Reasons for Moral-Based Opposition to Pornography in a U.S. Nationally Representative Sample.

Pornography use is a common-but-controversial activity that many people object to or morally disapprove of. Despite this, there is a limited understanding of the reasons for such moral opposition. Although some prior research has assessed characteristics that influence moral opposition to pornography, most research has done so using various forced-choice methods. The present study aimed to better understand the reasoning behind moral-based opposition to pornography by using open-ended questioning and exploring the relationship between these reasons and pornography use habits. To achieve these aims, we analyzed data from a nationally representative U.S. sample, specifically studying individuals who reported moral beliefs opposing pornography (N = 1,020). Results revealed 14 general themes (e.g., religion/spirituality; concerns about abuse; disgust) in the reasons participants reported for their moral disapproval of pornography, many of which were related to individual difference variables such as gender, age, religiousness, and political preferences. Implications, limitations, and directions for future research are also discussed.

Anxiety and Compulsive Sexual Behavior Disorder: A Systematic Review.

The inclusion of the novel diagnosis of Compulsive Sexual Behavior Disorder in the forthcoming 11th edition of the International Classification of Diseases has spurred increasing interest in the clinical profile of the disorder. Such attention has included a focus on potential comorbidities, risk factors, or symptoms resulting from such behaviors, including anxiety. Anxiety disorders have long been noted as comorbid with many other diagnoses, such as posttraumatic stress disorder, obsessive compulsive disorder, and substance use disorders. This review aims to understand the relationship between anxiety and compulsive sexual behavior in adults and adolescents, based on available quantitative studies. A search of PsycInfo and PubMed revealed 40 studies which quantitatively assessed a relationship between an anxiety measure and a Compulsive Sexual Behavior Disorder measure, including dissertations and published articles using clinical and community samples. A qualitative synthesis and risk of bias analysis of the studies was conducted, rather than a meta-analysis, due to the variety of methods. Overall, studies were primarily cross-sectional and the relationship between these two constructs was unclear, likely due to several factors, including inconsistent measurement of Compulsive Sexual Behavior Disorder, lack of gender diversity, and very little longitudinal data. Directions for future research are discussed.

Sexual addiction 25 years on: A systematic and methodological review of empirical literature and an agenda for future research.

In 1998, Gold and Heffner authored a landmark review in Clinical Psychology Review on the topic of sexual addiction that concluded that sexual addiction, though increasingly popular in mental health settings, was largely based on speculation, with virtually no empirical basis. In the more than two decades since that review, empirical research around compulsive sexual behaviors (which subsumes prior research about sexual addiction) has flourished, ultimately culminating in the inclusion of a novel diagnosis of Compulsive Sexual Behavior Disorder in the eleventh edition of the World Health Organization's International Classification of Diseases. The present work details a systematic review of empirical research published between January 1st, 1995 and August 1st, 2020 related to compulsive sexual behaviors, with a specific focus on evaluating the methodologies of that literature. This review yielded 371 papers detailing 415 individual studies. In general, the present review finds that, although research related to compulsive sexual behaviors has proliferated, much of this work is characterized by simplistic methodological designs, a lack of theoretical integration, and an absence of quality measurement. Moreover, the present review finds a virtual absence of high-quality treatment-related research published within this time frame. Implications of these findings for both clinical practice and future research are discussed.

Nebraska experience.

