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Although teachers and researchers frequently acknowledge that music education can benefit pupils’ academic achievement, health and well-being, and social development, classroom music-making can have long-lasting, detrimental impacts. Individuals’ experiences of failure, disappointment, and exclusion in the music classroom highlight an urgent need for music education to be reframed by an understanding of “musical vulnerability”: individuals’ inherent and situational openness to being affected—positively or negatively—by the semantic and somatic properties of music-making. Drawing on existing vulnerability studies, I evaluate how classroom music-making can foster both positive receptivity and negative susceptibility, depending on its delineation of identity and physical embodiment. I then present reductive analyses of phenomenologically-informed interviews in which 12 secondary music teachers described their past experiences of being pupils, and their present experiences of teaching pupils, in music classrooms in the United Kingdom. Using excerpts from their observations of teaching pupils, I describe how interactions between individuals’ interpersonal and personal vulnerabilities—including personality, musical, and neurological differences—affected occasions of musical receptivity and susceptibility. As individuals negotiated conflicting musical expectations, they sometimes fostered fruitful resilience but sometimes encountered profound resignation. I draw on these findings to construct a preliminary typology of musical vulnerability and emphasize the need for future research into proactive differentiation in the music classroom.

Participatory performance, as defined by Thomas Turino, holds the potential to contribute to enhanced social bonding, cooperation, and the realisation of community among participants – despite the ...

Background HIV self-tests increase HIV status awareness by providing convenience and privacy, although cost and access may limit use. Since 2015, the New York City (NYC) Health Department has conducted 5 waves of an online Home Test Giveaway. Methods We recruited adult cisgender men who have sex with men (MSM) and transgender and gender-nonconforming (TGNC) individuals who had sex with men, who were living in NYC, not previously HIV diagnosed, and using paid digital advertisements (4-8 weeks per wave). Eligible respondents were e-mailed a code to redeem on the manufacturer's website for a free HIV self-test and an online follow-up survey ~2 months later. For key process and outcome measures, we present means across 5 waves. Results Across the 5 waves of Home Test Giveaway, there were 28,921 responses to the eligibility questionnaire: 17,383 were eligible, 12,182 redeemed a code for a free HIV self-test, and 7935 responded to the follow-up survey (46% of eligible responses). Among eligible responses, approximately half were Latino/a (mean, 32%) or non-Latino/a, black (mean, 17%). Mean report of never testing before was 16%. Among 5903 follow-up survey responses who reported test use, 32 reported reactive results with no known previous diagnosis (0.54%), of whom 78% reported receiving confirmatory testing. Report of likelihood of recommending the Home Test Giveaway to friends was high (mean, 96%). Conclusions We recruited diverse NYC MSM and TGNC and distributed a large number of HIV self-tests to them. Among respondents who reported newly reactive tests, the majority reported confirmatory testing. This seems to be one acceptable way to reach MSM and TGNC for HIV testing, including those who have never tested before.

Background Intracavitary pulmonary aspergilloma is a chronic, debilitating fungal infection. Without definitive therapy, death can occur from massive hemoptysis, cachexia, or secondary infection. Although surgical resection is the standard therapy, it is not possible for many patients owing to poor pulmonary function or medical comorbidities. Aspergilloma removal through bronchoscopy is an important alternative therapy that may be available in select cases. Methods We retrospectively reviewed all cases referred to the University of Calgary Interventional Pulmonary Service for transbronchial removal of intracavitary aspergilloma from January 1, 2009, to January 1, 2014. Results Ten patients with intracavitary pulmonary aspergilloma were identified. In 3 patients, the aspergilloma cavity was not accessible by bronchoscopy. Successful removal of the aspergilloma with symptom improvement or resolution was achieved in 6 of 7 cases. One of the patients was lost to follow-up. Minor hypoxia lasting 12 to 72 hours was observed in 5 cases. Severe sepsis requiring an extended critical care unit stay occurred in 1 case. Follow-up ranged from 9 months to 5 years. Conclusions Although not without risk of minor hypoxia and possible sepsis, for carefully selected patients, bronchoscopic removal of symptomatic intracavitary pulmonary aspergilloma may be an alternative therapy to surgical resection for this life-threatening disease.

This study presents a combined analytical and empirical model for predicting the signal loss effects of metallic drilling rig structures on radio-frequency electromagnetic waves used by wireless sensor networks (WSNs) installed on a drilling rig. The model is based on the combination of free space path loss and the excess loss caused by the metallic structure separately. The authors combine both losses to predict the overall loss of signal strength. The model has been validated against field data collected from multiple drilling rigs. Further modification of the model to include the effects of different signal frequencies is under way. They present simulation results from OMNeT++ based on their model, to establish the packet loss and energy consumption expected for a real WSN. They also present a novel dynamic multi-hop routing protocol, which improves network performance by removing the constraints of single-hop forwarding. The algorithm directs packets to their destination via a selected node within a routing ‘cluster’. By combining their channel model and routing protocol, they are able to achieve 100% packet success, while setting transmit power levels appropriately to achieve the longest possible network lifetime.

