The effect of pain on involuntary and voluntary capture of attention

BACKGROUND: There is converging evidence for the notion that pain affects a broad range of attentional domains. This study investigated the influence of pain on the involuntary capture of attention as indexed by the P3a component in the event-related potential derived from the electroencephalogram. METHODS: Participants performed in an auditory oddball task in a pain-free and a pain condition during which they submerged a hand in cold water. Novel, infrequent and unexpected auditory stimuli were presented randomly in a series of frequent standard and infrequent target tones. P3a and P3b amplitudes were observed to novel, unexpected and target-related stimuli, respectively. RESULTS: Both electrophysiological components were characterized by reduced amplitudes in the pain compared with the pain-free condition. Hit rate and reaction time to target stimuli did not differ between the two conditions presumably because the experimental task was not difficult enough to exceed attentional capacities under pain conditions. CONCLUSIONS: These results indicate that voluntary attention serving the maintenance and control of ongoing information processing (reflected by the P3b amplitude) is impaired by pain. In addition, the involuntary capture of attention and orientation to novel, unexpected information (measured by the P3a) is also impaired by pain. Thus, neurophysiological measures examined in this study support the theoretical positions proposing that pain can reduce attentional processing capacity. These findings have potentially important implications at the theoretical level for our understanding of the interplay of pain and cognition, and at the therapeutic level for the clinical treatment of individuals experiencing ongoing pain.

MRI-guided and CT-guided cervical nerve root infiltration therapy: a cost comparison

PURPOSE To evaluate and compare the costs of MRI-guided and CT-guided cervical nerve root infiltration for the minimally invasive treatment of radicular neck pain. MATERIALS AND METHODS Between September 2009 and April 2012, 22 patients (9 men, 13 women; mean age: 48.2 years) underwent MRI-guided (1.0 Tesla, Panorama HFO, Philips) single-site periradicular cervical nerve root infiltration with 40 mg triamcinolone acetonide. A further 64 patients (34 men, 30 women; mean age: 50.3 years) were treated under CT fluoroscopic guidance (Somatom Definition 64, Siemens). The mean overall costs were calculated as the sum of the prorated costs of equipment use (purchase, depreciation, maintenance, and energy costs), personnel costs and expenditure for disposables that were identified for MRI- and CT-guided procedures. Additionally, the cost of ultrasound guidance was calculated. RESULTS The mean intervention time was 24.9 min. (range: 12 - 36 min.) for MRI-guided infiltration and 19.7 min. (range: 5 - 54 min.) for CT-guided infiltration. The average total costs per patient were EUR 240 for MRI-guided interventions and EUR 124 for CT-guided interventions. These were (MRI/CT guidance) EUR 150/60 for equipment use, EUR 46/40 for personnel, and EUR 44/25 for disposables. The mean overall cost of ultrasound guidance was EUR 76. CONCLUSION Cervical nerve root infiltration using MRI guidance is still about twice as expensive as infiltration using CT guidance. However, since it does not involve radiation exposure for patients and personnel, MRI-guided nerve root infiltration may become a promising alternative to the CT-guided procedure, especially since a further price decrease is expected for MRI devices and MR-compatible disposables. In contrast, ultrasound remains the less expensive method for nerve root infiltration guidance.

Canine rabies in Australia: a review of preparedness and research needs

Australia is unique as a populated continent in that canine rabies is exotic, with only one likely incursion in 1867. This is despite the presence of a widespread free-ranging dog population, which includes the naturalized dingo, feral domestic dogs and dingo-dog cross-breeds. To Australia's immediate north, rabies has recently spread within the Indonesian archipelago, with outbreaks occurring in historically free islands to the east including Bali, Flores, Ambon and the Tanimbar Islands. Australia depends on strict quarantine protocols to prevent importation of a rabid animal, but the risk of illegal animal movements by fishing and recreational vessels circumventing quarantine remains. Predicting where rabies will enter Australia is important, but understanding dog population dynamics and interactions, including contact rates in and around human populations, is essential for rabies preparedness. The interactions among and between Australia's large populations of wild, free-roaming and restrained domestic dogs require quantification for rabies incursions to be detected and controlled. The imminent risk of rabies breaching Australian borders makes the development of disease spread models that will assist in the deployment of cost-effective surveillance, improve preventive strategies and guide disease management protocols vitally important. Here, we critically review Australia's preparedness for rabies, discuss prevailing assumptions and models, identify knowledge deficits in free-roaming dog ecology relating to rabies maintenance and speculate on the likely consequences of endemic rabies for Australia.

