A phenomenologic investigation of pediatric residents' experiences being parented and giving parenting advice.

Factors surrounding pediatricians' parenting advice and training on parenting during residency have not been well studied. The primary purpose of this study was to examine pediatric residents' self-reported experiences giving parenting advice and explore the relationship between parenting advice given and types of parenting residents received as children. Thirteen OUHSC pediatric residents were individually interviewed to examine experiences being parented and giving parenting advice. Phenomenological methods were used to explicate themes and secondary analyses explored relationships of findings based upon Baumrind's parenting styles (authoritative, authoritarian, permissive). While childhood experiences were not specifically correlated to the parenting advice style of pediatric residents interviewed, virtually all reported relying upon childhood experiences to generate their advice. Those describing authoritative parents reported giving more authoritative advice while others reported more variable advice. Core interview themes related to residents' parenting advice included anxiety about not being a parent, varying advice based on families' needs, and emphasis of positive interactions and consistency. Themes related to how residents were parented included discipline being a learning process for their parents and recalling that their parents always had expectations, yet always loved them. Pediatric residents interviewed reported giving family centered parenting advice with elements of positive interactions and consistency, but interviews highlighted many areas of apprehension residents have around giving parenting advice. Our study suggests that pediatric residents may benefit from more general educational opportunities to develop the content of their parenting advice, including reflecting on any impact from their own upbringing.

Factors influencing planktonic, post-settlement dispersal of early juvenile blue crabs (Callinectes sapidus Rathbun).

An emerging body of literature points to post-settlement, planktonic dispersal as a key determinant of distribution and abundance patterns of aquatic organisms, yet little is known about mechanisms inducing such dispersal. Recent evidence suggests that early juvenile blue crabs (Callinectes sapidus Rathbun) may use planktonic emigration as a means of post-settlement dispersal. The goal of this study was to identify mechanisms inducing post-settlement, planktonic dispersal of early juvenile blue crabs. A combination of field mark-recapture experiments in large seagrass beds within a 2x3 km region near Oregon Inlet, North Carolina, USA, and a series of laboratory flume experiments examined the effects of day vs. night, crab size (first-second juvenile benthic instars: J1-J2 vs. third-fifth juvenile benthic instars: J3-J5), crab density and current speed on planktonic dispersal of early juvenile blue crabs. Transport of dead crabs in the flume experiment identified that planktonic dispersal was an active behavioral response rather than a passive response to increasing current speed. The experimental results demonstrated that planktonic dispersal can range from 4 to 18% under medium to high flow conditions. Planktonic dispersal of juvenile crabs is (1) an active behavioral response, (2) increased significantly with current speeds above 20 cms(-1), and (3) was higher for relatively large (J3-J5) than small (J1-J2) instars. There was a non-significant trend towards greater dispersal at night than during the day in the field experiment, and no effect of crab density on dispersal in the flume experiment. The results from this study highlight the need to consider mechanisms inducing post-settlement, planktonic dispersal when attempting to understand and predict recruitment and population dynamics of aquatic organisms, as well as when linking hydrodynamics, animal behavior and planktonic dispersal.

Caregiving in nursing homes. Views of licensed nurses and nursing assistants.

This investigation is a qualitative study of the views held by 36 licensed nurses (25 registered nurses and 11 licensed practical nurses) and 40 nursing assistants regarding caregiving in nursing homes. Because these care providers are most directly involved in the delivery of care, their views are important as determinants of quality of care. Study findings focus on the extent to which nurses and nursing assistants agree on what contributes to good care and how they perceive the work that each does. Also reported are their perceptions regarding factors that make care delivery easy or difficult. Results suggest that nurses and nursing assistants share selected perceptions about the division of labor in the nursing home. Also evident are areas of less agreement among these members of different status sets. A discussion of how these caregivers can work together as effective team members is presented.

Gene targeting of a CFTR allele in HT29 human epithelial cells.