Nebraska agencies and public health organizations collaboratively addressed cyanobacterial issues for the first time after two dogs died within hours of drinking water from a small private lake south of Omaha on May 4, 2004. A necropsy on one of the dogs revealed that the cause of death was due to ingestion of Microcystin toxins. Within two weeks after the dog deaths, state and local officials jointly developed strategies for monitoring cyanobacterial blooms and issuing public health alerts and advisories. Weekly sampling of public lakes for microcystin toxins and cyanobacteria was initiated during the week of May 17, 2004. ELISA laboratory equipment and supplies were purchased to achieve a quick turnaround time for measuring weekly lake samples for total microcystins so that public health advisories and alerts could be issued prior to each weekend's recreational activities. A conservative approach was selected to protect human health, pets, and livestock, which included collecting worst-case samples from cyanobacterial blooms; freezing and thawing of samples to lyse algal cells and release toxins prior to laboratory analysis; and using action levels of 15 ppb and 2 ppb of total microcystins, respectively, for issuing health alerts and health advisories. During 2004, five dog deaths, numerous wildlife and livestock deaths, and more than 50 accounts of human skin rashes, lesions, or gastrointestinal illnesses were reported at Nebraska lakes. Health alerts were issued for 26 lakes and health advisories for 69 lakes. Four lakes were on health alert for 12 or more weeks. The primary cyanobacterial bloom-forming genera identified in Nebraska lakes were Anabaena, Aphanizomenon, and Microcystis. Preliminary assessments of lake water quality data indicated that lower lake levels from the recent drought and low nitrogen to phosphorus ratios may have contributed, in part, to the increased numbers of cyanobacterial complaints and problems that occurred in 2004.

Resistance of the pulmonary epithelium to movement of buffer ions.

Exposure of the apical surfaces of alveolar monolayers to acidic and alkaline solutions has been reported to have little influence on intracellular pH compared with basolateral challenges (Joseph D, Tirmizi O, Zhang X, Crandall ED, and Lubman RL. Am J Physiol Lung Cell Mol Physiol 282: L675-L683, 2002). We have used fluorescent pH indicators and a trifurcated optical bundle to determine whether the apical surfaces are less permeable to ionized buffers than the membranes that separate the vasculature from the tissues in intact rat lungs. In the first set of experiments, the air spaces were filled with perfusate containing FITC-dextran (mol wt 60000) or 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Air space pH fell progressively from 7.4 to 6.61 +/- 0.03 (mean +/- SE, n = 11, air space buffers at 10 mM). Perfusion for 2 min with 2 mM NH4Cl increased air space pH by 0.142 +/- 0.019 unit, without a subsequent acidic overshoot. Infusions of NaHCO3 and sodium acetate reduced pH without a subsequent alkaline overshoot. In the second set of experiments, cellular pH was monitored in air-filled lungs after perfusion with BCECFAM. Injections of NH4Cl caused a biphasic response, with initial alkalinization of the cellular compartment followed by acidification after the NH4Cl was washed from the lungs. Subsequent return of pH to normal was slowed by infusions of 1.0 mM dimethyl amiloride. These studies suggest that lung cells are protected from air space acidification by the impermeability of the apical membranes to buffer ions and that the cells extrude excess H+ through basolateral Na+/H+ exchangers.

Protection of the lungs from acid during aspiration.

Unlike the thick mucosa that normally covers the upper gastrointestinal tract, the membranes that cover the distal surfaces of the lungs are remarkably attenuated. This permits rapid exchange of gases between the airspaces and pulmonary vasculature, and may make the lungs more susceptible to acid challenges associated with acid reflux and aspiration. Any injury to the alveolar epithelium could result in the movement of solute and water into the airspaces (chemical pneumonia) and impair gas exchange. In this study, we used a fluorescent approach to compare the relative permeability of the apical basolateral surfaces of the lungs to the exchange of the ionic forms of acids and bases. The apical membranes proved to be much less permeable to NH(4)(+) and HCO(3)(+) than the basolateral membranes. This asymmetry in permeability should enhance resistance of the epithelium to inspired acidic challenges by slowing entry of acid into the cells and by linking the intracellular pH of the alveolar cells to that of the plasma, which is a relatively large, well-buffered compartment. Evidence also was obtained that the acid is secreted by the membranes covering the lungs.

Abnormal pressure-natriuresis in hypertension: role of cytochrome P450 metabolites of arachidonic acid.

