Functional and Environmental Constraints on Prey Capture Speed in a Lizard.

Movement is an important component of animal behavior and determines how an organism interacts with its environment. The speed at which an animal moves through its environment can be constrained by internal (e.g., physiological state) and external factors (e.g., habitat complexity). When foraging, animals should move at speeds that maximize prey capture while minimizing mistakes (i.e., missing prey, slipping). We used experimental arenas containing obstacles spaced in different arrays to test how variation in habitat complexity influenced attack distance, prey capture speed, and foraging success in the Prairie Lizard. Obstacles spaced uniformly across arenas resulted in 15% slower prey capture speed and 30-38% shorter attack distance compared to arenas with no obstacles or with obstacles clustered in opposite corners of the arena. Prey capture probability was not influenced by arena type or capture speed, but declined with increasing attack distance. Similarly, the probability of prey consumption declined with attack distance across arena types. However, prey consumption probability declined with increasing prey capture speed in more open arenas but not in the cluttered arena. Foraging accuracy declined with increasing speed in more open arenas, and remained relatively constant when obstacles were in closer proximity. Foraging success was primarily constrained by intrinsic properties (speed-maneuverability tradeoff) when ample space was available, but environmental conditions had a greater impact on foraging success in "cluttered" habitats. This empirical test of theoretical predictions about optimal movement speeds in animals provides a step forward in understanding how animals select speeds in nature.

Hormone activities and the cell cycle machinery in immunity-triggered growth inhibition.

Biotic stress and diseases caused by pathogen attack pose threats in crop production and significantly reduce crop yields. Enhancing immunity against pathogens is therefore of outstanding importance in crop breeding. However, this must be balanced, as immune activation inhibits plant growth. This immunity-coupled growth trade-off does not support resistance but is postulated to reflect the reallocation of resources to drive immunity. There is, however, increasing evidence that growth-immunity trade-offs are based on the reconfiguration of hormone pathways, shared by growth and immunity signalling. Studies in roots revealed the role of hormones in orchestrating growth across different cell types, with some hormones showing a defined cell type-specific activity. This is apparently highly relevant for the regulation of the cell cycle machinery and might be part of the growth-immunity cross-talk. Since plants are constantly exposed to Immuno-activating microbes under agricultural conditions, the transition from a growth to an immunity operating mode can significantly reduce crop yield and can conflict our efforts to generate next-generation crops with improved yield under climate change conditions. By focusing on roots, we outline the current knowledge of hormone signalling on the cell cycle machinery to explain growth trade-offs induced by immunity. By referring to abiotic stress studies, we further introduce how root cell type-specific hormone activities might contribute to growth under immunity and discuss the feasibility of uncoupling the growth-immunity cross-talk.

Housing helpful invaders: the evolutionary and molecular architecture underlying plant root-mutualist microbe interactions.

Plant root rhizosphere interactions with mutualistic microbes are diverse and numerous, having evolved over time in response to selective pressures on plants to attain anchorage and nutrients. These relationships can be considered to be formed through a combination of architectural connections: molecular architecture interactions that control root-microbe perception and regulate the balance between host and symbiont and developmental architecture interactions that enable the microbes to be 'housed' in the root and enable the exchange of compounds. Recent findings that help to understand the common architecture that exists between nodulation and mycorrhizal interactions, and how this architecture could be re-tuned to develop new symbioses, are discussed here.

Gambusia quadruncus (Cyprinodontiformes: Poeciliidae): a new species of mosquitofish from east-central México.

Gambusia quadruncus n. sp., the llanos mosquitofish, is described from east-central México. The region inhabited by the species represents a hotspot of diversity of Gambusia, and G. quadruncus sometimes coexists with at least three congeners. The species differs from its closest relative, Gambusia affinis, in several characteristics with plausible effects on reproductive isolation, e.g. body size, body and fin morphology, male genital morphology (distal tip of gonopodium) and female anal spot morphology (colouration near the urogenital sinus). Moreover, combined analysis of mitochondrial and nuclear gene sequence data (c. 2158 total base pairs) indicates reciprocal monophyly of G. quadruncus and its sister species G. affinis, with levels of genetic divergence suggesting the two species diverged from one another over a million years ago. The origin of G. quadruncus may reflect a vicariant event associated with Pliocene orogenesis in the Tamaulipas Arch and a frontal section of the Sierra Madre Oriental (Lleran Mesas). Gambusia quadruncus inhabits a variety of freshwater habitats across several river drainages, with its range spanning at least 350 km from north to south, covering over 25 000 km(2). A key to aid identification of the species is provided.

