotting in some of the rabbits. No evidence of clinical disease was seen in our normal animals. These data underline the difficulties often associated with the reproduction of animal models in different laboratories.

Therapeutic actions of cyclosporine and anti-tumor necrosis factor alpha in collagen-induced arthritis and the effect of combination therapy.

OBJECTIVE: To define the mechanisms of action of 2 novel drugs, cyclosporine and anti-tumor necrosis factor alpha (TNFalpha), in collagen-induced arthritis and to determine the effect of combination therapy. METHODS: Type II collagen-immunized DBA/1 mice with established arthritis were treated with cyclosporine alone, anti-TNFalpha alone, cyclosporine plus anti-TNFalpha, or saline. RESULTS: Cyclosporine was found to ameliorate arthritis, suppress interferon-gamma (IFNgamma) production by CD4+ T cells, and reduce TNFalpha expression in arthritic joints. However, cyclosporine did not directly inhibit TNFalpha production by macrophages, indicating that the decrease in TNFalpha expression observed in vivo was probably an indirect consequence of the reduction in type 1 T helper cell activity. Anti-TNFalpha also reduced IFNgamma production by T cells, indicating that TNFalpha is involved in the cellular immune response to collagen. Combined treatment with cyclosporine plus anti-TNFalpha had an additive therapeutic effect. CONCLUSION: Although cyclosporine and anti-TNFalpha target different points in the inflammatory pathway, there is an overlap in the consequences of their actions in vivo.

Immunopathogenesis of SLE.

Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease characterized by the deposition of autoantibodies and immune complexes, leading to tissue damage. The immunopathogenesis of SLE is like a jigsaw puzzle, some pieces of which are missing or have not fallen into place. In predisposed individuals, the initial stimulus is likely to be one or more of the environmental agents interacting with susceptibility genes. Once the critical threshold is breached there is a failure of the immune system to downregulate the ensuing abnormal immune response, involving polyclonal B cell activation and hyperactive T cell help. Key questions include, what are the processes behind the availability of autoantigens and the breakdown of tolerance that give rise to the pathogenic autoantibodies? Current areas of research also involve the roles played by cytokines, adhesion molecules, co-stimulatory molecules and apoptosis.

DBA/1 mice expressing the human TNF-alpha transgene develop a severe, erosive arthritis: characterization of the cytokine cascade and cellular composition.

Arthritis spontaneously develops in mice expressing a human TNF-alpha transgene modified with the 3' untranslated region of beta-globin. We have backcrossed these mice onto the arthritis-susceptible DBA/1 background and found an acceleration of the onset of arthritis with successive generations of interbreeding. Bioactive TNF-alpha in primary synovial membrane cell cultures was significantly higher in the DBA/1 transgenic mice than in transgenic mice on the original background. Elevated levels of human TNF-alpha were accompanied by increases in synovial cell expression of murine IL-1beta and IL-6, but murine granulocyte-macrophage CSF, IFN-gamma, and IL-4 could not be detected. Interestingly, the anti-inflammatory cytokine IL-10 could be detected, but levels were not modulated by expression of the transgene. Analysis of the synovial membrane cell composition revealed that >50% of synovial cells were CD45-negative cells, presumably fibroblasts and endothelial cells, and the majority of CD45-expressing cells were neutrophils. Peritoneal macrophages and lymphocytes from the spleen, bone marrow, and lymph nodes required LPS stimulation to produce human TNF-alpha, indicating that, when activated, cells of these lineages were capable of expressing the transgene; however, few were found in synovial tissues. In contrast, fibroblasts derived from synovial tissue spontaneously released human TNF-alpha, and using immunohistochemical techniques, this cytokine was localized to fibroblast-like cells and chondrocytes. We propose that arthritis in DBA/1 human TNF-alpha transgenic mice is driven in part through the spontaneous expression of transgene by connective tissue cells, and there is little evidence of the participation of lymphocytes in this model.

Dynamics of proinflammatory cytokine expression in the joints of mice with collagen-induced arthritis (CIA).

This report contains a description of the cellular localization and kinetics of proinflammatory cytokine expression in murine CIA, a model for rheumatoid arthritis. Tissue cryostat sections of undecalcified paws from type II collagen-immunized DBA/1 mice, taken 1-10 days after the onset of clinical arthritis, were examined for the presence of tumour necrosis factor-alpha (TNF-alpha), IL-1beta and IL-6 using an indirect immunoperoxidase technique. In parallel, interferon-gamma (IFN-gamma) production by lymph node cells, stimulated in vitro with type II collagen, was assessed as a marker of T cell activity. The main areas of TNF-alpha, IL-1beta and IL-6 expression were in the synovial lining layer and in tissue contiguous with cartilage and bone (the marginal zone), in particular at sites of pannus formation and joint erosion. There was a progressive increase in the number of TNF-alpha-, IL-1beta- and IL-6-positive cells from day 1 to day 10 of arthritis, during which time IFN-gamma production by CD4+ T cells from draining lymph nodes declined sharply. A further finding of potential significance was that TNF-alpha was consistently detected at day 1 of arthritis, whereas IL- 1beta-positive cells were not found until day 3, suggesting that the expression of TNF-alpha precedes that of IL-1beta.

