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Previous research indicates speaking may be emotionally and socially risky for adults who stutter (AWS) due to psychological distress induced by others following a dysfluency. This may impact communication-related decision-making; however, no measure had been developed to objectively quantify this variable. The present study aimed to develop and validate the Probability Discounting for Communication (PDC) task, a behavioral measure of risk taking that characterizes decreasing subjective value of hypothetical communication engagement as the probability of stuttering and listener reaction change. AWS (n= 67) and adults who do not stutter (AWNS; n= 93) were recruited from an online listserv and MTurk. Across a series of trials, participants completed the PDC by using a visual analog scale to indicate their subjective value of communication as probabilities of stuttering (1%-99%) and magnitudes of negative listener reaction risk (10%, 50%, 90%) were manipulated. They also completed measures of stuttering, communication, and demographics. Results revealed communication was discounted hyperbolically across increasing dysfluency odds. AWS showed more systematic discounting patterns compared to AWNSsuggestingAWSmay be more sensitive to communication due to experiences with stuttering. A magnitude effect was found with both AWS and AWNS discounting communication more steeply with increasing negative listener reaction risk. Significant associations were observed between discounting, stuttering, and communication measures among AWS, which indicates that sensitivity to risk in the context of stuttering and social reaction may influence communication engagement. Overall, the PDC functions as a measure to assess underlying decisionmaking patterns related to communication among AWS, which may inform treatment. [ABSTRACT FROM AUTHOR]

Hispanic/Latino perspectives can help construct a hermeneutics that involves a reader's first impressions and position. This model of 'critical correspondence' depends on recognizing the separated nature of texts and readers and examines them through the reader's social location and theoretical framework in a quest for the liberation and survival of all people.

A survey of 134 physicians in pediatric residency programs showed they are not uniformly knowledgeable about pulse oximetry. Pulse oximetry is widely used for continuous, noninvasive monitoring of blood oxygen content and is relied upon in clinical decision making. Physicians, therefore, need to be better informed about how to use pulse oximeters and about what to do with the information gained. A little more than half the pediatric house officers surveyed knew what a pulse oximeter measures: the percentage of hemoglobin that is oxygenated (oxyhemoglobin). Knowledge of pulse oximeters on the part of pediatric house staff may be variable and inadequate for good clinical decision making, and may result in further illness for patients. Medical schools and residency training programs should offer more training in the use of pulse oximeters and in the application of data gained from them., Objective. Pulse oximetry is widely used to measure oxygen saturation in inpatient and outpatient settings. As with any medical technology, competence in interpretation and application of the data is essential for patient care. We therefore undertook a study to quantify pediatric house staff's knowledge of pulse oximetry and their ability to interpret the information. Methods. A 16-item multiple choice questionnaire (6 demographic, 10 knowledge) was developed to assess knowledge of pulse oximetry. The questionnaire was administered to a total of 134 pediatric house staff from five medical school-affiliated residency programs in New York City. Results. The mean test score and standard deviation was 64.3% [+ or -] 1.9, with a range of 10% to 100%. Regarding three questions related to the knowledge of the oxyhemoglobin deviation curve, only 17% of the the respondents answered all three questions correctly. In three questions pertaining to the accuracy of the pulse oximeter, 36% of the respondents answered all questions correctly. Forty-three percent of the house staff believed that training in the use of pulse oximetry was inadequate. Conclusions. The results showed that there is marked variability in pediatric house staff's knowledge of all aspects of pulse oximetry. This could contribute to patient morbidity. We suggest that medical schools and residency programs place more emphasis on teaching the principles and applications of pulse oximetry and the oxyhemoglobin dissociation curve. Pediatrics 1994;93:810-813; pulse oximetry, oxyhemoglobin dissociation curve, medical education.

ATP-binding cassette class A3 (ABCA3) is a lipid transporter that plays a critical role in pulmonary surfactant function. The substitution of valine for glutamic acid at codon 292 (E292V) produces a hypomorphic variant that accounts for a significant portion of ABCA3 mutations associated with lung disorders spanning from neonatal respiratory distress syndrome and childhood interstitial lung disease to diffuse parenchymal lung disease (DPLD) in adults including pulmonary fibrosis. The mechanisms by which this and similar ABCA3 mutations disrupt alveolar type 2 (AT2) cell homeostasis and cause DPLD are largely unclear. The present study, informed by a patient homozygous for the E292V variant, used an in vitro and a preclinical murine model to evaluate the mechanisms by which E292V expression promotes aberrant lung injury and parenchymal remodeling. Cell lines stably expressing enhanced green fluorescent protein (EGFP)-tagged ABCA3 isoforms show a functional deficiency of the ABCA3E292V variant as a lipid transporter. AT2 cells isolated from mice constitutively homozygous for ABCA3E292V demonstrate the presence of small electron-dense lamellar bodies, time-dependent alterations in macroautophagy, and induction of apoptosis. These changes in AT2 cell homeostasis are accompanied by a spontaneous lung phenotype consisting of both age-dependent inflammation and fibrillary collagen deposition in alveolar septa. Older ABCA3E292V mice exhibit increased vulnerability to exogenous lung injury by bleomycin. Collectively, these findings support the hypothesis that the ABCA3E292V variant is a susceptibility factor for lung injury through effects on surfactant deficiency and impaired AT2 cell autophagy. [ABSTRACT FROM AUTHOR]