Suppose that the function $f$ is analytic in the open unit disk $\unicode[STIX]{x1D6E5}$ in the complex plane. For each $\unicode[STIX]{x1D6FC}>0$ a function $f^{[\unicode[STIX]{x1D6FC}]}$ is defined as the Hadamard product of $f$ with a certain power function. The function $f^{[\unicode[STIX]{x1D6FC}]}$ compares with the fractional derivative of $f$ of order $\unicode[STIX]{x1D6FC}$. Suppose that $f^{[\unicode[STIX]{x1D6FC}]}$ has a limit at some point $z_{0}$ on the boundary of $\unicode[STIX]{x1D6E5}$. Then $w_{0}=\lim _{z\rightarrow z_{0}}f(z)$ exists. Suppose that $\unicode[STIX]{x1D6F7}$ is analytic in $f(\unicode[STIX]{x1D6E5})$ and at $w_{0}$. We show that if $g=\unicode[STIX]{x1D6F7}(f)$ then $g^{[\unicode[STIX]{x1D6FC}]}$ has a limit at $z_{0}$.

Petri net modeling enables us to verify the protocol of interest formally. However, aside from formal verification, a new protocol really needs to be tested in a relatively realistic environment in which it interworks (or at least co-exists) with earlier or different versions of the same or similar protocols. Simulation excels in meeting such challenges. But the correctness of a protocol can never be proved by simulation alone. In this paper, we present an innovative methodology that combines the use of colored Petri nets and simulation (in ns-2) to obtain the advantages of deep formal verification with the broad spectrum testing of simulation. A new version of SACK TCP, @a-min Paced SACK TCP, is used as the example protocol under test in our research. Our experimental results show that @a-min Paced SACK TCP could reduce the number of packets queued at the bottleneck router significantly, decreasing the possibility of packet discard due to limited buffer space. Of course, the proposed methodology is a generic approach that can be used to study the performance of any new network protocol that is intended to run in an existing, complex network environment.

Background Perioperative hypothermia has been reported to increase the occurrence of cardiovascular complications. By increasing the activity of sympathetic nervous system, perioperative hypothermia also has the potential to increase cardiac injury and dysfunction associated with subarachnoid hemorrhage. Methods The Intraoperative Hypothermia for Aneurysm Surgery Trial randomized patients undergoing cerebral aneurysm surgery to intraoperative hypothermia (n = 499, 33.3 degrees +/- 0.8 degrees C) or normothermia (n = 501, 36.7 degrees +/- 0.5 degrees C). Cardiovascular events (hypotension, arrhythmias, vasopressor use, myocardial infarction, and others) were prospectively followed until 3-month follow-up and were compared in hypothermic and normothermic patients. A subset of 62 patients (hypothermia, n = 33; normothermia, n = 29) also had preoperative and postoperative (within 24 h) measurement of cardiac troponin-I and echocardiography to explore the association between perioperative hypothermia and subarachnoid hemorrhage-associated myocardial injury and left ventricular function. Results There was no difference between hypothermic and normothermic patients in the occurrence of any single cardiovascular event or in composite cardiovascular events. There was no difference in mortality (6%) between groups, and there was only a single primary cardiovascular death (normothermia). There was no difference between hypothermic and normothermic patients in postoperative versus preoperative left ventricular regional wall motion or ejection fraction. Compared with preoperative values, hypothermic patients had no postoperative increase in cardiac troponin-I (median change 0.00 microg/l), whereas normothermic patients had a small postoperative increase (median change + 0.01 microg/l, P = 0.038). Conclusion In patients undergoing cerebral aneurysm surgery, perioperative hypothermia was not associated with an increased occurrence of cardiovascular events.

Background Although hypothermia and barbiturates improve neurologic outcomes in animal temporary focal ischemia models, the clinical efficacy of these interventions during temporary occlusion of the cerebral vasculature during intracranial aneurysm surgery (temporary clipping) is not established. Methods A post hoc analysis of patients from the Intraoperative Hypothermia for Aneurysm Surgery Trial who underwent temporary clipping was performed. Univariate and multivariate logistic regression methods were used to test for associations between hypothermia, supplemental protective drug, and short- (24-h) and long-term (3-month) neurologic outcomes. An odds ratio more than 1 denotes better outcome. Results Patients undergoing temporary clipping (n = 441) were assigned to intraoperative hypothermia (33.3 degrees +/- 0.8 degrees C, n = 208) or normothermia (36.7 degrees +/- 0.5 degrees C, n = 233), with 178 patients also receiving supplemental protective drug (thiopental or etomidate) during temporary clipping. Three months after surgery, 278 patients (63%) had good outcome (Glasgow Outcome Score = 1). Neither hypothermia (P = 0.847; odds ratio = 1.043, 95% CI = 0.678-1.606) nor supplemental protective drug (P = 0.835; odds ratio = 1.048, 95% CI = 0.674-1.631) were associated with 3-month Glasgow Outcome Score. The effect of supplemental protective drug did not significantly vary with temperature. The effects of hypothermia and protective drug did not significantly vary with temporary clip duration. Similar findings were made for 24-h neurologic status and 3-month Neuropsychological Composite Score. Conclusion In the Intraoperative Hypothermia for Aneurysm Surgery Trial, neither systemic hypothermia nor supplemental protective drug affected short- or long-term neurologic outcomes of patients undergoing temporary clipping.

BACKGROUND: Hepatic portal venous gas (HPVG) is a rare condition that occurs when intraluminal gas and/or gas produced by intestinal bacteria enters the portal venous circulation. The most common precipitating factors include ischemia, intra-abdominal abscesses and inflammatory bowel disease. However, HPVG has recently been recognized as a rare complication of endoscopic and radiological procedures. Earlier studies advised immediate surgical intervention, but according to current recommendations, in some settings, HPVG can be managed conservatively. The present study reports two cases of HPVG; one that occurred following colonoscopy in a patient with severe Crohn’s disease and one in a patient with graft-versus-host disease.METHODS: The epidemiology, pathogenesis, diagnosis and management of HPVG are reviewed. Two case reports are presented, followed by the development of a management algorithm.RESULTS: Of the two patients that developed HPVG, one was an outpatient undergoing a colonoscopy for assessment of Crohn’s disease activity and the other was an inpatient with graft-versus-host disease. Once the diagnosis of HPVG was made, both patients were managed conservatively with antibiotic therapy and management of their underlying disease.CONCLUSIONS: HPVG can occur in the setting of severe gastrointestinal disease states and following endoscopic procedures. It is critical that gastroenterologists are aware of the differential diagnosis, pathogenesis, diagnostic approach and management of HPVG.

