Navigating noisy waters: A review of field studies examining anthropogenic noise effects on wild fisha).

Anthropogenic noise is globally increasing in aquatic ecosystems, and there is concern that it may have adverse consequences in many fish species, yet the effects of noise in field settings are not well understood. Concern over the applicability of laboratory-conducted bioacoustic experiments has led to a call for, and a recent increase in, field-based studies, but the results have been mixed, perhaps due to the wide variety of techniques used and species studied. Previous reviews have explored the behavioral, physiological, and/or anatomical costs of fish exposed to anthropogenic noise, but few, if any, have focused on the field techniques and sound sources themselves. This review, therefore, aims to summarize, quantify, and interpret field-based literature, highlight novel approaches, and provide recommendations for future research into the effects of noise on fish.

Infrared photoconductivity and photovoltaic response from nanoscale domains of PbS alloyed with thorium and oxygen.

Thin films of lead sulfide alloyed with thorium and oxygen were deposited on GaAs substrates and processed to produce a photo-diode structure. Structural, optical and electrical characterizations indicate the presence of small nanoscale domains (NDs) that are characterized by dense packaging, high quality interfaces and a blue-shift of the energy bandgap toward the short wavelength infrared range of the spectrum. Photocurrent spectroscopy revealed a considerable photoconductivity that is correlated with excitation of carriers in the NDs of lead sulfide alloyed with thorium and oxygen. Furthermore, the appearance of a photovoltaic effect under near infrared illumination indicates a quasi-type II band alignment at the interface of the GaAs and the film of NDs.

A case of near-drowning: a case for routine cerebral monitoring.

UNLABELLED: A 6-week-old infant presenting with near-drowning was medically paralysed and ventilated on admission. Status epilepticus was found on cerebral function monitoring, without which the diagnosis would have been missed or delayed for many hours. This case illustrates the value of cerebral function monitoring for patients in intensive care, where clinical signs of seizure activity are frequently masked by paralysis and sedation. CONCLUSION: Limited availability of electroencephalogram (EEG) and cerebral function monitoring (CFM) in paediatric intensive care may inadvertently delay diagnosis and appropriate treatments and so adversely affect outcomes. We propose that round-the-clock cerebral function and/or EEG monitoring should be available in all centres that provide paediatric intensive care.

Mosquitoes: biting behavior inhibited by ecdysone.

Biting in Anopheles freeborni is inhibited during ovarian development. Biting inhibition is triggered by ecdysone, a hormone produced by the ovary during oogenesis. Biting inhibition does not occur in females after the removal of ovaries, but is restored by replacing ovaries or injecting ecdysone. Ecdysone also inhibits biting behavior when it is fed to females. This is the first example of ecdysone controlling a nonmolt-related behavior in insects.

Gestational zinc deprivation in mice: persistence of immunodeficiency for three generations.

Pregnant Swiss Webster mice were fed a diet moderately deficient in zinc from day 7 of gestation until parturition. Offspring of these mice showed depressed immune function through 6 months of age. In addition, the second and third filial generations, all of which were fed only the normal control diet, continued to manifest reduced immunocompetence, although not to the same degree as in the first generation.

Respecting autonomy in young people.

Paediatricians have a duty to protect the life and health of their patients and to respect their autonomy. Usually, there will be no conflict between these duties. Both children and parents want effective care and agree to the medical interventions that that are most likely to provide it. However, when children refuse or resist such interventions, it may be unclear when the duty to protect trumps the duty to respect. This is because children may have differing levels of autonomy, sometimes making them competent to make medical decisions for themselves and at other times not. Further, there may be conflict between the children and their parents in such circumstances. Children may refuse treatments that parents desire or vice versa. Sometimes paediatricians may agree with the child in the face of legal powers of parental guardianship. At other times they may agree with the parents, facing the prospect of forcing treatment on an unwilling child with potentially devastating psychological consequences. This paper will explore this potential ethical and legal minefield by evaluating some practical clinical cases based on the experiences of the primary author. It provides a range of examples of these different types of conflicts, including especially problematic "hard cases" that concern the withdrawal of life-sustaining treatment and child protection. The goal of the article is not simply to morally and legally outline the boundaries of such tensions in paediatric care. It also provides concrete advice about how they should best be resolved in everyday clinical practice.

Estimation of the Rigid-Body Motion from Three-Dimensional Images Using a Generalized Center-of-Mass Points Approach.