The pressure-natriuresis relationship is shifted to higher pressures in genetic and experimental models of hypertension; however, the factors responsible for altering kidney function remain to be determined. In spontaneously hypertensive (SHR) and Lyon hypertensive rats, the resetting of pressure-natriuresis results from increased preglomerular renal vascular tone, whereas sodium reabsorption is elevated in the thick ascending loop of Henle (TALH) of Dahl S rats. Recently, a new route for the renal metabolism of arachidonic acid (AA) has been described, and there is evidence that this pathway contributes to the resetting of renal function in hypertension. In the kidney, cytochrome P450 (CYP) enzymes metabolize AA primarily to 20-HETE and EETs. 20-HETE is a potent constrictor of renal arterioles that has an important role in autoregulation of renal blood flow and tubuloglomerular feedback. 20-HETE and EETS also inhibit sodium reabsorption in the proximal tubule and TALH. In the SHR, the renal production of 20-HETE is elevated and inhibitors of the formation of 20-HETE decrease arterial pressure. Blockade of 20-HETE formation also reduces blood pressure or improves renal function in deoxycorticosterone acetate (DOCA)-salt, angiotensin II--infused, and Lyon hypertensive rats. In contrast, 20-HETE formation is reduced in the TALH of Dahl S rats and this contributes to elevated sodium reabsorption. Induction of 20-HETE synthesis improves pressure-natriuresis and lowers blood pressure in Dahl S rats, whereas inhibitors of the synthesis of 20-HETE promote the development of hypertension in Lewis rats. These findings indicate that the renal production of CYP metabolites of AA is altered in genetic and experimental models of hypertension and that this system contributes to the resetting of pressure-natriuresis and the development of hypertension in some models.

Effects of converting enzyme inhibitors on renal P-450 metabolism of arachidonic acid.

The effects of blockade of the renin-angiotensin system on the renal metabolism of arachidonic acid (AA) were examined. Male Sprague-Dawley rats were treated with vehicle, captopril (25 mg x kg(-1) x day(-1)), enalapril (10 mg x kg(-1) x day(-1)), or candesartan (1 mg x kg(-1) x day(-1)) for 1 wk. The production of 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) by renal cortical microsomes increased in rats treated with captopril by 59 and 24% and by 90 and 58% in rats treated with enalapril. Captopril and enalapril increased 20-HETE production in the outer medulla by 100 and 143%, respectively. In contrast, blockade of ANG II type 1 receptors with candesartan had no effect on the renal metabolism of AA. Captopril and enalapril increased cytochrome P-450 (CYP450) reductase protein levels in the renal cortex and outer medulla and the expression of CYP450 4A protein in the outer medulla. The effects of captopril on the renal metabolism of AA were prevented by the bradykinin-receptor antagonist, HOE-140, or the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester. These results suggest that angiotensin-converting enzyme inhibitors may increase the formation of 20-HETE and EETs secondary to increases in the intrarenal levels of kinins and NO.

Intrarenal infusion of bradykinin elicits a pressor response in conscious rats via a B2-receptor mechanism.

Bradykinin (BK) is a peptide known to activate afferent nerve fibers from the kidney and elicit reflex changes in the cardiovascular system. The present study was specifically designed to test the hypothesis that bradykinin B2 receptors mediated the pressor responses elicited during intrarenal bradykinin administration. Pulsed Doppler flow probes were positioned around the left renal artery to measure renal blood flow (RBF). A catheter, to permit selective intrarenal administration of BK, was advanced into the proximal left renal artery. The femoral artery was cannulated to measure mean arterial pressure (MAP). MAP, heart rate (HR), and RBF were recorded from conscious unrestrained rats while five-point cumulative dose-response curves during an intrarenal infusion of BK (5-80 microg x kg(-1) x min(-1)) were constructed. Intrarenal infusion of BK elicited dose-dependent increases in MAP (maximum pressor response, 26+/-3 mmHg), accompanied by a significant tachycardia (130+/-18 beats/min) and a 28% increase in RBF. Ganglionic blockade abolished the BK-induced increases in MAP (maximum response, -6+/-5 mmHg), HR (maximum response 31+/-14 beats/min), and RBF (maximum response, 7+/-2%). Selective intrarenal B2-receptor blockade with HOE-140 (50 microg/kg intrarenal bolus) abolished the increases in MAP and HR observed during intrarenal infusion of BK (maximum MAP response, -2+/-3 mmHg; maximum HR response, 15+/-11 beats/min). Similarly, the increases in RBF were prevented after HOE-140 treatment. In fact, after HOE-140, intrarenal BK produced a significant decrease in RBF (22%) at the highest dose of BK. Results from this study show that the cardiovascular responses elicited by intrarenal BK are mediated predominantly via a B2-receptor mechanism.