For α > 0 let α denote the set of functions which can be expressed where μ is a complex-valued Borel measure on the unit circle. We show that if f is an analytic function in Δ = {z ∈ : |z| < 1} and there are two nonparallel rays in /f(Δ) which do not meet, then f ∈ α where απ denotes the largest of the two angles determined by the rays. Also if the range of a function analytic in Δ is contained in an angular wedge of opening απ and 1 < α < 2, then f ∈ α.

Many disasters take place in urban areas, affecting millions of people each year through loss of life, serious injury and loss of assets and livelihoods. Poorer groups are generally most affected. The impact of these disasters and their contribution to poverty are underestimated, as is the extent to which rapidly growing and poorly managed urban development increases the risks. But urban specialists do not see disasters and disaster prevention as being within their remit. At the same time, few national and international disaster agencies have worked with urban governments and community organizations to identify and act on the urban processes that cause the accumulation of disaster risk in and around urban areas. This paper summarizes the discussions from a workshop funded by UNDP on the links between disasters and urban development in Africa, highlighting the underestimation of the number and scale of urban disasters, and the lack of attention to the role of urban governance. It notes the difficulties in getting action in Africa, since the region’s problems are still perceived as “rural” by disaster and development specialists, even though two-fifths of its population live in urban areas. It emphasizes the need for an understanding of risk that encompasses events ranging from disasters to everyday hazards and which understands the linkages between them – in particular, how identifying and acting on risks from “small” disasters can reduce risks from larger ones. It also stresses the importance of integrating such an understanding into poverty reduction strategies.

Vfr of Pseudomonas aeruginosa is 91% similar to the cAMP receptor protein (CRP) of Escherichia coli. Based on the high degree of sequence homology between the two proteins, the question arose whether Vfr had a global regulatory effect on gene expression for P. aeruginosa as CRP did for E. coli. This report provides two-dimensional polyacrylamide gel electrophoretic evidence that Vfr is a global regulator of gene expression in P. aeruginosa. In a vfr101::aacC1 null mutant, at least 43 protein spots were absent or decreased when compared to the proteome pattern of the parent strain. In contrast, 17 protein spots were absent or decreased in the parent strain when compared to the vfr101::aacC1 mutant. Thus, a mutation in vfr affected production of at least 60 proteins in P. aeruginosa. In addition, the question whether Vfr and CRP shared similar mechanistic characteristics was addressed. To ascertain whether Vfr, like CRP, can bind cAMP, Vfr and CRP were purified to homogeneity and their apparent dissociation constants (K(d)) for binding to cAMP were determined. The K(d) values were 1.6 microM for Vfr and 0.4 microM for CRP, suggesting that these proteins have a similar affinity for cAMP. Previously the authors had demonstrated that Vfr could complement a crp mutation and modulate catabolite repression in E. coli. This study presents evidence that Vfr binds to the E. coli lac promoter and that this binding requires the presence of cAMP. Finally, the possible involvement of Vfr in catabolite repression control in P. aeruginosa was investigated. It was found that succinate repressed production of mannitol dehydrogenase, glucose-6-phosphate dehydrogenase, amidase and urocanase both in the parent and in two vfr null mutants. This implied that catabolite repression control was not affected by the vfr null mutation. In support of this, the cloned vfr gene failed to complement a mutation in the P. aeruginosa crc gene. Thus, although Vfr is structurally similar to CRP, and is a global regulator of gene expression in P. aeruginosa, Vfr is not required for catabolite repression control in this bacterium.

Crc (catabolite repression control) protein of Pseudomonas aeruginosa has shown to be involved in carbon regulation of several pathways. In this study, the role of Crc in catabolite repression control has been studied in Pseudomonas putida . The bkd operons of P. putida and P. aeruginosa encode the inducible multienzyme complex branched-chain keto acid dehydrogenase, which is regulated in both species by catabolite repression. We report here that this effect is mediated in both species by Crc. A 13-kb cloned DNA fragment containing the P. putida crc gene region was sequenced. Crc regulates the expression of branched-chain keto acid dehydrogenase, glucose-6-phosphate dehydrogenase, and amidase in both species but not urocanase, although the carbon sources responsible for catabolite repression in the two species differ. Transposon mutants affected in their expression of BkdR, the transcriptional activator of the bkd operon, were isolated and identified as crc and vacB ( rnr ) mutants. These mutants suggested that catabolite repression in pseudomonads might, in part, involve control of BkdR levels.