HT29 cells endogenously express the cystic fibrosis transmembrane conductance regulator (CFTR) and have been used previously as a model to examine cellular regulation of CFTR expression and chloride secretory function. Homologous recombination has been used to specifically disrupt CFTR transcription in the HT29-18-C1 subclone. Experiments demonstrate successful disruption of a CFTR allele by DNA constructs, which target insertion of the neomycin phosphotransferase gene into CFTR exon 1 via homologous recombination. The mutation of one allele is a partial knockout because this cell line has multiple CFTR alleles. The mutation is confirmed by polymerase chain reaction (PCR) and genomic Southern blot analysis. A 52-68% reduction in CFTR mRNA levels is observed in the mutant cell line by both Northern and PCR analysis. However, Western blots show no decrease in total CFTR protein levels. Consistent with the lack of reduction in CFTR protein, the partial knockout mutant does not demonstrate alterations in cyclic AMP or calcium stimulation of chloride efflux or net osmolyte loss. Results suggest that posttranscriptional regulation of CFTR levels may contribute to maintenance of cellular chloride transport function.

Cellular chloride depletion inhibits cAMP-activated electrogenic chloride fluxes in HT29-18-C1 cells.

Cyclic AMP-activated chloride fluxes have been analyzed in HT29-18-C1 cells (a clonal cell line derived from a human colon carcinoma) using measurements of cell volume (electronic cell sizing), cell chloride content (chloride titrator) and intracellular chloride activity (6-methoxy-N-(3-sulfopropyl)quinolinium; SPQ). HT29-18-C1 was shown to mediate polarized chloride transport. In unstimulated cells, the apical membrane was impermeable to chloride and net chloride flux was mediated by basolateral furosemide-sensitive transport. Forskolin (10 microM) increased furosemide-insensitive chloride permeability of the apical membrane, and decreased steady-state intracellular chloride concentration approximately 9%. Cellular chloride depletion (substitution of medium chloride by nitrate or gluconate), caused greater than fourfold reduction in cellular chloride concentration. When chloride-depleted cells were returned to normal medium, cells regained chloride and osmolytes via bumetanide-sensitive transport, but forskolin did not stimulate bumetanide-insensitive chloride uptake. The inhibition of cAMP-activated chloride reuptake was not explained by limiting cation conductance, cell shrinkage, choice of substitute anion, or decreased generation of cAMP in chloride-depleted cells. When cells with normal chloride content were depolarized (135 mM medium potassium + 10 microM valinomycin), cAMP activated electrogenic chloride uptake permselective for Cl- approximately Br- > NO3- > I-. The electrogenic transport pathway was inhibited in chloride-depleted cells. Results suggest that chloride depletion limits activation of electrogenic chloride flux.

The role of rehabilitation medicine in the management of chronic pain: description of a pain control program and longitudinal outcomes.

Longitudinal outcomes of 35 patients with chronic benign pain were studied following their participation in a 3-week multidisciplinary pain management program. Pretreatment status with respect to activity levels, health care utilization, medication use, and subjective pain intensity was compared statistically with post-treatment status at three follow-up assessments (discharge, 1.6 months, and 22.7 months post-discharge). Results suggest a positive impact of treatment on activity levels, health care utilization, and medication use post-discharge, with diminution of that impact over time. Pain management programs increasingly will need to demonstrate cost effectiveness, including finding ways to maximize program gains over time.

Propionate activates multiple ion transport mechanisms in the HT29-18-C1 human colon cell line.