Readiness: observations and comments from a medical team deployment.

The evolving strategy of the United States in dealing with the changing world order calls for a force structure capable of fighting and winning two nearly simultaneous major regional conflicts and conducting a range of other military operations. Readiness is a key factor in this new strategy. Consequently, major paradigm shifts are occurring within the Air Force Medical Service. Maintaining current and accurate medical records on personnel to meet deployment requirements is a significant challenge. Historically, time and resources are consumed determining the deployability of troops prior to a deployment. This adds to the cost of doing business and increases the time required to clear the deploying team, even though there is an established process to avoid these very problems. The experience of a recent medical team deployment to Bosnia is discussed. Future directions given the implementation of TRI-CARE, the Preventive Health Assessment Program, and the Strategic Health Resourcing Plan are also considered.

Suppression of TNF-alpha expression, inhibition of Th1 activity, and amelioration of collagen-induced arthritis by rolipram.

Rolipram is a type IV phosphodiesterase inhibitor that suppresses inflammation and TNF-alpha production. As anti-TNF-alpha therapy is effective in rheumatoid arthritis, we investigated the effect of rolipram on collagen-induced arthritis (CIA), a murine model of rheumatoid arthritis. Rolipram was administered after the onset of clinical arthritis at doses of 0.5, 3, 5, or 10 mg/kg twice daily, with a dose-dependent therapeutic effect on clinical severity and joint erosion. Immunohistochemical analysis of joints of rolipram-treated mice revealed 67% reduction in TNF-alpha-expressing cells compared with control arthritic mice. In vitro studies using bone marrow-derived macrophages confirmed that rolipram directly suppressed TNF-alpha and IL-12 production following stimulation with IFN-gamma and LPS. The effect of rolipram on T cell activity was studied by measuring Th1/Th2 cytokine production by collagen-stimulated draining lymph node cells from arthritic mice treated in vivo with rolipram. Rolipram reduced IFN-gamma production and increased IL-10, indicating that rolipram down-regulated the ongoing Th1 response to type II collagen. Finally, the effect on CIA of combination therapy was studied using rolipram plus either anti-TNF-alpha or anti-CD4 mAbs. Rolipram plus anti-TNF-alpha was not therapeutically additive, whereas rolipram plus anti-CD4 mAb was clearly additive. This result indicates that the therapeutic effects of rolipram overlap with TNF-alpha blockade, but are complementary to anti-CD4 treatment. It is therefore proposed that a major mechanism of action of rolipram in CIA is suppression of TNF-alpha activity. These findings suggest that type IV phosphodiesterase inhibitors may be effective in pathologic conditions, such as RA, with overexpression of TNF-alpha.

Surgical intervention and anesthetic management of the patient with Parkinson's disease.

With estimates as high as 1 million patients in the United States, Parkinson's disease is a relatively common neurological disorder. It has long been thought that the primary biochemical disturbance in Parkinson's disease is dopamine related. Accordingly, many drugs have been developed that increase the supply of dopamine, affect the biochemical balance of dopamine, or act as a dopamine substitute. These drugs may have significant interactions with anesthetic agents. In addition, there are several disease and drug-induced physiological aberrancies that can have profound anesthetic implications in the patient with Parkinson's disease (e.g., aspiration pneumonitis, myocardial irritability, hypotension, hypertension, and respiratory impairment). Although surgical therapy for Parkinson's disease has a long history, with the advent of advanced neuroimaging techniques there has been a resurgence of these procedures (e.g., pallidotomy and thalamotomy) for advanced stages of Parkinson's disease. It is likely that these surgical procedures will become more commonplace, possibly prolonging the lifespan of patients with Parkinson's disease. Even though these cases are typically performed with local anesthesia, there are several important caveats to consider in the management of these patients (e.g., airway access with CNS changes, hypertension, and tremor). It's incumbent on anesthesiologists to become familiar with the special needs of patients with Parkinson's disease and alter the "days in hell" attitude among these patients toward surgery and anesthesia.

Synergy between anti-CD4 and anti-tumor necrosis factor in the amelioration of established collagen-induced arthritis.