Patients undergoing hypothermic cardiopulmonary bypass are often receiving aspirin therapy. Hypothermia, aspirin and cardiopulmonary bypass can each induce a platelet function defect, but it is not known if the effects of aspirin and hypothermia are additive in this regard. To address this question in humans in vivo, the forearm skin temperature of healthy volunteers was equilibrated and maintained at either normothermia (32 degrees C) or hypothermia (28 degrees C or 22 degrees C) before and 16 h after the ingestion of 650 mg aspirin. A standardized template bleeding time was performed on the forearm and the shed blood emerging from the wound was assayed for platelet surface P-selectin expression by whole blood flow cytometry (reflecting alpha granule secretion) and thromboxane B2 (the stable metabolite of thromboxane A2) by radioimmunoassay. Hypothermia resulted in marked prolongation of the bleeding time. Aspirin resulted in prolongation of the bleeding time under normothermic conditions, but only minimally augmented the hypothermia-induced prolongation of the bleeding time. Platelet surface P-selectin up-regulation in shed blood was abolished by hypothermia. Aspirin had no effect on maximal platelet surface P-selectin expression under normothermic or hypothermic conditions. Both hypothermia and aspirin resulted in markedly reduced shed blood thromboxane B2. Although aspirin slightly augmented the hypothermia-induced reduction in shed blood thromboxane B2, the concentration of thromboxane generated in shed blood under hypothermic conditions in the absence of aspirin had no effect on platelet surface P-selectin or platelet aggregation in whole blood. In conclusion, as determined by three independent parameters of the shed blood emerging from a standardized bleeding time wound (bleeding time, platelet surface P-selectin, and thromboxane B2), aspirin did not significantly augment hypothermia-induced platelet dysfunction in vivo.

This paper studies conditions on an analytic function that imply it belongs to Mα, the set of multipliers of the family of functions given by where μ is a complex Borel measure on the unit circle and α > 0. There are two main theorems. The first asserts that if 0 < α < 1 and sup. The second asserts that if 0 < α < 1, ƒ ∈ H∞ and supt. The conditions in these theorems are shown to relate to a number of smoothness conditions on the unit circle for a function analytic in the open unit disk and continuous in its closure.

for |z| < 1. Fα is a Banach space with respect to the norm defined by ‖f‖Fα = inf ‖μ‖ where μ varies over all measures in M for which (1) or (2) holds and where ‖μ‖ is the total variation norm of μ. The spaces Fα have been studied in a number of recent papers and earlier work was extensively done corresponding to the case α = 1. This paper gives a survey of some recent results about Fα which focus on questions about radial limits. We will summarize work contained in [3], [4] and [5]. This material was presented in a talk by the author at the Complex Analysis Semester held at the Banach Center in Warsaw during the fall, 1992. The author wishes to thank the organizers for their invitation to participate in that conference and for their hospitality, especially to Professor Jan Krzyz.

In this paper we investigate functions analytic and nonvanishing in the unit disk, with the property that the logarithmic derivative is contained in some domain Ω \Omega . We obtain conditions on Ω \Omega which imply that the functions are bounded and that their first derivatives belong to H p {H^p} for some p ⩾ 1 p \geqslant 1 . For certain domains Ω \Omega the sufficient conditions that we give are also, in some sense, necessary. Examples of domains to which the results apply are given.

This prospective study was designed to determine whether use of nonwashed shed mediastinal blood exacerbated platelet and related hematologic dysfunctions after cardiopulmonary bypass, compared with the alternative use of autologous and homologous standard liquid preserved blood for volume support. Thirty-two patients undergoing cardiopulmonary bypass for open heart operations were randomized to receive either nonwashed shed mediastinal blood (group 1; n = 16) or liquid preserved packed red blood cells (group 2; n = 16) for transfusion therapy in the management of postoperative bleeding. Patient blood samples and bleeding times were obtained preoperatively, after cardiopulmonary bypass but before transfusions, 2 and 24 hours after transfusion, and on postoperative days 2, 3, and 7. Group 1 patients received an average of 710 +/- 90 mL (range, 300 to 1,700 mL) of nonwashed shed mediastinal blood containing significantly greater (p < 0.0001) amounts of fibrin degradation products and D-dimer protein. Of the hematologic, microaggregate, and plasma protein measurements performed, only the protein C level was significantly greater in group 1 (p < 0.05) after transfusion. Patient bleeding times were not significantly different between the groups at any of the time points, and the total postoperative blood loss was not different between the groups. There was a trend toward less need for homologous transfusion in group 1 (p < 0.1). This study documents the safety and ease of using nonwashed shed mediastinal blood as a primary blood volume support after an open heart operation.

This paper considers the radial and nontangential growth of a function f given bywhere α>0 and μ is a complex-valued Borel measure on the unit circle. The main theorem shows how certain local conditions on μ near eiθ affect the growth of f(z) as z→eiθ in Stolz angles. This result leads to estimates on the nontangential growth of f where exceptional sets occur having zero β-capacity.

Pathogen transmission in animal populations is contingent on interactions between and within species. Often standard ornithological data (e.g. total counts at a wetland) are the only data available for assessing the risks of avian pathogen transmission. In this paper we ask whether these data can be used to infer fine-scale transmission patterns. We tested for non-randomness in waterbird assemblages and explored waterbird interactions using social network analysis. Certain network parameter values were then compared to a data set on avian influenza prevalence in southern Africa. Our results showed that species associations were strongly non-random, implying that most standard ornithological data sets would not provide adequate information on which to base models of pathogen spread. In both aquatic and terrestrial networks, all species regularly associated closely with other network members. The spread of pathogens through the community could thus be rapid. Network analysis together with detailed, fine-scale observations offers a promising avenue for further research and management-oriented applications.