DNA-DAMAGING REACTIONS OF NEOCARZINOSTATIN (ANTIBIOTICS, DNA REPAIR, CYTOTOXICITY)

Sensitive assays utilizing a cell-free and an intracellular system were employed to study the molecular bases of the DNA-damaging reactions of neocarzinostatin (NCS). In the cell-free DNA system, super-helical form I DNA from the bacteriophage PM2 was used as the substrate. The three forms of DNA present after treatment with NCS were separated by agarose gel electrophoresis. When NCS-damaged DNA was assayed under neutral conditions, there was a progressive decrease in the amount of surviving form I DNA and a corresponding increase in form II (nicked, relaxed circular) DNA, but very little increase in form III (linear duplex) DNA. This indicates that NCS introduces primarily single-strand breaks. However later studies showed that there were some site-specific double-strand breaks mediated by NCS on PM2 DNA. Seven such specific sites were mapped on the PM2 genome. When the damage was assayed under nondenaturing alkaline conditions or with the apurinic/apyrimidinic endonuclease IV, there was a slightly greater decrease in the amount of surviving form I DNA compared with neutral conditions indicating the presence of some alkali-labile sites.^ NCS-mediated DNA damage and repair were examined with cultured Chinese hamster ovary (CHO) cells using either alkaline elution for analysis of single-strand breaks or neutral elution for analysis of double-strand breaks. Most of the strand breaks introduced by NCS were capable of being rejoined. However, there was a small amount of residual DNA damage remaining unrejoined at 24-hr after removal of the drug. The amount of residual DNA damage was higher in a CHO mutant cell line (EM9) having a higher sensitivity to killing by NCS than its parental strain (AA8). Other lesions, DNA-protein complexes and alkali-labile sites, were detected after NCS treatment but they constituted only a small fraction of the DNA damage.^ Based on the above information, it can be postulated that NCS introduces some very lethal DNA damage. It is likely that the lethal lesions are a subset of the total DNA lesions representing the residual DNA damage. This DNA damage may be composed of site-specific, unrejoinable double-strand breaks and are thus the primary lesion leading to NCS-mediated lethality.^

The functions of pitx2 and Bmp signaling in craniofacial development

The formation of the vertebrate face is an extremely complex developmental process, which needs to coordinate the outgrowth of several facial primordia. Facial primordia are small buds made up of mesenchymal masses enclosed by an epithelial layer that surrounds the primitive mouth. The upper jaw is formed by the maxillary process, the lateral nasal process, and the frontonasal process while the mandibular process forms the lower jaw. Recent experiments using genetics in mice and bead implantation approaches have shown that the pitx2 homeobox gene and Bmp signaling play important roles in this complex developmental process. However, the molecular mechanisms underlying the function of pitx2 and Bmp in these events are still unclear. Here, we show that pitx2 is required for oral epithelium maintenance, and branchial arch signaling is pitx2 dosage sensitive by using pitx2 allelic combinations that encode varying levels of pitx2. Maintenance of fgf8 signaling requires only low pitx2 dosage while repression of Bmp signaling requires high pitx2 levels. Different incisor and molar phenotypes in low level pitx2 mutant embryos suggest a distinct requirement for pitx2 in tooth-type development. The results show that pitx2 is required for craniofacial muscle formation and expanded Bmp signaling results in excess bone formation in pitx2 mutant embryos. Fate-mapping studies show that ectopic bone results from excessive bone growth, instead of muscle transformation. Moreover, by using cre/loxp system we show that partial loss of Bmpr-IA in the facial primordia results in cleft lip/palate, abnormal teeth, ectopic teeth and tooth transformation. These phenotypes suggest that Bmp signaling has multiple functions during craniofacial development. The mutant palate shelves can fuse with each other when cultured in vitro, suggesting that cleft palate is secondary to the partial loss of Bmpr-IA. Furthermore, we prove that Bmp4, one of the ligands of Bmpr-IA, plays a role during lip fusion developmental process and partial loss of Bmp4 in the facial primordia results in the lip fusion delay. These results have provided insight to understand the complex signaling cascades that regulate craniofacial development. ^

The heparan sulfate-fibroblast growth factor signaling system in liver growth and function