Variable correction of host defense following gene transfer and bone marrow transplantation in murine X-linked chronic granulomatous disease.

Chronic granulomatous disease (CGD) is an inherited immunodeficiency in which the absence of the phagocyte superoxide-generating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase results in recurrent bacterial and fungal infections. A murine model of X-linked CGD (X-CGD) was used to explore variables influencing reconstitution of host defense following bone marrow transplantation and retroviral-mediated gene transfer. The outcomes of experimental infection with Aspergillus fumigatus, Staphylococcus aureus, or Burkholderia cepacia were compared in wild-type, X-CGD mice, and transplanted X-CGD mice that were chimeric for either wild-type neutrophils or neutrophils with partial correction of NADPH oxidase activity after retroviral-mediated gene transfer. Host defense to these pathogens was improved in X-CGD mice even with correction of a limited number of neutrophils. However, intact protection against bacterial pathogens required relatively greater numbers of oxidant-generating phagocytes compared to protection against A fumigatus. The host response also appeared to be influenced by the relative level of cellular NADPH oxidase activity, particularly for A fumigatus. These results may have implications for developing effective approaches for gene therapy of CGD. (Blood. 2001;97:3738-3745)

Retroviral-mediated gene transfer of gp91phox into bone marrow cells rescues defect in host defense against Aspergillus fumigatus in murine X-linked chronic granulomatous disease.

The X-linked form of chronic granulomatous disease (X-CGD), an inherited deficiency of the respiratory burst oxidase, results from mutations in the X-linked gene for gp91phox, the larger subunit of the oxidase cytochrome b. The goal of this study was to evaluate the impact of retroviral-mediated gene transfer of gp91phox on host defense against Aspergillus fumigatus in a murine model of X-CGD. Retrovirus vectors constructed using the murine stem cell virus (MSCV) backbone were used for gene transfer of the gp91phox cDNA into murine X-CGD bone marrow cells. Transduced cells were transplanted into lethally irradiated syngeneic X-CGD mice. After hematologic recovery, superoxide production, as monitored by the nitroblue tetrazolium (NBT) test, was detected in up to approximately 80% of peripheral blood neutrophils for at least 28 to 35 weeks after transplantation. Neutrophil expression of recombinant gp91phox and superoxide production were significantly less than wild-type neutrophils. However, 9 of 9 mice with approximately 50% to 80% NBT+ neutrophils after gene transfer did not develop lung disease after respiratory challenge with 150 to 500 A fumigatus spores, doses that produced disease in 16 of 16 control X-CGD mice. In X-CGD mice transplanted with mixtures of wild-type and X-CGD bone marrow, > or = 5% wild-type neutrophils were required for protection against A fumigatus challenge. These data suggest that expression of even low levels of recombinant gp91phox can substantially improve phagocyte function in X-CGD, although correction of very small percentage of phagocytes may not be sufficient for protection against A fumigatus.

Absence of respiratory burst in X-linked chronic granulomatous disease mice leads to abnormalities in both host defense and inflammatory response to Aspergillus fumigatus.

Mice with X-linked chronic granulomatous disease (CGD) generated by targeted disruption of the gp91phox subunit of the NADPH-oxidase complex (X-CGD mice) were examined for their response to respiratory challenge with Aspergillus fumigatus. This opportunistic fungal pathogen causes infection in CGD patients due to the deficient generation of neutrophil respiratory burst oxidants important for damaging A. fumigatus hyphae. Alveolar macrophages from X-CGD mice were found to kill A. fumigatus conidia in vitro as effectively as alveolar macrophages from wild-type mice. Pulmonary disease in X-CGD mice was observed after administration of doses ranging from 10(5) to 48 spores, none of which produced disease in wild-type mice. Higher doses produced a rapidly fatal bronchopneumonia in X-CGD mice, whereas progression of disease was slower at lower doses, with development of chronic inflammatory lesions. Marked differences were also observed in the response of X-CGD mice to the administration of sterilized Aspergillus hyphae into the lung. Within 24 hours of administration, X-CGD mice had significantly higher numbers of alveolar neutrophils and increased expression of the proinflammatory cytokines IL-1 beta and TNF-alpha relative to the responses seen in wild-type mice. By one week after administration, pulmonary inflammation was resolving in wild-type mice, whereas X-CGD mice developed chronic granulomatous lesions that persisted for at least six weeks. This is the first experimental evidence that chronic inflammation in CGD does not always result from persistent infection, and suggests that the clinical manifestations of this disorder reflect both impaired microbial killing as well as other abnormalities in the inflammatory response in the absence of a respiratory burst.