An incomplete major pulmonary fissure can make anatomic lung resection technically more difficult and may increase the risk of complications, such as prolonged postoperative air leak. The objective of this study was to determine if preoperative computed tomography (CT) of the chest could accurately predict the completeness of the major pulmonary fissure observed at the time of surgery.From October 2008 to June 2009, patients at a single university institution were enrolled if they underwent surgery for a pulmonary nodule, mass or known cancer. At the time of surgery, completeness of the major pulmonary fissure was graded 1 if pulmonary lobes were entirely separate, 2 if the visceral cleft was complete with an exposed pulmonary artery at the base with some parenchyma fusion, 3 if the visceral cleft was only evident for part of the fissure without a visible pulmonary artery and 4 if the fissure was absent. The preoperative CT scan of each patient was graded by a single, blinded chest radiologist using the same scale. We used the Pearson χ2 test with 2-tailed significance to test the independence of the operative and radiologic grading.In 48% (29 of 61) of patients, the radiologic and operative grading were the same. Of those graded differently, 94% (30 of 32) were within 1 grade. Despite this agreement, we observed no statistically significant correlation between the operative and radiologic grading (p = 0.24).The major fissure can often be well-visualized on a preoperative CT scan, but preoperative CT cannot accurately predict the completeness of the major pulmonary fissure discovered at surgery.

The use of cardiopulmonary bypass (CPB) during cardiac surgery is associated with a hemostatic defect, the hallmark of which is a markedly prolonged bleeding time. However, the nature of the putative platelet function defect is controversial. In this study, blood was analyzed at 10 time points before, during, and after CPB. We used a whole-blood flow cytometric assay to study platelet surface glycoproteins in (1) peripheral blood, (2) peripheral blood activated in vitro by either phorbol myristate acetate, the thromboxane (TX)A2 analog U46619, or a combination of adenosine diphosphate and epinephrine, and (3) the blood emerging from a bleeding-time wound (shed blood). Activation-dependent changes were detected by monoclonal antibodies directed against the glycoprotein (GP)Ib-IX and GPIIb-IIIa complexes and P-selectin. In addition, we measured plasma glycocalicin (a proteolytic fragment of GPIb) and shed-blood TXB2 (a stable breakdown product of TXA2). In shed blood emerging from a bleeding-time wound, the usual time-dependent increase in platelet surface P-selectin was absent during CPB, but returned to normal within 2 hours. This abnormality paralleled both the CPB-induced prolongation of the bleeding time and a CPB-induced marked reduction in shed-blood TXB2 generation. In contrast, there was no loss of platelet reactivity to in vitro agonists during or after CPB. In peripheral blood, platelet surface P-selectin was negligible at every time point, demonstrating that CPB resulted in a minimal number of circulating degranulated platelets. CPB did not change the platelet surface expression of GPIb in peripheral blood, as determined by the platelet binding of a panel of monoclonal antibodies, ristocetin-induced binding of von Willebrand factor, and a lack of increase in plasma glycocalicin. CPB did not change the platelet surface expression of the GPIIb-IIIa complex in peripheral blood, as determined by the platelet binding of fibrinogen and a panel of monoclonal antibodies. In summary, CPB resulted in (1) markedly deficient platelet reactivity in response to an in vivo wound, (2) normal platelet reactivity in vitro, (3) no loss of the platelet surface GPIb-IX and GPIIb-IIIa complexes, and (4) a minimal number of circulating degranulated platelets. These data suggest that the “platelet function defect” of CPB is not a defect intrinsic to the platelet, but is an extrinsic defect such as an in vivo lack of availability of platelet agonists. The near universal use of heparin during CPB is likely to contribute substantially to this defect via its inhibition of thrombin, the preeminent platelet activator.

For α > 0 \alpha > 0 let F α {\mathcal {F}_\alpha } denote the class of functions defined for | z | > 1 |z| > 1 by integrating 1 / ( 1 − x z ) α 1/{(1 - xz)^\alpha } against a complex measure on | x | = 1 |x|= 1 . A function g g holomorphic in | z | > 1 |z| > 1 is a multiplier of F α {\mathcal {F}_\alpha } if f ∈ F α f \in {\mathcal {F}_\alpha } implies g f ∈ F α gf \in {\mathcal {F}_\alpha } . The class of all such multipliers is denoted by M α {\mathcal {M}_\alpha } . Various properties of M α {\mathcal {M}_\alpha } are studied in this paper. For example, it is proven that α > β \alpha > \beta implies M α ⊂ M β {\mathcal {M}_\alpha } \subset {\mathcal {M}_\beta } , and also that M α ⊂ H ∞ {\mathcal {M}_\alpha } \subset {H^\infty } . Examples are given of bounded functions which are not multipliers. A new proof is given of a theorem of Vinogradov which asserts that if f ′ f’ is in the Hardy class H 1 {H^1} , then f ∈ M 1 f \in {\mathcal {M}_1} . Also the theorem is improved to f ′ ∈ H 1 f’ \in {H^1} implies f ∈ M α f \in {\mathcal {M}_\alpha } , for all α > 0 \alpha > 0 . Finally, let α > 0 \alpha > 0 and let f f be holomorphic in | z | > 1 |z| > 1 . It is known that f f is bounded if and only if its Cesàro sums are uniformly bounded in | z | ≤ 1 |z| \leq 1 . This result is generalized using suitable polynomials defined for α > 0 \alpha > 0 .

Trauma care benefits from the use of imaging technologies. Trauma patients and trauma team members are exposed to radiation during the continuum of care. Knowledge of exposure amounts and effects are important for trauma team members.We performed a review of the published literature; keywords included "trauma," "patients," "trauma team members," "wounds," "injuries," "radiation," "exposure," "dose" and "computed tomography" (CT). We also reviewed the Board on Radiation Effects Research (BEIR VII) report, published in 2005 and 2006.We found no randomized controlled trials or studies. Relevant studies demonstrated that CT accounts for the single largest radiation exposure in trauma patients. Exposure to 100 mSv could result in a solid organ cancer or leukemia in 1 of 100 people. Trauma team members do not exceed the acceptable occupation radiation exposure determined by the National Council of Radiation Protection and Management. Modern imaging technologies such as 16- and 64-slice CT scanners may decrease radiation exposure.Multiple injured trauma patients receive a substantial dose of radiation. Radiation exposure is cumulative. The low individual risk of cancer becomes a greater public health issue when multiplied by a large number of examinations. Though CT scans are an invaluable resource and are becoming more easily accessible, they should not replace careful clinical examination and should be used only in appropriate patients.