We present an analytical method for the estimation of rigid-body motion in sets of three-dimensional SPECT and PET slices. This method utilizes mathematically defined generalized center-of-mass points in images, requiring no segmentation. It can be applied to compensation of the rigid-body motion in both SPECT and PET, once a series of 3D tomographic images are available. We generalized the formula for the center-of-mass to obtain a family of points co-moving with the object's rigid-body motion. From the family of possible points we chose the best three points which resulted in the minimum root-mean-square difference between images as the generalized center-of-mass points for use in estimating motion. The estimated motion was used to sum the sets of tomographic images, or incorporated in the iterative reconstruction to correct for motion during reconstruction of the combined projection data. For comparison, the principle-axes method was also applied to estimate the rigid-body motion from the same tomographic images. To evaluate our method for different noise levels, we performed simulations with the MCAT phantom. We observed that though noise degraded the motion-detection accuracy, our method helped in reducing the motion artifact both visually and quantitatively. We also acquired four sets of the emission and transmission data of the Data Spectrum Anthropomorphic Phantom positioned at four different locations and/or orientations. From these we generated a composite acquisition simulating periodic phantom movements during acquisition. The simulated motion was calculated from the generalized center-of-mass points calculated from the tomographic images reconstructed from individual acquisitions. We determined that motion-compensation greatly reduced the motion artifact. Finally, in a simulation with the gated MCAT phantom, an exaggerated rigid-body motion was applied to the end-systolic frame. The motion was estimated from the end-diastolic and end-systolic images, and used to sum them into a summed image without obvious artifact. Compared to the principle-axes method, in two of the three comparisons with anthropomorphic phantom data our method estimated the motion in closer agreement to than of the Polaris system than the principal-axes method, while the principle-axes method gave a more accurate estimation of motion in most cases for the MCAT simulations. As an image-driven approach, our method assumes angularly complete data sets for each state of motion. We expect this method to be applied in correction of respiratory motion in respiratory gated SPECT, and respiratory or other rigid-body motion in PET.

Expression of the sea urchin MyoD homologue, SUM1, is not restricted to the myogenic lineage during embryogenesis.

SUM1 (sea urchin myogenic factor 1) is a sea urchin homologue of the myogenic basic helix-loop-helix transcription factors of the MyoD family. SUM1 was initially cloned from Lytechinus variegatus where immunocytochemistry demonstrated restricted expression in precursors of the circumesophageal muscles, the only identified muscle cells in the early embryo. Subsequent in situ hybridization analysis indicates that SUM1 embryonic expression is not restricted to the myogenic lineage; a distinct population of nonmyogenic cells also expresses SUM1. For comparative purposes, we cloned the SUM1 orthologue in the distantly related sea urchin, Strongylocentrotus purpuratus, where we found SpSUM1 transcripts in the same population of nonmyogenic cells.

Specific nutrient abnormalities in asymptomatic HIV-1 infection.

OBJECTIVE: To determine whether specific nutrient abnormalities occur in earlier stages of HIV-1 infection, thereby preceding the marked wasting and malnutrition that accompany later stages of the infection. DESIGN: A longitudinal investigation to determine biological, psychological and social factors thought to influence the progression and outcome of HIV-1 infection. Nutritional status was assessed using biochemical measurement of nutrient levels, dietary history, anthropometry and clinical examination for the signs and symptoms of nutritional deficiency or excess. SETTING: The study was performed on an outpatient basis at the University of Miami School of Medicine. PARTICIPANTS: One hundred homosexual men, aged between 20 and 55 years, who were asymptomatic other than persistent generalized lymphadenopathy (Centers for Disease Control stage III) and 42 age-matched homosexual men demonstrated to be free of HIV-1 infection at two 6-month intervals. MAIN OUTCOME MEASURES: Biochemical measurement of nutrient status, dietary history, anthropometry, clinical signs or symptoms of nutritional excess or deficiency were obtained for all participants. RESULTS: Despite few differences in mean blood levels of specific nutrients, prevalence of specific nutrient abnormalities was widespread among HIV-1-infected subjects, compared with non-infected male homosexual controls. Overtly and marginally low blood levels of vitamins A (18%), E (27%), riboflavin (26%), B6 (53%), and B12 (23%), together with copper (74%) and zinc (50%) were documented in HIV-1-seropositive subjects. With the exception of riboflavin, zinc, and copper, a similar prevalence of abnormalities among HIV-1-seronegative controls was not observed. CONCLUSION: Specific nutrient abnormalities occur with relative frequency in asymptomatic HIV-1 infection and may contribute to the rate and form of HIV-1 disease progression.

Dopamine fails to inhibit renal tubular sodium pump in hypertensive rats.