Bradykinin B2-receptors mediate the pressor and renal hemodynamic effects of intravenous bradykinin in conscious rats.

Bradykinin (BK) is a peptide which evokes remarkably different changes in cardiovascular function. Systemic bolus injection of BK results in a rapid drop in blood pressure via an endothelium-dependent mechanism. On the other hand, local administration of BK can activate a powerful pressor reflex by stimulating afferent nerves located in the abdominal viscera, the heart, and the kidney. In the present study, the cardiovascular and renal hemodynamic effects during sustained (intravenous infusion) and transient (intravenous bolus injection) elevations in circulating BK were characterized and the receptor mechanism eliciting these effects was investigated. Mean arterial pressure (MAP), heart rate (HR), and renal blood flow (RBF) were recorded from conscious unrestrained rats while five-point cumulative dose-response curves were constructed during infusion or bolus injection of BK (5-80 microg kg(-1)). Infusion of BK produced dose-dependent increases in MAP (maximum response = 27 +/- 3 mmHg) accompanied by a significant tachycardia (maximum response = 159 +/- 20 bpm), a 28 +/- 6% increase in RBF, and no changes in renal vascular resistance (RVR). The BK-induced increases in MAP, HR, and RBF were abolished after treatment with a ganglion blocker (maximum responses: MAP = 2 +/- 3 mmHg, HR = 13 +/- 4 bpm, RBF = 4 +/- 2%) or with an agent which blocks B2-receptors (maximum responses: MAP = 1 +/- 1 mmHg, HR = 6 +/- 5 bpm, RBF = 6 +/- 2%). In marked contrast, bolus administration of BK resulted in hypotensive responses (maximum decline in MAP = -37 +/- 4 mmHg), reflex tachycardia (maximum increase in HR = 45 +/- 9 bpm), increases in RBF (maximum response = 13 +/- 4%), and significant reductions in RVR (maximum response = 38 +/- 5%). These responses were also prevented when B2-receptors were blocked (maximum responses: MAP = 3 +/- 2 mmHg, HR = 17 +/- 6 bpm, RBF = 3 +/- 3%, RVR = 9 +/- 4%). In summary, BK infusions activated a cardiopressor reflex while BK injections caused hypotension. These opposite effects were both mediated via B2-receptors. These findings suggest that BK can have complex effects on the cardiovascular system that may be dependent on the sites, magnitude, and duration of elevated BK concentrations.

Extracellular Matrix Assembly in Diatoms (Bacillariophyceae) (I. A Model of Adhesives Based on Chemical Characterization and Localization of Polysaccharides from the Marine Diatom Achnanthes longipes and Other Diatoms).