Modern multislice computed tomography (CT) scanners produce isotropic CT images with a thickness of 0.6 mm. These CT images offer detailed information of lung cavities, which could be used for better surgical planning of treating lung cancer. The major challenge for developing a surgical planning system is the automatic segmentation of lung lobes by identifying the lobar fissures. This paper presents a lobe segmentation algorithm that uses a two-stage approach: (1) adaptive fissure sweeping to find fissure regions and (2) wavelet transform to identify the fissure locations and curvatures within these regions. Tested on isotropic CT image stacks from nine anonymous patients with pathological lungs, the algorithm yielded an accuracy of 76.7%-94.8% with strict evaluation criteria. In comparison, surgeons obtain an accuracy of 80% for localizing the fissure regions in clinical CT images with a thickness of 2.5-7.0 mm. As well, this paper describes a procedure for visualizing lung lobes in three dimensions using software-amira-and the segmentation algorithm. The procedure, including the segmentation, needed about 5 min for each patient. These results provide promising potential for developing an automatic algorithm to segment lung lobes for surgical planning of treating lung cancer.

The male hypermethylated (MHM) region, located near the middle of the short arm of the Z chromosome of chickens, consists of approximately 210 tandem repeats of a BamHI 2.2-kb sequence unit. Cytosines of the CpG dinucleotides of this region are extensively methylated on the two Z chromosomes in the male but much less methylated on the single Z chromosome in the female. The state of methylation of the MHM region is established after fertilization by about the 1-day embryonic stage. The MHM region is transcribed only in the female from the particular strand into heterogeneous, high molecular-mass, non-coding RNA, which is accumulated at the site of transcription, adjacent to the DMRT1 locus, in the nucleus. The transcriptional silence of the MHM region in the male is most likely caused by the CpG methylation, since treatment of the male embryonic fibroblasts with 5-azacytidine results in hypo-methylation and active transcription of this region. In ZZW triploid chickens, MHM regions are hypomethylated and transcribed on the two Z chromosomes, whereas MHM regions are hypermethylated and transcriptionally inactive on the three Z chromosomes in ZZZ triploid chickens, suggesting a possible role of the W chromosome on the state of the MHM region.

Chromomeres 1 and 3 of the chicken W lampbrush chromosome contain most of the EcoRI and XhoI repeat sequence families respectively. These chromomeres were stained with DAPI and their sizes relative to other W chromomeres were observed. Their relative contents of EcoRI and XhoI repeats were determined using fluorescence in situ hybridization with genomic probes for each of the two repeat families. There were two types of W chromosome in the chickens (White Leghorn and Rhode Island Red) used in this study with respect to the amount of EcoRI repeat. A high-copy-number type has about 4000 copies of the 1.2-kb repeat per genome and shows a large fluorescence signal on W chromomere 1. A low-copy-number type has about 700 copies per genome and does not have a detectable chromomere 1 on W chromosome, nor does it show FISH labelling in the region normally occupied by chromomere 1. The genome of Fayoumi chickens has about one-sixth the amount of the XhoI sequence family of White Leghorns. W lampbrush chromomere 3 is much smaller and its FISH labelling with the XhoI probe is much weaker in Fayoumis than in White Leghorns. These results demonstrate that in the chicken W chromosome, specific chomomeres are occupied by specific DNA repeat sequence families.

To examine the hypothesis that surface P-selectin-positive (degranulated) platelets are rapidly cleared from the circulation, we developed novel methods for tracking of platelets and measurement of platelet function in vivo. Washed platelets prepared from nonhuman primates (baboons) were labeled with PKH2 (a lipophilic fluorescent dye), thrombin-activated, washed, and reinfused into the same baboons. Three-color whole blood flow cytometry was used to simultaneously (i) identify platelets with a mAb directed against glycoprotein (GP)IIb-IIIa (integrin alpha 11b beta 3), (ii) distinguish infused platelets by their PKH2 fluorescence, and (iii) analyze platelet function with mAbs. Two hours after infusion of autologous thrombin-activated platelets (P-selectin-positive, PKH2-labeled), 95 +/- 1% (mean +/- SEM, n = 5) of the circulating PKH2-labeled platelets had become P-selectin-negative. Compared with platelets not activated with thrombin preinfusion, the recovery of these circulating PKH2-labeled, P-selectin-negative platelets was similar 24 h after infusion and only slightly less 48 h after infusion. The loss of platelet surface P-selectin was fully accounted for by a 67.1 +/- 16.7 ng/ml increase in the plasma concentration of soluble P-selectin. The circulating PKH2-labeled, P-selectin-negative platelets were still able to function in vivo, as determined by their (i) participation in platelet aggregates emerging from a bleeding time wound, (ii) binding to Dacron in an arteriovenous shunt, (iii) binding of mAb PAC1 (directed against the fibrinogen binding site on GPIIb-IIIa), and (iv) generation of procoagulant platelet-derived microparticles. In summary, (i) circulating degranulated platelets rapidly lose surface P-selectin to the plasma pool, but continue to circulate and function; and (ii) we have developed novel three-color whole blood flow cytometric methods for tracking of platelets and measurement of platelet function in vivo.