We have previously reported that dopamine-1 receptor-mediated activation of phospholipase C is diminished in renal cortical slices of adult spontaneously hypertensive rats. To determine the potential consequences of this phenomenon, we performed the present studies in which renal proximal tubule suspensions obtained from spontaneously hypertensive and Wistar-Kyoto rats of 10-12 weeks of age were used. The tubule suspensions were incubated with dopamine in the presence or absence of dopamine receptor antagonists, and sodium, potassium adenosine trisphosphatase (sodium pump) activity was measured as the ouabain-sensitive adenosine trisphosphate hydrolysis. We found that dopamine produced a concentration-related inhibition of sodium pump activity in the normotensive rats but not in the hypertensive rats. Dopamine-induced inhibition of sodium pump activity in the normotensive rats was abolished by the phospholipase C inhibitor U-73122 or the protein kinase C inhibitor sphingosine, suggesting the involvement of a phospholipase C-coupled protein kinase C pathway in this response. Dopamine-induced inhibition in the normotensive rats was attenuated by the dopamine-1 receptor antagonist SCH 23390 but not by the dopamine-2 receptor antagonist domperidone. To identify possible sites of defect in dopamine-1 receptor-coupled signaling pathways in the hypertensive rats, we incubated the proximal tubules with phorbol 12,13-dibutyrate or the synthetic diacylglycerol analogue 1-oleoyl-2-acetyl-rac-glycerol. The results showed that both compounds inhibited sodium pump activity as effectively in the hypertensive as in the normotensive rats, suggesting that the protein kinase C-coupled sodium pump pathway was not defective in the hypertensive animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Cloning of the alpha-subunit of GS protein from spontaneously hypertensive rats.

Enhanced sodium reabsorption by the kidney has a significant role in the development of genetic hypertension. In the spontaneously hypertensive rat (SHR) model of genetic hypertension, the enhanced sodium reabsorption likely arises from abnormal hormonal regulation of tubular transport. Since hormonal signaling pathways are coupled frequently via GTP binding proteins, one explanation for hormonal abnormalities in SHR would be a defect in a GTP binding protein or proteins. Recent work has suggested that the regulation of Na+,K(+)-ATPase activity by cholera toxin-sensitive GTP binding proteins is abnormal in SHR. The purpose of the present studies was to clone the alpha S-subunit, which is the subunit ADP ribosylated by cholera toxin, of GS protein to determine whether it is abnormal in SHR. Reverse transcription-polymerase chain reaction was able to detect mRNA for alpha S in both Wistar-Kyoto (WKY) rats and SHR. Northern analysis indicated that equivalent amounts of alpha S mRNA were present in WKY rats and SHR. S1 nuclease analysis demonstrated that there was no difference in the amount of alpha S short and long forms between WKY rats and SHR. Subcloning and sequencing of polymerase chain reaction products from WKY rats and SHR indicated that the alpha S forms present in renal cortex were identical. ADP ribosylation studies with cholera toxin demonstrated the presence of equivalent amounts of alpha S protein in WKY rats and SHR. Taken together, these results suggest that the abnormal regulation of Na+,K(+)-ATPase activity by a cholera toxin-sensitive pathway in SHR does not arise from a defect in the alpha S subunit.

The identification of neurotrophic factor as a transferrin.

Partially purified neurotrophic factor (NTF) from chicken nerves comigrated with transferrin and a component in several preparations known to have neurotrophic effects on cultured skeletal muscle cells. One-dimensional gel electrophoretograms of proteolytic fragments of NTF and fragments obtained from transferrins purified from chicken eggs, serum and embryos were indistinguishable. These purified transferrins, like NTF, all stimulated the incorporation of [3H]thymidine and supported myotube formation to a similar degree as NTF. These studies suggest that NTF is a transferrin-like protein and that both transferrins and NTF act by initially promoting myoblast proliferation and subsequently supporting myogenesis in chick muscle cultures.

Persistent immunological consequences of gestation zinc deprivation.