This study evaluated the natural prey preferences and spatial variability of predation pressure (PP = proportion of colonies with snails and/or clear predation signs) by the gastropod Cyphoma gibbosum on octocoral communities off the La Parguera Natural Reserve, Puerto Rico. All octocoral colonies were checked for presence of C. gibbosum and/or clear predation signs in four permanent band-transects (2 x 10 m), along three depth intervals (0-5, 7-12, >15 m deep) in each of six reefs along an inshore offshore gradient. Results indicate that C. gibbosum preys on at least 16 species, six of which (Briareum asbestinum, Gorgonia ventalina, Pseudoterogorgia americana, P. acerosa, Plexaura flexuosa, and Pseudoplexaura porosa) consistently showed significantly higher (K-W, P < 0.05) (17-37%) PP compared to all other species. Plexaura flexuosa, P. americana, and P. porosa had significantly higher PP (11-38%) among inner and mid-shelf reefs, and G. ventalina had higher PP in shelf-edge reefs (16-20%). A combination of differential spatial distributions and octocoral species abundances seems to explain the observed patterns of predation by C. gibbosum. Prey preference and higher abundances of 3-dimensional octocorals providing increased refuge or microhabitats utilized for mating or egg-deposition could be driving the spatial distribution of C. gibbosum and the observed differential predation pressure. [ABSTRACT FROM AUTHOR]

Discusses the development of Hispanic hermeneutics, in four representatives of Hispanic/Latino theology. Reference to the work of Fernando F. Segovia, an interpreter of Hispanic/Latino hermeneutics.

COVID-19 syndrome is characterized by acute lung injury, hypoxemic respiratory failure, and high mortality. Alveolar type 2 (AT2) cells are essential for gas exchange, repair, and regeneration of distal lung epithelium. We have shown that the causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and other members of the β-coronavirus genus induce an endoplasmic reticulum (ER) stress response in vitro; however, the consequences for host AT2 cell function in vivo are less understood. To study this, two murine models of coronavirus infection were used-mouse hepatitis virus-1 (MHV-1) in A/J mice and a mouse-adapted SARS-CoV-2 strain. MHV-1-infected mice exhibited dose-dependent weight loss with histological evidence of distal lung injury accompanied by elevated bronchoalveolar lavage fluid (BALF) cell counts and total protein. AT2 cells showed evidence of both viral infection and increased BIP/GRP78 expression, consistent with activation of the unfolded protein response (UPR). The AT2 UPR included increased inositol-requiring enzyme 1α (IRE1α) signaling and a biphasic response in PKR-like ER kinase (PERK) signaling accompanied by marked reductions in AT2 and BALF surfactant protein (SP-B and SP-C) content, increases in surfactant surface tension, and emergence of a reprogrammed epithelial cell population ( Krt8 + and Cldn4 + ). The loss of a homeostatic AT2 cell state was attenuated by treatment with the IRE1α inhibitor OPK-711. As a proof-of-concept, C57BL6 mice infected with mouse-adapted SARS-CoV-2 demonstrated similar lung injury and evidence of disrupted surfactant homeostasis. We conclude that lung injury from β-coronavirus infection results from an aberrant host response, activating multiple AT2 UPR stress pathways, altering surfactant metabolism/function, and changing AT2 cell state, offering a mechanistic link between SARS-CoV-2 infection, AT2 cell biology, and acute respiratory failure. NEW & NOTEWORTHY COVID-19 syndrome is characterized by hypoxemic respiratory failure and high mortality. In this report, we use two murine models to show that β-coronavirus infection produces acute lung injury, which results from an aberrant host response, activating multiple epithelial endoplasmic reticular stress pathways, disrupting pulmonary surfactant metabolism and function, and forcing emergence of an aberrant epithelial transition state. Our results offer a mechanistic link between SARS-CoV-2 infection, AT2 cell biology, and respiratory failure.

ATP-binding cassette class A3 (ABCA3) is a lipid transporter that plays a critical role in pulmonary surfactant function. The substitution of valine for glutamic acid at codon 292 (E292V) produces a hypomorphic variant that accounts for a significant portion of ABCA3 mutations associated with lung disorders spanning from neonatal respiratory distress syndrome and childhood interstitial lung disease to diffuse parenchymal lung disease (DPLD) in adults including pulmonary fibrosis. The mechanisms by which this and similar ABCA3 mutations disrupt alveolar type 2 (AT2) cell homeostasis and cause DPLD are largely unclear. The present study, informed by a patient homozygous for the E292V variant, used an in vitro and a preclinical murine model to evaluate the mechanisms by which E292V expression promotes aberrant lung injury and parenchymal remodeling. Cell lines stably expressing enhanced green fluorescent protein (EGFP)-tagged ABCA3 isoforms show a functional deficiency of the ABCA3 E292V variant as a lipid transporter. AT2 cells isolated from mice constitutively homozygous for ABCA3 E292V demonstrate the presence of small electron-dense lamellar bodies, time-dependent alterations in macroautophagy, and induction of apoptosis. These changes in AT2 cell homeostasis are accompanied by a spontaneous lung phenotype consisting of both age-dependent inflammation and fibrillary collagen deposition in alveolar septa. Older ABCA3 E292V mice exhibit increased vulnerability to exogenous lung injury by bleomycin. Collectively, these findings support the hypothesis that the ABCA3 E292V variant is a susceptibility factor for lung injury through effects on surfactant deficiency and impaired AT2 cell autophagy.

The middle cranial fossa is bounded anteriorly by the sphenoid ridge, medially by the lateral wall of the cavernous sinus and Meckel's cave, posteriorly by the sphenoid wing and petrous bone, and laterally by the greater wing of sphenoid and squamous temporal bone. In normal individuals, unnamed venous channels within the dura and arachnoid granulations can be seen on the floor of this fossa by the operating surgeon. Meningiomas arising mainly from the dura of the floor are uncommon, and middle fossa meningiomas have been arbitrarily named so based on an attachment of more than 75% to this location. They tend to present clinically at a large size and require special considerations for surgical treatment., (Copyright © 2020 Elsevier B.V. All rights reserved.)