1. Whole-cell patch clamp recordings were made from Chinese hamster ovary (CHO) cells stably expressing homomeric mouse Kv1.1 (delayed rectifier K+; mKv1.1) channels. The effects of internal application of a number of different peptides, based on part of the amino terminal sequence of the human Kv3.4 channel subunit (hKv3.4), were examined in order to determine their influence on N-type inactivation. 2. For the native hKv3.4 peptide, the association rate constant (kon) increased with membrane depolarization, whilst the dissociation rate constant (koff) had little dependence on voltage. This resulted in the apparent dissociation constant (KD) of the hKv3.4 peptide tending to increase with depolarization. 3. In general, kon increased and apparent KD decreased with positive charge of the hKv3.4 peptide variants; in peptides lacking a hydrophobic amino terminal this correlation was not maintained. In contrast, the rate of dissociation of the variant peptides (koff) was independent of net charge. 4. The blocking activity of the hKv3.4 peptide was not dependent on a disulphide bridge between cysteine residues C6 and C24 and the presence of cysteine residues in the hKv3.4 peptide was not a prerequisite for rapid inactivation. All cysteine-substituted variants, especially at C6, showed a more rapid recovery from inactivation than the hKv3.4 peptide. Substitutions at C24, and not C6, reduced kon. 5. The present results concerning the action of the mammalian hKv3.4 channel inactivation particle on mKv1.1 channels complement earlier models for the invertebrate Shaker K+ channel. It is proposed that the hydrophobic amino terminal region of the hKv3.4 inactivation peptide blocks the channel pore, whilst the adjacent positively charged region interacts with negative charges on the channel protein.

The gene (crc) responsible for catabolite repression control in Pseudomonas aeruginosa has been cloned and sequenced. Flanking the crc gene are genes encoding orotate phosphoribosyl transferase (pyrE) and RNase PH (rph). New crc mutants were constructed by disruption of the wild-type crc gene. The crc gene encodes an open reading frame of 259 amino acids with homology to the apurinic/apyrimidinic endonuclease family of DNA repair enzymes. However, crc mutants do not have a DNA repair phenotype, nor can the crc gene complement Escherichia coli DNA repair-deficient strains. The crc gene product was overexpressed in both P. aeruginosa and in E. coli, and the Crc protein was purified from both. The purified Crc proteins show neither apurinic/apyrimidinic endonuclease nor exonuclease activity. Antibody to the purified Crc protein reacted with proteins of similar size in crude extracts from Pseudomonas putida and Pseudomonas fluorescens, suggesting a common mechanism of catabolite repression in these three species.

Platelet dysfunction and increased fibrinolysis are the most important etiologic factors in the hemostatic defect observed following the institution of cardiopulmonary bypass. This study examined the effects of heparin per se, administered before the institution of cardiopulmonary bypass, on platelet function and fibrinolysis.Sampling was performed in 55 patients undergoing cardiac operations before and 5 minutes after the routine administration of heparin, before the institution of cardiopulmonary bypass.Heparin administration resulted in a significant prolongation of the bleeding time (from 6.3 +/- 2.1 to 12.6 +/- 4.9 minutes; p0.00001), a significant reduction in the level of shed blood thromboxane B2 (from 1,152 +/- 669 to 538 +/- 187 pg/0.1 mL; p = 0.00002), and an increase in the plasma levels of plasmin (from 11.8 +/- 9.7 to 125.4 +/- 34.8 U/L; p0.0001) and D-dimer (from 571.3 +/- 297.1 to 698.5 +/- 358.6 micrograms/mL; p = 0.05). There were no significant differences before and after heparin administration in the plasma levels of fibrinogen, plasminogen, tissue plasminogen activator, antiplasmin, antithrombin III, and von Willebrand factor.Heparin, independent of cardiopulmonary bypass, causes both platelet dysfunction and increased fibrinolysis. The use of an alternative anticoagulant or a lower dose of heparin in conjunction with heparin-coated surfaces might improve the hemostatic balance during open heart operations.

Background Distortion of the left ventricular (LV) cavity in patients with right ventricular pressure overload (RVPO) is well known. However, no direct measurements of regional myocardial function in terms of myocardial shortening and wall thickening are available; therefore, exactly how RVPO disturbs LV regional performance remains unclear. By using three-dimensional (3D) tagged magnetic resonance imaging, we were able to measure regional systolic function directly. Our objective was to study the relation between the distortion of the LV circular shape and regional LV function. Methods and Results In nine patients with RVPO and six healthy volunteers, four parallel short-axis images (with 12 radial tags) and two mutually orthogonal long-axis images (with four parallel tags) were generated, and endocardial and epicardial borders were manually traced. By integration of the short- and long-axis images, 3D reconstruction of the LV tracking points from end diastole to end systole was obtained. Data from the midventricular two short-axis image slices were analyzed. These were then divided into anterior, lateral, posterior, and septal regions. Circumferential and longitudinal shortening were then calculated from the endocardial and epicardial tag intersection points. Wall thickness and thickening were calculated by the 3D volume-element approach. An eccentricity index (EI), the ratio of septum-to-free-wall to anteroposterior diameters, was used to describe the shape of the LV cavity. The regional curvature was also measured. The RVPO group was characterized by flattening of the septum and LV lateral wall, decreased EI reflecting the distorted LV shape, altered distribution of endocardial circumferential shortening, and preserved ejection fraction. Changes in EI closely correlated with the septal curvature. The EI was smaller at end systole, reflecting further shape distortion relative to end diastole. Reduced myocardial performance, as measured by wall thickening and circumferential and longitudinal shortening fractions, was observed for the septum. A reduction in endocardial circumferential shortening of the septal and lateral walls was directly related to the end-systolic EI. In addition, whereas for healthy subjects a linear relation between area ejection fraction and endocardial circumferential shortening was observed, in RVPO patients a curvilinear (quadratic) relation was observed. Conclusions In patients with RVPO, compared with healthy subjects, the septal function was reduced, as evidenced by reduced thickening and shortening fractions. The distortion in LV cavity at end systole due to the flattening of the septum contributes to preserved systolic ventricular function and nonuniform distribution in endocardial circumferential shortening.