Recent work has shown that offspring of outbred mice deprived of adequate dietary zinc during the latter two-thirds of gestation exhibited a defective direct plaque-forming cell response to immunization with heterologous erythrocytes, as well as impaired ontogenesis of serum IgM. Moreover, such aberrant immunological measurements continued to be observed, although to a lesser degree, in F2 and F3 progeny. We now demonstrate that offspring of mice moderately deprived of zinc (5 ppm zinc diet) between days 7 and 20 of gestation also show an aberrant pattern of development of serum levels of IgG2a and IgA, despite complete nutritional rehabilitation beginning at birth. Only by 6 months of age were concentrations of these serum immunoglobulins similar to those in offspring of control dams. In contrast, levels of IgG1 and IgG2b were within normal ranges by 6 wk of age. Cross-fostering of zinc-deprived offspring to dams adequately nourished during pregnancy did little to ameliorate their aberrant pattern of serum immunoglobulin development. Defective maturation of serum IgG2a and IgA did not persist in F2 and F3 progeny. Nonetheless such 2nd and 3rd generation offspring continued to have higher than normal perinatal mortality. The alterations of immune ontogenesis in these mice could not be attributed to the persistence of abnormal plasma zinc levels, as these were within normal ranges. It would appear that zinc deficiency during gestation may alter the basic mechanism of development of immunological competence.

Use of an expanded-whole-wheat product in the reduction of body weight and serum lipids in obese females.

To achieve weight reduction and alter serum lipid profiles, an air-expanded whole-wheat protein product (SNW) was used by moderately obese women as a meal substitute for 12 wk. Results were compared with those from a standard low-calorie diet (LCD). The SNW group lost 3.9 kg (means) over the first 6 wk and a further 1.6 kg between weeks 6 and 12. In contrast, the LCD group lost 2.8 kg during the initial 6 wk but failed to achieve weight loss during the second 6 wk. Consequently, the SNW group lost nearly twice as much weight over the 12-wk period as did LCD participants. A beneficial effect of SNW on serum cholesterol and triglycerides was noted; both measures declined in conjunction with the weight loss. Such alterations were greater in the SNW group than in LCD participants. Both schemes proved safe. SNW is safe and effective in weight reduction and serum lipid modification in moderately obese women.

Plasma vitamin B12 level as a potential cofactor in studies of human immunodeficiency virus type 1-related cognitive changes.

Studies of cognitive function in subjects with human immunodeficiency virus type 1 (HIV-1) infection who remain relatively asymptomatic (ie, Centers for Disease Control stages II and III) have provided widely variable estimates of cognitive impairment. In view of the finding that approximately 25% of asymptomatic HIV-1-infected subjects demonstrate either marginal or overt vitamin B12 deficiency, we have investigated plasma vitamin B12 status as a potential cofactor in studies of HIV-1-related cognitive impairment. When cognition was assessed in asymptomatic (Centers for Disease Control stages II and III) HIV-1-infected participants taking into consideration vitamin B12 status, those subjects with low plasma vitamin B12 levels (less than 180 pmol/L) performed more poorly than did those with normal (greater than or equal to 180 pmol/L) vitamin B12 status on specific measures of information processing speed and visuospatial problem-solving skills. These findings suggest that concurrent vitamin B12 deficiency may be a cofactor in subtle cognitive changes observed in the asymptomatic stages of HIV-1 infection. These differences in prevalence of low plasma vitamin B12 levels may help to explain differences among studies in the proportion of HIV-1-infected subjects showing cognitive impairment.

Association of vitamin B6 status with parameters of immune function in early HIV-1 infection.

Nutritional deficiencies have been documented to affect immune function. The present study indicates that vitamin B6 deficiency is prevalent in CDC stage III HIV-1-infected subjects, despite adequate dietary vitamin B6 intake. As vitamin B6 deficiency has been previously shown to affect immune function, these relatively asymptomatic HIV-1-infected patients were examined for evidence of a relationship between vitamin B6 deficiency and immune dysregulation. Vitamin B6 status in HIV-1-infected subjects was significantly associated with functional parameters of immunity [multivariate F(3,36) = 3.70, p less than or equal to 0.02]. Additional analyses indicated that overtly deficient participants exhibited significantly decreased lymphocyte responsiveness to the mitogens phytohemagglutinin and pokeweed, and reduced natural killer cell cytotoxicity, compared to subjects with clearly adequate vitamin B6 status (chi 2 = 8.78, df = 3, p less than 0.04). Vitamin B6 status was not related to immune cell subpopulations, e.g., CD4, CD8 cell number, or level of serum immunoglobulins. The results of this study indicate that while vitamin B6 status is not a primary etiological factor in HIV-1-related immunological dysregulation, it appears to be an important cofactor of immune function.

Zidovudine-associated adverse reactions in a longitudinal study of asymptomatic HIV-1-infected homosexual males.