Short-chain fatty acids (SCFAs) are the major solutes and the major anions in the colonic lumen. We studied the response of suspended HT29-18-C1 cells (an epithelial cell line derived from a human colon carcinoma) to SCFA exposure. Cellular response was evaluated by measurement of cell volume (Coulter counter), intracellular pH [pHi; measured fluorometrically with 2',7'-bis(2-carboxyethyl)-5-(6)-carboxyfluorescein (BCECF)], and intracellular Na+, K+, and Cl- content (flame photometry and chloride titrator). Exposure to 130 mM propionate in isosmotic medium causes a rapid decrease in pHi and activates pHi recovery via amiloride-sensitive Na-H exchange. In the presence of propionate, Na-H exchange also causes cell swelling to a peak volume 11% above control cells and causes a 2.8-fold increase in intracellular Na+ content. After peak swelling, a regulatory-volume decrease (RVD) significantly reduced volume and intracellular Na+ returned to baseline. Other SCFAs (acetate, butyrate, and valerate) also elicit swelling and RVD. Activation of the Na(+)-K(+)-adenosinetriphosphatase (ATPase) is required to return Na+ to normal levels and to indirectly provide ion gradients required for propionate-induced RVD, but Na(+)-K(+)-ATPase activity does not directly mediate RVD. When 1 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) is added in the presence of propionate, RVD was inhibited and cell Na+ content increased. Cl- depletion inhibited propionate-induced RVD and diminished the effect of SITS.

Use of self-administered joint counts in the evaluation of rheumatoid arthritis patients.

The validity and reliability of self-administered joint counts are reported in a group of 32 rheumatoid arthritis patients being followed at a university-based practice located in the Southeast region of the United States, serving low to middle income urban and rural patients. Adequate inter-rater reliability among the patients' and the research assistant's joint counts was obtained for upper (r = 0.74), lower (r = 0.96), and upper and lower extremities (r = 0.89). Convergent validity correlations for pain, helplessness, and the Joint Alignment and Motion scale were found to be adequate. We conclude that rheumatoid arthritis patients can reliably assess their joint counts. Self joint counts along with other validated self-reports of health status may be applicable to busy outpatient settings, as well as in clinical research.

Regulation of cystic fibrosis transmembrane conductance regulator (CFTR) gene transcription and alternative RNA splicing in a model of developing intestinal epithelium.

Transcriptional and post-transcriptional regulation of CFTR (cystic fibrosis transmembrane conductance regulator) gene expression was studied in HT29 cells. It is known that the abundance of CFTR mRNA increases during differentiation of pluripotent HT29-18 cells and is maintained at high levels in the stably differentiated HT29-18-C1 subclone. Nuclear run-on assays suggest that increased transcription of the CFTR gene explains the increased abundance of total CFTR mRNA in differentiated HT29 cells. The increased transcription cannot be ascribed to cell cycle-dependent expression of the CFTR gene or to changes in CFTR gene copy number between subcloned cells. Similar to native tissue cells, differentiated HT29 cells contain low copy numbers of CFTR transcripts (1-5/cell), and a portion of the CFTR transcripts are alternatively spliced to remove exon 9 (and make 9-mRNA). During differentiation of HT29-18 cells, the absolute amount of full-length CFTR mRNA increases 8-fold, whereas the amount of 9- mRNA increases 18-fold. The fraction of 9- mRNA in the CFTR mRNA pool is increased in differentiated HT29 cells. The results show that gene transcription regulates the abundance of CFTR transcripts and that regulatory control of alternative RNA splicing may also be a cellular mechanism to modulate CFTR function.

Assay of apical membrane enzymes based on fluorogenic substrates.

A series of enzymatic rate assays are described. The assays are based on coumarin derivatives that are fluorogenic substrates for the enzymes dipeptidase IV, aminopeptidase N, alkaline phosphatase, and gamma-glutamyltransferase. These simple assays are rapid and offer improved sensitivity over established colorimetric methods. The substrates have apparent affinities for the enzymes of 5-250 microM. L-Glutamic acid gamma-(7-amido-4-methylcoumarin) is characterized as a substrate of gamma-glutamyltransferase on the basis of inhibition of enzymatic cleavage when the glycylglycine acceptor molecule is omitted and inhibition of the enzymatic reaction by addition of glycine. Assay conditions for the four enzymes are established such that less than 0.6% of the substrate is consumed, fluorescence is proportional to enzymatic product, and results may be directly compared to established colorimetric assays. Intestinal epithelial cells are used both to establish appropriate assay conditions and to demonstrate the utility of the assays.