The heparan sulfate (HS)-fibroblast growth factor (FGF) signaling system is a ubiquitous regulator that senses local environmental changes and mediates cell-to-cell communication. This system consists of three mutually interactive components. These are regulatory polypeptides (FGF), FGF receptor (FGFR) and heparan sulfate proteoglycans (FGFRHS). All four FGFR genes are expressed in the adult liver. Expression of the FGFR1–3 genes is generally associated with non-parenchymal cells while expression of the FGFR4 gene is associated with parenchymal hepatocytes. We showed that livers of mice lacking FGFR4 exhibited normal morphology and regenerated normally in response to partial hepatectomy. However, the FGFR4 (−/−) mice exhibited depleted gallbladders, an elevated bile acid pool and elevated excretion of bile acids. Cholesterol- and bile acid-controlled liver cholesterol 7α-hydroxylase (Cyp7a), the limiting enzyme for bile acid synthesis, was elevated, unresponsive to dietary cholesterol, but repressed normally by dietary cholate. These results indicated that FGFR4 was not directly involved in liver growth but exerted negative control on liver bile acid synthesis. This was confirmed in transgenic mice overexpressing the constitutively active human FGFR4 in livers. The transgenic mice exhibited decreased fecal bile acid excretion, bile acid pool size, and expression of Cyp7a. Introduction of this constitutively active human FGFR4 into FGFR4 (−/−) mice restored the inhibition of bile acid synthesis. Activation of the c-Jun N-terminal Kinase (JNK) pathway by FGFR4 correlated with the repressive effect on bile acid synthesis. ^ To determine whether FGFR4 played a broader role in liver-specific metabolic function, we examined the impact of both acute and chronic exposure to CCl 4 in FGFR4 (−/−) mice. Following acute CCl4 exposure, the FGFR4 (−/−) mice exhibited accelerated liver injury, a significant increase in liver mass and delayed hepatolobular repair, with no apparent effect on liver cell proliferation and restoration of cellularity. Chronic CCl4 exposure resulted in severe fibrosis in livers of FGFR4 (−/−) mice compared to normal mice. Analysis at both mRNA and protein levels indicated an 8 hr delay in FGFR4-deficient mice in the down-regulation of cytochrome P450 2E1 (CYP2E1) protein, the major enzyme whose products underlie CCl 4-induced injury. These results show that hepatocyte FGFR4 protects against acute and chronic insult to the liver and prevents accompanying fibrosis. ^ Of the 23 FGF polypeptides, FGF1 and FGF2 are present at significant levels in the liver. To determine whether FGF1 and FGF2 played a role in CCl 4-induced liver injury and fibrosis, we examined the impact of both acute and chronic exposure to CCl4 in both wild-type and FGF1-FGF2 double-knockout mice. Following acute CCl4 exposure, FGF1(−/−)FGF2(−/−) mice exhibited accelerated liver injury, overall normal liver growth and repair, and decreased liver collagen α1(I) induction. Liver fibrosis resulting from chronic CCl4 exposure was markedly decreased in livers of FGF1(−/−)FGF2(−/−) mice compared to wild-type mice. This study suggests a role for FGF1 and FGF2 in hepatic fibrogenesis. ^ In summary, our three part study shows that specific components of the ubiquitous HS-FGF signaling family in the liver context interfaces with metabolite- and xenobiotic-controlled networks to regulate liver function, but has no apparent direct effect on liver cell growth. ^

Occupational beryllium exposure: Reconciling federal policies, regulations and contractor implementation guides to protect worker health