Chemotherapeutic regimens frequently interact with and may influence nutritional factors. To determine the possible effects of zidovudine (ZDV) treatment on nutrient status, this study examined and compared the nutritional, immunological, and hematological status of asymptomatic, CDC stage III, HIV-1-seropositive males (n = 15) provided with ZDV (500-1,200 mg/day) and 22 nontreated, CD4-matched HIV-1-seropositive subjects. Prior to ZDV administration, hematological and plasma nutrient levels were similar in both groups. Following ZDV treatment, drug-treated subjects demonstrated alterations in hematological and nutritional parameters. A large proportion of the ZDV-treated participants exhibited decreased levels of zinc and copper along with a significant increase in red cell folate. The level of plasma zinc appeared to be particularly important in maintaining immune function in the ZDV-treated group. Whereas ZDV-treated subjects with adequate zinc levels displayed a significant increase in the response of peripheral blood lymphocytes to mitogens, this enhancement was not demonstrated in zinc-deficient, ZDV-treated participants or in untreated individuals whose lymphocyte response significantly declined over time, despite adeqaute zinc status. The findings of this study reveal a zidovudine-induced effect on nutritional parameters, indicating the importance of monitoring nutritional status with drug therapeutic regimens.

Contrast agent neurotoxicity presenting as subarachnoid hemorrhage.

A patient developed signs, symptoms, and radiologic findings compatible with acute subarachnoid hemorrhage after receiving a large dose of heparin and intravascular contrast medium for coronary angiography and stent placement. Subsequent CT indicated the subarachnoid enhancement was due to contrast. Neurotoxicity from contrast agents is well-known, however this is an unusual report of toxicity mimicking subarachnoid hemorrhage clinically and radiologically.

P504S immunohistochemical detection in 405 prostatic specimens including 376 18-gauge needle biopsies.

P504S is a recently described, prostate cancer-specific gene that encodes a protein involved in the beta-oxidation of branched chain fatty acids. A recent study has shown that immunohistochemical detection of P504S gene product is a sensitive and specific marker of prostatic carcinoma in formalin-fixed, paraffin-embedded tissues. We performed a detailed analysis of P504S protein expression in a large series of prostate and bladder specimens with special emphasis on staining in specific morphologic patterns of prostatic adenocarcinoma, posthormonal and radiation therapy cases, and invasive urothelial carcinoma. A total of 366 prostate needle core biopsies from 124 patients with prostate cancer, 10 biopsies from 2 patients without prostate cancer, 28 prostatectomy specimens (16 with specific morphologic patterns, 7 posthormonal therapy and 5 postradiation therapy specimens), 5 bladder specimens with invasive urothelial carcinoma, and a single transurethral resection specimen from a patient with hormonally treated prostate cancer and invasive urothelial carcinoma were stained with P504S monoclonal antibody at a 1:250 dilution using standard heat-induced epitope retrieval and avidin-biotin technique. Extent (0, no staining; 1+, 1-10% staining; 2+, 11-50% staining; 3+, > or =51% staining) and location (luminal, subluminal, and diffuse cytoplasmic) of immunoreactivity in carcinoma and benign tissues were recorded. A total of 153 of 186 biopsies (82%) with prostatic adenocarcinoma stained for P504S. Pseudohyperplastic, atrophic, ductal, and mucinous prostatic carcinomas stained similarly, as did cases treated with hormone or radiotherapy. In 81 of 377 (21%) foci of benign prostatic tissue there was staining that was almost always focal, faint, and noncircumferential. Seminal vesicles did not stain for P504S. Five of six (83%) specimens with invasive urothelial carcinoma had 2+ staining and one case had focal staining. We conclude that immunohistochemistry for P504S has potential utility in the diagnosis of prostate cancer, including those treated by hormones and radiation. Circumferential luminal to subluminal and diffuse cytoplasmic staining is the most specific staining pattern for prostatic carcinoma and is almost never associated with benign prostatic tissue. However, a negative P504S immunostain does not automatically rule out prostate cancer, as 18% of cases were negative. Additionally, occasional benign glands, high-grade prostatic intraepithelial neoplasia, atypical adenomatous hyperplasia, and urothelial carcinoma may express P504S. Therefore, we think that P504S is best used only in conjunction with strict light microscopic correlation and preferably with high molecular weight cytokeratin immunostaining.

Production of human chorionic gonadotrophin by a hepatoblastoma resulting in precocious puberty.

A two year old boy presented with precocious puberty associated with hepatoblastoma. Serum concentrations of beta human chorionic gonadotrophin and alpha-fetoprotein were raised. An aggressive chemotherapeutic regimen resulted in useful palliation and interesting changes in the beta human chorionic gonadotrophin and alpha-fetoprotein concentrations. In contrast to a previous report, the ultrastructure of the tumour showed frequent Golgi apparatus but no other electron dense membrane bound vesicles.