Effects of sometribove on zinc metabolism and tissue mineral concentration in dairy calves.

The metabolism of Zn and tissue mineral concentrations were studied after a single oral 65Zn dose in 10 6-wk-old Holstein calves injected subcutaneously daily with 0 (control) or 10 mg of sometribove (recombinant methionyl bST) for 6 wk. Zinc-65 absorption was not significantly affected by bST; its concentration in the semitendinosus muscle was reduced by 32% in the bST calves, but concentrations in liver, pancreas, spleen, kidney, heart, small intestine, testicle, and rib were not different from controls. Manganese content was reduced by 27% in liver, 60% in kidney, 99% in spleen, 92% in testicles, and 33% in rib. Iron content of pancreas, spleen, and testicle and Zn content of rib were increased in the bST calves. The data indicate that Zn metabolism was not affected adversely by bST. Manganese content of several tissues was significantly reduced in the bST calves; however, no clinical signs of an Mn deficiency were evident.

Effects of sometribove on performance, carcass composition, and chemical blood characteristics of dairy calves.

Ten intact male Holstein calves averaging 75 kg of BW and 59 d of age were used to study the effects of daily injections of 0 (control) or 10 mg of sometribove (recombinant methionyl bST) for 6 wk on performance, health, carcass composition, N metabolism, chemical blood characteristics, and hormone profiles. Average daily gain, feed intake, feed:gain ratio, and height at withers, hip, and hock were not influenced by bST. Carcasses from bST-treated calves contained 5% more protein and 36% less lipid than controls. Circulating concentrations of Ca, P, glucose, urea N, alkaline phosphatase, creatine phosphokinase, insulin-like growth factor-I, and insulin were not affected by bST. Packed cell volume was decreased about 7% (29.9 vs. 32.4%) in the bST calves. Hormone injection did not adversely affect health of the calves as measured by body temperature and by pulse and respiration rates. The most profound effects of sometribove were a reduction in carcass lipid and an increase in body proteins. These effects may be of some practical importance when leanness of carcass is desirable.

Zinc absorption, metabolism, and endogenous excretion in zinc-deficient and normal calves over an extended time.

Zinc metabolism was studied in Zn-deficient and control Holstein calves over a 2-mo period following a single oral or i.v. 65Zn dose. In both orally and i.v. dosed animals, all gastrointestinal tissue sections from Zn-deficient animals contained more 65Zn than comparable tissues of controls. Contents of proximal small intestinal sections of Zn-deficient calves contained more 65Zn 8 to 10 wk after dosing than did those from controls; however, the reverse occurred in the distal small intestine, cecum, and large intestine. With both dosing methods, Zn-deficient calves retained more 65Zn throughout the study. Daily 65Zn excretion rate as a percentage of that retained declined for 6 wk after dosing, indicating a constantly increasing biological half-life. For deficient calves, the biological half-life was about 500 d in the later weeks of the experiments. In orally dosed, Zn-deficient animals, specific activity of fecal 65Zn exceeded that of serum Zn throughout the study. This shows a shortcoming in the basic assumption of measuring endogenous Zn loss from fecal and serum specific activities and total fecal stable Zn. Thus, endogenously excreted Zn is not representative of that remaining.

Influence of dietary aluminum and phosphorus on zinc metabolism in dairy calves.

The metabolism of a single oral zinc-65 dose was studied in young dairy calves fed two concentrations of added A1 (0 and .20% A1) and two concentrations of added P (0 and .22% P) for 7 wk. The four treatments were 1) normal P-low A1, 2) low P-low A1, 3) normal P-high A1 and 4) low P-high A1. The basal diet (low P-low AL) contained, by analysis, .132% P, .74% Ca, .021% A1 and 59 ppm Zn. Zinc-65 absorption was greater (66.5 vs 63.2% of dose, P less than .10) with the low-P diet; added A1 reduced (P less than .05) 65Zn absorption. Calves fed low-P diets had higher (P less than .10) concentrations of 65Zn in liver, kidney, spleen, heart, small intestine and testicle than those fed normal-P diets. Zinc-65 was reduced (P less than .10) in pancreas, heart, testicle and muscle of calves fed high A1. Iron was increased in liver and kidney (P less than .10), Zn (P less than .10) and Mn (P less than .01) were increased in liver, but Fe in small intestine and Cu in muscle and tibia shaft were decreased (P less than .10) in calves fed the low-P diets compared to those fed adequate-P diets. High A1 reduced (P less than .10) Cu in small intestine and tibia shaft. The results suggest that zinc metabolism may be moderately affected in calves fed either low-P or high-A1 diets.