Beryllium is a widely distributed, highly toxic metal. When beryllium particulates enter the body, the body's defense mechanisms are engaged. When the body's defenses cannot easily remove the particulates, then a damage and repair cycle is initiated. This cycle produces chronic beryllium disease (CBD), a progressive, fibrotic respiratory involvement which eventually suffocates exposed individuals. ^ Beryllium disease is an occupational disease, and as such it can be prevented by limiting exposures. In the 1940s journalists reported beryllium deaths at Atomic Energy Commission (AEC) facilities, the Department of Energy's (DOE) predecessor organization. These reports energized public pressure for exposure limits, and in 1949 AEC implemented a 2 μg/m3 permissible exposure limit (PEL). ^ The limits appeared to stop acute disease. In contrast, CBD has a long latency period between exposure and diagnosable disease, between one and thirty years. The lack of immediate adverse health consequences masked the seriousness of chronic disease and pragmatically removed CBD from AEC/DOE's political concern. ^ Presently the PEL for beryllium at DOE sites remains at 2 μg/m 3. This limit does not prevent CBD. This conclusion has long been known, although denied until recently. In 1999 DOE acknowledged the limit's ineffectiveness in its federal regulation governing beryllium exposure, 10 CFR 850. ^ Despite this admission, the PEL has not been reduced. The beryllium manufacturer and AEC/DOE have a history of exerting efforts to maintain and protect the status quo. Primary amongst these efforts has been creation and promotion of disinformation within peer reviewed health literature which discusses beryllium, exposures, health effects and treatment, and targeting graduate school students so that their perspective is shaped early. ^ Once indoctrinated with incorrect information, professionals tend to overlook aerosol and respiratory mechanics, immunologic and carcinogenic factors. They then apply tools and perspectives derived from the beryllium manufacturer and DOE's propaganda. Conclusions drawn are incorrect. The result is: health research and associated policy is conducted with incorrect premises. Effective disease management practices are not implemented. ^ Public health protection requires recognition of the disinformation and its implications. When disinformation is identified, then effective health policies and practices can be developed and implemented. ^

Characterization of cytochrome P450 4F subfamily: Functional role and response in inflammation

CYP4F subfamily comprises a group of enzymes that metabolize LTB4 to biologically less active metabolites. These inactive hydroxy products are incapable of chemotaxis and recruitment of inflammatory cells. This has led to a hypothesis that CYP4Fs may modulate inflammatory conditions serving as a signal of resolution. ^ We investigated the regulation of rat CYP4F gene expression under various inflammatory prompts including a bacterial lipopolysaccharide (LPS) treated model system, controlled traumatic brain injury (TBI) model as well as using direct cytokine challenges. CYP4Fs showed an isoform specific response to LPS. The pro-inflammatory cytokines IL-1β, IL-6 and TNF-α produced an overall inductive CYP4F response whereas IL-10, an anti-inflammatory cytokine, suppressed CYP4F gene expression in primary hepatocytes. The molecular mechanism behind IL-6 mediated CYP4F induction was partially STAT3 dependent. ^ An alternate avenue of triggering the inflammatory cascade is TBI, which is known to cause several secondary effects leading to multiorgan dysfunction syndrome. The results from this study elicited that trauma to the brain can produce acute inflammatory changes in organs distant from the injury site. Local production of LTB4 after CNS injury caused mobilization of inflammatory cells such as neutrophils to the lung. In the resolution phase, CYP4F expression increased with time along with the associated activity causing a decline in LTB4 concentration. This marked a significant reduction in neutrophil recruitment to the lung which led to subsequent recovery and repair. In addition, we showed that CYP4Fs are localized primarily in pulmonary endothelium. We speculate that the temporally regulated LTB4 clearance in the endothelium may be a novel target for treatment of pulmonary inflammation following injury. ^ In humans, several CYP4F isoforms have been identified and shown to metabolize LTB4 and other endogenous eicosanoids. However, the specific activity of the recently cloned human CYP4F11 is unknown. In the final part of this thesis, CYP4F11 protein was expressed in yeast in parallel to CYP4F3A. To our surprise, CYP4F11 displayed a different substrate profile than CYP4F3A. CYP4F3A metabolized eicosanoids while CYP4F11 was a better catalyst for therapeutic drugs. Thus, besides their endogenous function in clearing inflammation, CYP4Fs also may play a part in drug metabolism. ^

The INO80 chromatin remodeling complex is involved in the nucleotide excision repair pathway