Human memory for odour following monorhinal presentation with and without verbal elaboration.

With 14 target odours, 7 via each nostril, 20 subjects' correct recognition was lower for the right nostril than for the left with verbal elaboration, but nonsignificant without verbal elaboration.

Mouse model of X-linked chronic granulomatous disease, an inherited defect in phagocyte superoxide production.

Chronic granulomatous disease (CGD) is a recessive disorder characterized by a defective phagocyte respiratory burst oxidase, life-threatening pyogenic infections and inflammatory granulomas. Gene targeting was used to generate mice with a null allele of the gene involved in X-linked CGD, which encodes the 91 kD subunit of the oxidase cytochrome b. Affected hemizygous male mice lacked phagocyte superoxide production, manifested an increased susceptibility to infection with Staphylococcus aureus and Aspergillus fumigatus and had an altered inflammatory response in thioglycollate peritonitis. This animal model should aid in developing new treatments for CGD and in evaluating the role of phagocyte-derived oxidants in inflammation.

Restitution of superoxide generation in autosomal cytochrome-negative chronic granulomatous disease (A22(0) CGD)-derived B lymphocyte cell lines by transfection with p22phax cDNA.

The respiratory burst oxidase of phagocytes and B lymphocytes is a multicomponent enzyme that catalyzes the one-electron reduction of oxygen by NADPH. It is responsible for the O2-production that occurs when these cells are exposed to phorbol 12-myristate 13-acetate or physiologic stimuli, such as phagocytosis in phagocytes or cross-linking of surface immunoglobulin in B lymphocytes. The activity of this enzyme is greatly diminished or absent in patients with chronic granulomatous disease (CGD), an inherited disorder characterized by a severe defect in host defense against bacteria and fungi. In every CGD patient studied so far, an abnormality has been found in a gene encoding one of the four components of the respiratory burst oxidase: the membrane proteins p22phox or gp91phox which together form the cytochrome b558 protein, or the cytosolic proteins p47phox or p67phox. Autosomal recessive cytochrome-negative CGD (A22(0) CGD) is associated with mutations in the gene coding for p22phox. We report here that the capacity for O2- production and cytochrome b558 protein expression were restored to Epstein-Barr virus-transformed B lymphocytes from two A22(0) CGD patients by transfection with an expression plasmid containing a p22phox cDNA. No detectable O2- was generated by untransfected p22phox-deficient lymphocytes. The genetic reconstitution of the respiratory burst in A22(0) CGD B lymphocytes by transfer of the wild-type p22phox cDNA represents a further step towards somatic gene therapy for this subgroup of A22(0) CGD. This system will also be useful for expression of genetically engineered mutant p22phox proteins in intact cells, facilitating the structure-function analysis of cytochrome b558.

Quality, access, and clinical issues in a nurse practitioner colposcopy outreach program.

From 8/89 to 7/92 a NP-colposcopist performed 593 colposcopy examinations including cervical biopsies, endocervical curettages, and Pap smears. Procedures were performed in selected health departments in north-central Florida. This portable outreach program expanded services to a primarily rural, medically indigent population. Specimen results were 21.1% negative, 5.6% human papilloma virus (HPV) only, 37.3% CIN I, 17.4% CIN II, 11.9% CIN III, 2.4% CIS, 0.3% carcinoma, and 4% other. Many CIN lesions also included HPV, yielding an overall incidence of HPV at 62.7%. Using the Bethesda system, 42.8% were low grade lesions, 32.1% high grade. Fourteen cases of CIS and two of carcinoma (one invasive, one microinvasive) were found. An 87.7% colposcopic diagnostic acumen level is favorable compared with published physician studies. One third of undercalls were due to occult canal lesions. Significant risk factors were smoking (48.6%), first coitus at < 18 years old (74%), history of HPV (49.6%), and life-time sexual partners > 2 (61.3%). Holistic prevention enabled 209 non-colposcopy problems.

Diode-pumped Nd:YLF regenerative amplifier.