Anti-CD4 treatment is reported to prevent collagen-induced arthritis if administered before the onset of clinical disease but has relatively little effect on established arthritis. In contrast, we have recently shown that anti-tumor necrosis factor alpha/beta (TNF) treatment reduces the severity of established arthritis. We now study the effect of combined administration of anti-CD4 monoclonal antibody (YTS 191.1.2/YTA 3.1.2) and anti-TNF monoclonal antibody (TN3-19.12) in established arthritis. Anti-CD4 treatment caused some reduction in paw-swelling but did not significantly prevent joint erosion. A suboptimal dose of anti-TNF alone had no significant effect on arthritis. In contrast, anti-CD4 plus suboptimal anti-TNF significantly reduced paw-swelling, limb involvement, and joint erosion. As previously reported, an optimal dose of anti-TNF alone inhibited paw-swelling, limb involvement, and joint erosion. However, optimal anti-TNF combined with anti-CD4 caused significantly greater reductions in paw-swelling and joint erosion than those achieved by optimal anti-TNF alone. Coadministration of anti-CD4 was also effective in preventing an antibody response to the hamster anti-TNF antibody, which may have implications for long-term therapy in human disease. Thus anti-CD4 acts synergistically with anti-TNF in ameliorating established collagen-induced arthritis and this combined therapeutic approach may provide effective long-term control of rheumatoid arthritis.

Sampling range of male sweetpotato weevils (Cylas formicarius elegantulus) (Summers) (Coleoptera: Curculionidae) to pheromone traps: Influence of pheromone dosage and lure age.

Studies were conducted to determine the effects of sex pheromone dosage and lure age on movement of male sweetpotato weevils (SPW),Cylas formicarius elegantulus (Summers), using mark-release-recapture techniques. SPW trap counts from various downwind distances were compared for dosages ranging from 0.01 to 10.0 µg and lure ages ranging from fresh (0 days old) to 64 days old. The percentages of male SPW recaptured decreased with an increase in release distance and decreased with a decrease in dosage at each corresponding distance. Most SPW were caught within the first 16-hr period. Slopes of percent recapture vs. release distance for the two higher dosages (10 µg and 1.0 µg) differed from those of the two lower dosages (0.1 and 0.01 µg) but did not differ from each other. Intercepts were similar among the three higher dosages. Slopes did not differ among the five lure ages examined. Intercepts differed between fresh (0 days old) and 24-day-old septa at 16 hr and between fresh (0 days old) and 34-day-old septa at 40 hr. Previous exposure to pheromone (conditioning) did not increase percentages of SPW recaptured. Results indicate that male SPW are capable of traversing distances of at least 280 m in 16 hr. The pheromone tested in this study appears to be effective at dosages lower than any other coleopteran sex-pheromone system. Incorporation of this pheromone into a SPW management system may effectively reduce the use of insecticides.

Effects of scale insect herbivory and shading on net gas exchange and growth of a subtropical tree species (Guaiacum sanctum L.).

The scale insect, Toumeyella sp., feeds exclusively on the subtropical hammock tree lignum vitae (Guaiacum sanctum L.). The combined effects of scale herbivory and shading on leaf gas exchange characteristics and growth of lignum vitae trees were studied using a factorial design. Trees grown in full sun or in 75% shade were manually infested with scale or left noninfested. Beginning 4 weeks after infestation, net CO2 assimilation, stomatal conductance, transpiration, internal partial pressure of CO2, and water-use efficiency were determined on single-leaves at 4-week intervals for trees in each treatment. At the end of the experiment, net CO2 assimilation was determined for whole plants. Total leaf area, leaf, stem, and root dry weights, and leaf chlorophyll and nitrogen concentrations were also determined. Scale infested trees generally had lower net CO2 assimilation, stomatal conductance, and transpiration rates as well as less leaf area, and root, stem, and leaf dry weights than noninfested trees. Twenty four weeks after the shade treatment was imposed, sun-grown trees had approximately twice the leaf area of shade-grown trees. Shade-grown trees compensated for the reduced leaf area by increasing their photosynthetic efficiency. This resulted in no difference in light saturated net CO2 assimilation on a whole plant basis between sun-grown and shade-grown trees. Chlorophyll and nitrogen concentrations per unit leaf area were greater in leaves of shade-grown trees than in leaves of sun-grown trees. Shading and herbivory by Toumeyella sp. each resulted in decreased growth of Guaiacum sanctum. Scale insect herbivory did not result in greater detrimental effects on leaf gas exchange characteristics for shade-grown than for sun-grown trees. Herbivory by Toumeyella resulted in a greater decrease in tree growth for sun-grown than for shade-grown trees.

Temperature instability as an early predictive factor of brain death in paediatric near-drowning victims.

Predicting outcome after near-drowning has been extensively studied. During four years, 42 near drowned children were aggressively treated with positive pressure ventilation, barbiturates and hypothermia. This mode of treatment makes it difficult to clinically assess the child's prognosis. Temperature instability after rewarming is an early negative predictive factor following treatment of near-drowning, and in conjunction with cerebral flow studies avoids the potential commitment to prolonged and unwarranted cardiovascular and respiratory support.