The genomic DNA of eukaryotic cells is well organized into chromatin structures. However, these repressed structures present barriers that block the access of regulatory factors to the genome during various nuclear events. To overcome the obstacle, two major cellular processes, post-modification of histone tails and ATP-dependent chromatin remodeling, are involved in reconfiguring chromatin structure and creating accessible DNA. Despite the current research progress, much remains to be explored concerning the relationship between chromatin remodeling and DNA repair. Recently, one member of the ATP-dependent chromatin remodeling complexes, INO80, has been found to play a crucial role in DNA damage repair. However, the functions of this complex in higher eukaryotes have yet to be determined. The goal of my study is to generate a human somatic INO80 conditional knockout model and investigate the functions of Ino80 in damage repair.^ By homologous targeting of the INO80 locus in human HCT116 colon epithelial cells, I established a human somatic INO80 conditional knockout model. I have demonstrated that the conditional INO80 cells exhibited a sufficiently viable period when the INO80 protein is removed. Moreover, I found that loss of INO80 resulted in deficient UV lesion repair in response to UV while the protein levels of the NER factors such as XPC, XPA, XPD were not affected. And in vitro repair synthesis assay showed that the NER incision and repair synthesis activities were intact in the absence of INO80. Examination on the damage recognition factor XPC showed its recruitment to damage sites was impaired in the INO80 mutant cells. Loss of INO80 also led to reduced enrichment of XPA at the site of UV lesions. Despite the reduced recruitment of XPC and XPA observed in INO80 mutants, no direct interaction was detected. Meanwhile, direct interaction between INO80 and DDB1, the initial UV lesion detector, was detected by coimmunoprecipitation. UV-induced chromosome relaxation was reduced in cells devoid of INO80. These results demonstrate the INO80 complex may participates in the NER by interacting with DDB1 and having a critical role of in creating DNA accessibility for the nucleotide excision pathway. ^

Get ur 60: A social marketing campaign to promote and facilitate physical activity among Central Texas middle school students

If allowed to continue unabated, the obesity epidemic may lead to the first decline in life expectancy in the developed world (Olshansky et al., 2005). Similar to the relationship between smoking habits in youth and adulthood, obesogenic dietary and physical activity habits in childhood may persist into adulthood (Kelder et al., 2002). Teaching children how to establish healthy eating habits and activity levels, as well as providing them the necessary resources to internalize and maintain these behaviors, may be the key to curbing this epidemic.^ A school-based obesity prevention approach is advantageous for many reasons including exposure to large captive audiences, reduced costs of sustainability and long-term maintenance, and generalizability of models and results across multiple populations. The effectiveness of school-based programs has been researched over the past 20 years, with promising results.^ Social marketing is a program-planning process that “facilitates the acceptance, rejection, modification, abandonment, or maintenance of particular behaviors” (Grier & Bryant, 2005). Social marketing has been shown to be effective in a variety of public health applications including improving diet, increasing physical activity, and preventing substance abuse. It is hypothesized that social marketing could further enhance the effectiveness of the Coordinated Approach To Child Health (CATCH) Central Texas Middle School Project, a school-based obesity prevention program.^ The development, implementation, and initial evaluation of the get ur 60 campaign, to promote the Center for Disease Control and Prevention (CDC) recommended sixty minutes of daily activity, is described in this paper. Various components of the get ur 60 campaign were assessed to evaluate the effectiveness of the campaign during the first semester of implementation. At the end of the spring semester focus groups were held to collect student reactions to the first semester of the get ur 60 campaign.^ The initial results from the first semester of get ur 60 have demonstrated that the campaign as designed was feasible to implement, accepted at all intervention schools, and resulted in a measure of success. ^

Development and Characterization of an in vitro Four-species Anaerobic Dental Biofilm Model