A diode-pumped Nd:YLF regenerative amplifier operating at 1047 nm produces 88-microJ, 11-ps pulses at a 1-kHz repetition frequency. Switching of the 250-MHz seed pulses with a Pockels cell in the half-wave configuration is achieved with a contrast ratio of 20:1. After 50 round trips, the amplified pulse experiences an overall energy gain of 73 dB when the amplifier is seeded with 4-pJ pulses (1-mW average seed power). At 1 kHz, doubling and quadrupling yields 46 microJ/pulse at 524 nm and 8.1 microJ/pulse at 262 nm, with corresponding conversion efficiencies of 52% and 23%. At 3.5 kHz, the amplifier generated 97 mW of power at 524 nm and 15.8 mW of power at 262 nm.

Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers. III. Tuning curves and thresholds at CF.

In order to study the effects of efferent activity, olivocochlear efferents were stimulated with an electrode in the fourth ventricle at the decussation of the crossed olivocochlear bundle (midline-OCB stimulation) or with an electrode at the brainstem origin of medial efferents (MOC stimulation). Tuning curves, or similar measures of threshold, were obtained from auditory-nerve fibers in the presence or absence of efferent stimulation. Efferent stimulation raised the thresholds of fibers for tones at the characteristic frequency (CF) by an amount which varied with the spontaneous rate (SR) of the auditory-nerve fiber. On the average, high-SR fibers had the smallest threshold shifts, and low-SR fibers had the largest threshold shifts. The distribution of threshold shifts as a function of CF peaked at CFs of 3-8 kHz for high-SR and medium-SR fibers but appeared to peak at higher CFs for low-SR fibers. Within the high-SR or medium-SR groups, the fibers with the lowest thresholds had the largest threshold shifts. Efferent stimulation decreased the Q20 of the tuning curves from most fibers (i.e. it made the tuning curves wider), but increased the Q20 from some fibers with CFs below 2 kHz. For fibers with CFs above 4 kHz, efferent stimulation shifted the tuning-curve tails to higher sound levels by about 1 dB on the average. The qualitative patterns of the effects due to midline-OCB stimulation or to MOC stimulation were similar. The distribution of high-SR threshold shifts vs. CF appears to be displaced apically in the cochlea compared to the distribution of MOC endings on outer hair cells. This can be understood in terms of efferent activity depressing basilar membrane motion and affecting regions at, and apical to, the activated efferent synapses. To explain the low-SR threshold shifts, an additional way in which efferent activity inhibits responses appears to be required. The data are consistent with one function of the medial efferents being to raise the thresholds of auditory-nerve fibers and thereby adjust the effective range of the auditory system.

Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers. II. Spontaneous rate.

In order to increase our understanding of cochlear mechanisms, we measured changes in the rate of spontaneous firing (SR) of single auditory-nerve fibers in response to the stimulation of medial olivocochlear efferents in cats. During the first second of efferent stimulation, SR was depressed by up to 35%, except in one very sensitive animal in which depressions up to 80% were found. With data from this aberrant cat excluded, the SR depression, on the average, increased as auditory-nerve fiber sensitivity increased, increased as the original SR decreased (data were not obtained for SRs less than two spikes/sec), and had a broad maximum at CFs of about 10 kHz. After the efferent stimulation was turned off, there was an "overshoot" in which the SR increased past the original rate in some fibers. The "overshoot" was larger for fibers with lower SRs and for fibers which showed larger "adaptation" in the efferent-induced depression of SR. The data on SR depression during efferent stimulation are consistent with two hypotheses: (1) that the stronger than usual efferent suppression of "spontaneous" rate found in some very sensitive fibers occurs because the "spontaneous" firing was, in part, a response to sound, and (2) that "true spontaneous" firing is reduced by the efferent-induced hyperpolarization of outer hair cells (OHCs) being electrically coupled through the endocochlear potential to inner hair cells (IHCs). It is suggested that (1) the efferent-induced suppression of "true spontaneous" activity is largest at CFs near 10 kHz because this CF region receives the greatest OHC innervation from medial efferents and the efferent-induced change in OHCs is electrically coupled to IHCs, whereas (2) the efferent suppression of responses to sound is largest at lower CFs because the efferent endings on OHCs act to decrease the motion of the basilar membrane and this change is propagated apically from the active efferent synapses on OHCs.

Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers. I. Rate-level functions.