Extracellular adhesives from the diatoms Achnanthes longipes, Amphora coffeaeformis, Cymbella cistula, and Cymbella mexicana were characterized by monosaccharide and methylation analysis, lectin-fluorescein isothiocyanate localization, and cytochemical staining. Polysaccharide was the major component of adhesives formed during cell motility, synthesis of a basal pad, and/or production of a highly organized shaft. Hot water-insoluble/hot 0.5 M NaHCO3-soluble anionic polysaccharides from A. longipes and A. coffeaeformis adhesives were primarily composed of galactosyl (64-70%) and fucosyl (32-42%) residues. In A. longipes polymers, 2,3-, t-, 3-, and 4-linked/substituted galactosyl, t-, 3-, 4-, and 2-linked fucosyl, and t- and 2-linked glucuronic acid residues predominated. Adhesive polysaccharides from C. cistula were EDTA-soluble, sulfated, consisted of 83% galactosyl (4-, 4,6-, and 3,4-linked/substituted) and 13% xylosyl (t-, 4f/5p-, and 3p-linked/substituted) residues, and contained no uronosyl residues. Ulex europaeus agglutinin uniformly localized [alpha](1,2)-L-fucose units in C. cistula and Achnanthes adhesives formed during motility and in the pads of A. longipes. D-Galactose residues were localized throughout the shafts of C. cistula and capsules of A. coffeaeformis. D-Mannose and/or D-glucose, D-galactose, and [alpha](t)-L-fucose residues were uniformly localized in the outer layers of A. longipes shafts by Cancavalia ensiformis, Abrus precatorius, and Lotus tetragonolobus agglutinin, respectively. A model for diatom cell adhesive structure was developed from chemical characterization, localization, and microscopic observation of extracellular adhesive components formed during the diatom cell-attachment process.

Extracellular Matrix Assembly in Diatoms (Bacillariophyceae) (II. 2,6-Dichlorobenzonitrile Inhibition of Motility and Stalk Production in the Marine Diatom Achnanthes longipes).

The cellulose synthesis inhibitor 2,6-dichlorobenzonitrile (DCB) and the DCB analogs 2-chloro-6-fluorobenzonitrile, 3-amino-2,6-dichlorobenzonitrile, and 5-dimethylamino-naphthalene-1-sulfonyl-(3-cyano-2, 4-dichloro)aniline (DCBF) inhibited extracellular adhesive production in the marine diatom Achnanthes longipes, resulting in a loss of motility and a lack of permanent adhesion. The effect was fully reversible upon removal of the inhibitor, and cell growth was not affected at concentrations of inhibitors adequate to effectively interrupt the adhesion sequence. Video microscopy revealed that the adhesion sequence was mediated by the export and assembly of polymers, and consisted of initial attachment followed by cell motility and eventual production of permanent adhesive structures in the form of stalks that elevated the diatom above the substratum. A. longipes adhesive polymers are primarily composed of noncellulosic polysaccharides (B.A. Wustman, M.R. Gretz, and K.D. Hoagland [1997] Plant Physiol 113: 1059-1069). These results, together with the discovery of DCB inhibition of extracellular matrix assembly in noncellulosic red algal unicells (S.M. Arad, O. Dubinsky, and B. Simon [1994] Phycologia 33: 158-162), indicate that DCB inhibits synthesis of noncellulosic extracellular polysaccharides. A fluorescent probe, DCBF, was synthesized and shown to inhibit adhesive polymer production in the same manner as DCB. DCBF specifically labeled an 18-kD polypeptide isolated from a membrane fraction. Inhibition of adhesion by DCB and its analogs provides evidence of a direct relationship between polysaccharide synthesis and motility and permanent adhesion.

Critical point drying: contamination in transitional fluid supply cylinders.

We call attention to the occurrence of an oily residue in the CPD bomb after critical point drying, as well as the presence of rust, dirt, and an oily residue in CO2 and Freon supply cylinders. Bottled gas is often tested for purity once after manufacturing and then is pumped and stored, perhaps several times, before the consumer's cylinders are filled. The cylinders may be in use for over 40 years, and may never be chemically cleaned, although they are hydrostatically pressure tested every five years, with the date of each test stamped on the cylinder. To the bottled gas industry we recommend regular inspection of tanks for bottom contamination, and vacuum and chemical cleaning when contamination is found. To users of bottled gas for critical point drying, we recommend becoming aware of the procedures of cylinder inspection, cleaning, and circulation among users. We suggest reporting to the gas supplier any contamination produced by inadvertently backfilling the supply cylinder. Although a common awareness of the problem of supply cylinder residues should lead to failures, the best assurance of clean, oil-free, dry liquid CO2 and other transitional fluids may be in the development of in-line filters which would remove particles, oil and moisture between the supply cylinder and the CPD bomb. We also suggest the use of gas grades higher than commercial, such as welding anhydrous (CO2) or specialty gases.