Dental caries is the most common chronic disease worldwide. It is characterized by the demineralization of tooth enamel caused by acid produced by cariogenic dental bacteria growing on tooth surfaces, termed bacterial biofilms. Cariogenesis is a complex biological process that is influence by multiple factors and is not attributed to a sole causative agent. Instead, caries is associated with multispecies microbial biofilm communities composed of some bacterial species that directly influence the development of a caries lesion and other species that are seemingly benign but must contribute to the community in an uncharacterized way. Clinical analysis of dental caries and its microbial populations is challenging due to many factors including low sensitivity of clinical measurement tools, variability in saliva chemistry, and variation in the microbiota. Our laboratory has developed an in vitro anaerobic biofilm model for dental carries to facilitate both clinical and basic research-based analyses of the multispecies dynamics and individual factors that contribute to cariogenicity. The rational for development of this system was to improve upon the current models that lack key elements. This model places an emphasis on physiological relevance and ease of maintenance and reproducibility. The uniqueness of the model is based on integrating four critical elements: 1) a biofilm community composed of four distinct and representative species typically associated with dental caries, 2) a semi-defined synthetic growth medium designed to mimic saliva, 3) physiologically relevant biofilm growth substrates, and 4) a novel biofilm reactor device designed to facilitate the maintenance and analysis. Specifically, human tooth sections or hydroxyapatite discs embedded into poly(methyl methacrylate) (PMMA) discs are incubated for an initial 24 hr in a static inverted removable substrate (SIRS) biofilm reactor at 37°C under anaerobic conditions in artificial saliva (CAMM) without sucrose in the presence of 1 X 106 cells/ml of each Actinomyces odontolyticus, Fusobacterium nucleatum, Streptococcus mutans, and Veillonella dispar. During days 2 and 3 the samples are maintained continually in CAMM with various exposures to 0.2% sucrose; all of the discs are transferred into fresh medium every 24 hr. To validate that this model is an appropriate in vitro representation of a caries-associated multispecies biofilm, research aims were designed to test the following overarching hypothesis: an in vitro anaerobic biofilm composed of four species (S. mutans, V. dispar, A. odontolyticus, and F. nucleatum) will form a stable biofilm with a community profile that changes in response to environmental conditions and exhibits a cariogenic potential. For these experiments the biofilms as described above were exposed on days 2 and 3 to either CAMM lacking sucrose (no sucrose), CAMM with 0.2% sucrose (constant sucrose), or were transferred twice a day for 1 hr each time into 0.2% sucrose (intermittent sucrose). Four types of analysis were performed: 1) fluorescence microscopy of biofilms stained with Syto 9 and hexidium idodine to determine the biofilm architecture, 2) quantitative PCR (qPCR) to determine the cell number of each species per cm2, 3) vertical scanning interferometry (VSI) to determine the cariogenic potential of the biofilms, and 4) tomographic pH imaging using radiometric fluorescence microscopy after exposure to pH sensitive nanoparticles to measure the micro-environmental pH. The qualitative and quantitative results reveal the expected dynamics of the community profile when exposed to different sucrose conditions and the cariogenic potential of this in vitro four-species anaerobic biofilm model, thus confirming its usefulness for future analysis of primary and secondary dental caries.

Cost -effectiveness of services and treatments for ambulatory dually diagnosed CMHC clients: Implications for managed care

This paper reports a cost-effectiveness analysis of standard therapeutic interventions received by ambulatory dually diagnosed clients of a Community Mental Health Center (CMHC). For the purposes of this study dually diagnosed was defined as a DSM-III-R or IV diagnosis of a major mental disorder and a concomitant substance abuse disorder. The prevalence of dually diagnosed people among the mentally ill and their unique and problematic nature continues to challenge and encumber CMHCs and poses grave public health risks. An absence of research on these clients in community-based settings and the cost-effectiveness of their standard CMHC care has hindered the development of effective community-based intervention strategies. This exploratory and descriptive effort is a first step toward providing information on which to base programmatic management decisions.^ Data for this study were derived from electronic client records of a CMHC located in a large Southwestern, Sun-belt metropolitan area. A total of 220 records were collected on clients consecutively admitted during a two-and-one-half year period. Information was gathered profiling the clients' background characteristics, receipt of standard services and treatments, costs of the care they received, and length of CMHC enrollment and subsequent psychiatric hospitalizations. The services and treatments were compared with regard to their costs and predicted contributions toward maintaining clients in the community and out of public psychiatric hospitals.^ This study investigated: (1) the study groups' background, mental illness, and substance abuse characteristics; (2) types, extent, and patterns of their receipt of standard services and treatments; (3) associations between the receipt of services and treatments, community tenure, and risk of psychiatric hospitalization; and, (4) comparisons of average costs for services and treatments in terms of their contributions toward maintaining the clients in the community.^ The results suggest that substance abuse and other lifestyle factors were related to the dually diagnosed clients' admissions to the CMHC. The dually diagnosed clients' receipt of care was associated strongly with their insurability and global functioning. Medication Services were the most expensive yet effective service or treatment. Supported Education was the third most expensive and second most effective. Psychosocial Services, the second most expensive, were only effective in terms of maintaining clients in the community. Group Counseling, the fourth most expensive, had no effect on community maintenance and increased the risk of hospitalization when accompanied by Medication Services. Individual Counseling, the least expensive, had no effect on community maintenance. But it reduced the risk of hospitalization when accompanied by Medication Services. Networking/Referral, the fifth most expensive service or treatment, was ineffective.^ The study compared the results with findings in the literature. Implications are discussed regarding further research, study limitations, practical applications and benefits, and improvements to theoretical understandings, in particular, concepts underscoring Managed Care. ^