In previous studies describing the effects of electrically stimulating the olivocochlear bundle, it seems possible that both medial and lateral (MOC and LOC) efferents may have been stimulated. To selectively stimulate MOC efferents, we used an electrode placed at the origin of the MOC efferents in the brainstem (MOC stimulation). For comparison, a stimulating electrode was placed in the fourth ventricle at the decussation of the crossed olivocochlear bundle where both MOC and LOC efferents are present (midline-OCB stimulation). Rate versus sound level functions from auditory-nerve fibers were obtained with and without efferent stimulation. Stimulation at either location shifted rate vs. level functions to higher sound levels and depressed the rate in the plateau. For fibers with high spontaneous rates, the level shifts and plateau depressions had slightly different distributions as a function of characteristic frequency. The average amplitudes of these effects were largest for midline-OCB stimulation, next largest for crossed MOC stimulation and smallest for uncrossed MOC stimulation. The qualitative pattern of the effects, however, did not depend on the location of the stimulus electrode. The amplitudes of the efferent-induced effects were different for auditory-nerve fibers with different spontaneous rates (by as much as a factor of three for the plateau depression). The results support several hypotheses: (1) the effects of midline-OCB stimulation are due only to the action of MOC efferents, (2) individual crossed and uncrossed MOC fibers produce similar effects, and (3) efferents differentially change the information carrying properties of auditory-nerve fibers in different spontaneous-rate categories. These results, taken together with anatomical data in the literature, are consistent with the hypothesis that, in the cat, MOC and midline-OCB stimulation have their effect solely through synapses on outer hair cells. The data are consistent with the hypothesis that the level shifts are produced by MOC efferents acting on outer hair cells to reduce the mechanical stimulus to inner hair cells. It seems likely that some other mechanism is required to produce the plateau depressions, at least for auditory-nerve fibers with high spontaneous rates.

Effects of electrical stimulation of medial olivocochlear neurons on ipsilateral and contralateral cochlear responses.

Recent anatomical evidence has cast doubt on the interpretation of the neural elements involved in past experiments in which efferents were electrically stimulated. To separate effects produced by medial olivocochlear (MOC) efferents from effects produced by lateral olivocochlear (LOC) efferents, MOC efferents were selectively stimulated by an electrode in the region of the MOC cell bodies in cats. For comparison, efferents were also stimulated with an electrode in the fourth ventricle (OCB stimulation, previously called COCB stimulation). MOC stimulation and fourth-ventricle OCB stimulation both produced qualitatively similar results bilaterally in that auditory-nerve compound action potential (N1) and endocochlear potential were reduced, and cochlear microphonic (CM) was increased. Both efferent-induced changes were affected in similar ways by changes in shock parameters, and were blocked by strychnine. At low sound levels, the decrease in N1 amplitude was approximately equivalent to a shift (decrease) in sound level but the change in N1 latency was not. The ratio of the CM increase to the N1 sound-level shift was independent of shock level or location. MOC stimulation typically produced an N1 sound-level shift of 11-16 dB in the contralateral ear and 4-7 dB in the ipsilateral ear. The ratio of these shifts almost equals the ratio of MOC neurons which had cell bodies on the stimulating-electrode side. Previous results reported by others with 'UOCB stimulation' now seem attributable to excitation of uncrossed MOC efferents rather than to excitation of uncrossed LOC efferents as previously thought. There is no effect reported in the literature or seen by us which can definitely be attributed to LOC neurons. Fourth-ventricle OCB stimulation typically produced an N1 sound-level shift in both ears of 19-22 dB which is approximately the sum of the crossed and uncrossed MOC shifts. Considering also that many uncrossed-MOC fibers course close to the midline (i.e. near the stimulating electrode), it seems likely that fourth-ventricle OCB stimulation excites both crossed and uncrossed MOC efferents. Referring to such stimulation in the cat as 'COCB stimulation' is therefore inaccurate and may lead to wrong conclusions about the functional role of various components of the olivocochlear fibers.

The 1980 patient urgency study: further analysis of the data.

The patient urgency study was a comprehensive nationwide evaluation of patient and physician perceptions of the urgency of need for medical care. Half of the patients in the study were between the ages of 13 and 21. The necessity for immediate care, specifically emergency department care, and admission varied proportionately with increasing age. There was little variation in patient volume by day of the week, although the 8:00 AM to 4:00 PM shift was demonstrably the busiest; the midnight to 8:00 AM shift, however, had proportionately more sick patients. Sixty percent of the patients came to the ED because they believed that they had an emergency problem; 62% of patients had a personal physician. The average number of patients admitted in the ED population was 12.5%, with a range of 4.1% to 22.9%. ED residents underestimated the urgency of need for medical care 6.7% of the time, in comparison with only 3.7% for career emergency physicians. Physicians noted that 7.4% of patients who left without being seen initially required immediate care.