The use of cardiopulmonary bypass (CPB) during cardiac surgery is associated with a hemostatic defect, the hallmark of which is a markedly prolonged bleeding time. However, the nature of the putative platelet function defect is controversial. In this study, blood was analyzed at 10 time points before, during, and after CPB. We used a whole-blood flow cytometric assay to study platelet surface glycoproteins in (1) peripheral blood, (2) peripheral blood activated in vitro by either phorbol myristate acetate, the thromboxane (TX)A2 analog U46619, or a combination of adenosine diphosphate and epinephrine, and (3) the blood emerging from a bleeding-time wound (shed blood). Activation-dependent changes were detected by monoclonal antibodies directed against the glycoprotein (GP)Ib-IX and GPIIb-IIIa complexes and P-selectin. In addition, we measured plasma glycocalicin (a proteolytic fragment of GPIb) and shed-blood TXB2 (a stable breakdown product of TXA2). In shed blood emerging from a bleeding-time wound, the usual time-dependent increase in platelet surface P-selectin was absent during CPB, but returned to normal within 2 hours. This abnormality paralleled both the CPB-induced prolongation of the bleeding time and a CPB-induced marked reduction in shed-blood TXB2 generation. In contrast, there was no loss of platelet reactivity to in vitro agonists during or after CPB. In peripheral blood, platelet surface P-selectin was negligible at every time point, demonstrating that CPB resulted in a minimal number of circulating degranulated platelets. CPB did not change the platelet surface expression of GPIb in peripheral blood, as determined by the platelet binding of a panel of monoclonal antibodies, ristocetin-induced binding of von Willebrand factor, and a lack of increase in plasma glycocalicin. CPB did not change the platelet surface expression of the GPIIb-IIIa complex in peripheral blood, as determined by the platelet binding of fibrinogen and a panel of monoclonal antibodies. In summary, CPB resulted in (1) markedly deficient platelet reactivity in response to an in vivo wound, (2) normal platelet reactivity in vitro, (3) no loss of the platelet surface GPIb-IX and GPIIb-IIIa complexes, and (4) a minimal number of circulating degranulated platelets. These data suggest that the "platelet function defect" of CPB is not a defect intrinsic to the platelet, but is an extrinsic defect such as an in vivo lack of availability of platelet agonists. The near universal use of heparin during CPB is likely to contribute substantially to this defect via its inhibition of thrombin, the preeminent platelet activator.

Mutants which are defective in catabolite repression control (CRC) of multiple independently regulated catabolic pathways have been previously described. The mutations were mapped at 11 min on the Pseudomonas aeruginosa chromosome and designated crc. This report describes the cloning of a gene which restores normal CRC to these Crc- mutants in trans. The gene expressing this CRC activity was subcloned on a 2-kb piece of DNA. When this 2-kb fragment was placed in a plasmid behind a phage T7 promoter and transcribed by T7 RNA polymerase, a soluble protein with a molecular weight (MW) of about 30,000 was produced in Escherichia coli. A soluble protein of identical size was overproduced in a Crc- mutant when it contained the 2-kb fragment on a multicopy plasmid. This protein could not be detected in the mutant containing the vector without the 2-kb insert or with no plasmid. When a 0.3-kb AccI fragment was removed from the crc gene and replaced with a kanamycin resistance cassette, the interrupted crc gene no longer restored CRC to the mutant, and the mutant containing the interrupted gene no longer overproduced the 30,000-MW protein. Pools of intracellular cyclic AMP and the activities of adenylate cyclase and phosphodiesterase were measured in mutant and wild-type strains with and without a plasmid containing the crc gene. No consistent differences between any strains were found in any case. These results provide original evidence for a 30,000-MW protein encoded by crc+ that is required for wild-type CRC in P. aeruginosa and confirms earlier reports that the mode of CRC is cyclic AMP independent in this bacterium.

Independently controlled, inducible, catabolic genes in Pseudomonas aeruginosa are subject to strong catabolite repression control by intermediates of the tricarboxylic acid cycle. Mutants which exhibited a pleiotropic loss of catabolite repression control of multiple pathways were isolated. The mutations mapped in the 11-min region of the P. aeruginosa chromosome near argB and pyrE and were designated crc. Crc- mutants no longer showed repression of mannitol and glucose transport, glucose-6-phosphate dehydrogenase, glucokinase, Entner-Doudoroff dehydratase and aldolase, and amidase when grown in the presence of succinate plus an inducer. These activities were not expressed constitutively in Crc- mutants but exhibited wild-type inducible expression.

The authors present a case of multiple intrahepatic pseudoaneurysms complicating acute gallstone pancreatitis, and they review the relevant literature. The complementary roles of ultrasonography, computed tomography and arteriography are illustrated. Although necrotizing vasculitis with resultant aneurysmal changes in peripancreatic vessels is a recognized complication of chronic pancreatitis, similar pseudoaneurysms have rarely been described in association with acute pancreatitis.