Escape performance of temperate king scallop, Pecten maximus under ocean warming and acidification

Among bivalves, scallops are exceptional due to their capacity to escape from predators by swimming which is provided by rapid and strong claps that are produced by the phasic muscle interspersed with tonic muscle contractions. Based on the concept of oxygen and capacity-limited thermal tolerance, the following hypothesis was tested: ocean warming and acidification (OWA) would induce disturbances in aerobic metabolic scope and extracellular acid-case status and impair swimming performance in temperate scallops. Following long-term incubation under near-future OWA scenarios [20 vs. 10 °C (control) and 0.112 kPa CO2 (hypercapnia) vs. 0.040 kPa CO2 (normocapnic control)], the clapping performance and metabolic rates (MR) were measured in resting (RMR) and fatigued (maximum MR) king scallops, Pecten maximus, from Roscoff, France. Exposure to OA, either alone or combined with warming, left MR and swimming parameters such as the total number of claps and clapping forces virtually unchanged. Only the duration of the escape response was affected by OA which caused earlier exhaustion in hyper- than in normocapnic scallops at 10 °C. While maximum MR was unaffected, warm exposure increased RMR in both normocapnic and hypercapnic P. maximus resulting in similar Q 10 values of ~2.2. The increased costs of maintenance and the observation of strongly reduced haemolymph PO2 levels indicate that at 20 °C scallops have reached the upper thermal pejus range with unbalanced capacities for aerobic energy metabolism. As a consequence, warming to 20 °C decreased mean phasic force during escape performance until fatigue. The observed prolonged recovery time in warm incubated scallops might be a consequence of elevated metabolic costs at reduced oxygen availability in the warmth.

(Table 1) Diving behaviour of male Adélie penguins (Pygoscelis adeliae) with and without corticosterone implants at Pointe Géologie

The amount of energy that organisms can allocate to self-maintenance and/or reproduction largely depends on their foraging strategies. Because of corticosterone (CORT) involvement in the control of energy metabolism, food intake and locomotor activity, recent studies have sought to demonstrate the role of this hormone in foraging decisions and performance. Moreover, considerable recent advances in animal-attached loggers now allow the study of behaviour in free-living animals. In order to assess the effects of CORT administration on the foraging behaviour of free-living Adelie Penguins Pygoscelis adeliae, we studied a group with CORT implants and a control group without CORT implants, by attaching time-depth recorders to the two groups and monitoring them throughout up to seven consecutive foraging trips during the guard stage (in Adelie Land, Antarctica). We found that foraging trips duration was similar between both groups. Dive durations, time spent at the bottom phase of dives, and the number of undulations per dive of CORT-implanted birds were all significantly higher than those of controls. However, CORT-implanted birds performed fewer dives overall (ca. 4,400) than controls (ca. 6,250) and spent many (13 and 6 times for penguins #3 and #4, respectively) long periods (>3 h) without diving. The low foraging effort and long resting periods support the view that CORT-implanted birds probably gained less energy than did the control birds. CORT treatment appears then to result in redirecting bird behaviour from costly activity (i.e. reproduction) to a behaviour promoting the preservation of energy reserves. Future studies are therefore needed to assess body condition and reproductive success of CORT-manipulated birds in parallel with the recording of their diving performances.

(Tables 1+4) Sample site substratum and morphometrics and damage levels of different populations of Laternula elliptica around Antarctica

We document differences in shell damage and shell thickness in a bivalve mollusc (Laternula elliptica) from seven sites around Antarctica with differing exposures to ice movement. These range from 60% of the sea bed impacted by ice per year (Hangar Cove, Antarctic Peninsula) to those protected by virtually permanent sea ice cover (McMurdo Sound). Patterns of shell damage consistent with blunt force trauma were observed in populations where ice scour frequently occurs; damage repair frequencies and the thickness of shells correlated positively with the frequency of iceberg scour at the different sites with the highest repair rates and thicker shells at Hangar Cove (74.2% of animals damaged) compared to the other less impacted sites (less than 10% at McMurdo Sound). Genetic analysis of population structure using Amplified Fragment Length Polymorphisms (AFLPs) revealed no genetic differences between the two sites showing the greatest difference in shell morphology and repair rates. Taken together, our results suggest that L. elliptica exhibits considerable phenotypic plasticity in response to geographic variation in physical disturbance.