Effects of high dietary lead on the metabolism of intravenously dosed selenium-75 in dairy calves.

The metabolism of intravenously dosed 75Se was studied in 10 Holstein bull calves fed for ad libitum access a control diet containing no added Pb or a control diet supplemented with 1000 ppm Pb as PbSO4 for 4 wk. The Pb-supplemented calves exhibited no clinical signs often ascribed to lead toxicity. Likewise, feed intake and body weight gains were not affected adversely. The lead content of rib, kidney, liver, and brain was increased. Serum glutamic oxaloacetate transaminase activity increased in the calves fed Pb during the last 2 wk of the experiment. The kidneys of the calves supplemented with lead were 34% larger than those of controls. The total endogenous 75Se in the feces over the 4-d collection period was not different between treatments (4.14% of dose versus 3.31% of dose). Likewise, urinary 75Se excretion values were similar. About 97% of the 75Se dose disappeared from the blood within 6 h after dosing four calves on both treatments. Tissue concentrations of 75Se were reduced in kidney, spleen, pancreas, brain, and spinal cord. In summary, ingested Pb had very little effect on the endogenous excretion of 75Se in urine and feces; therefore, the data are consistent with earlier research in which the main effect of Pb on Se occurs at the absorption site.

Effects of dietary aluminum and phosphorus on magnesium metabolism in dairy calves.

The metabolism of Mg was studied in young dairy calves fed two levels of added Al (0 and .20% Al) and two levels of added P (0 and .22% P) for 7 wk. The four treatments were 1) normal P-low Al, 2) low P-low Al, 3) normal P-high Al and 4) low P-high Al. The basal diet (low P-low Al) contained, by analysis, .132% P, .021% Al and .17% Mg. Added Al did not affect (P greater than .10) serum Mg. An Al x P interaction on bone Mg was detected (P less than .01). Magnesium was reduced in tibia shaft (.34 vs .44%) and in tibia joint (.43 vs .53%) in calves fed high Al in the presence of normal dietary P, but Mg was not reduced in the calves fed low-P diets. Apparent absorption of Mg was reduced by approximately five-fold (.18 g/d vs -.84 g/d, P less than .01); urinary Mg excretion was reduced 31% (1.12 g/d vs .77 g/d, P less than .01); and Mg retention declined 41% (-95 g/d vs -1.61 g/d, P less than .01) in calves fed added A1. Compared with calves fed low-P diets, calves fed normal levels of P had a higher Mg concentration in tibia shaft (P less than .01) and tibia joint (P less than .05). The data indicate that supplemental Al may adversely affect Mg metabolism in calves.

Influence of high dietary aluminum on performance and phosphorus bioavailability in dairy calves.

Sixteen male intact Holstein calves averaging 72 kg and 64 d of age were used to study the effects of high dietary Al on calf performance and P bioavailability. The main effects were two concentrations of added aluminum (0 and .20% Al) and two of added P (0 and .22% P). The basal diet contained, by analysis, .132% P, .74% Ca, and .021% Al. The calves were assigned to four treatment groups balanced according to body weight. The four treatments were 1) normal P, low Al; 2) low P, low Al; 3) low P, high Al; and 4) normal P, high Al. Calved had ad libitum access to their respective diets for 7 wk. Metabolism of a single oral 32P dose was determined during wk 6. The adverse effects of high dietary Al include a 17% reduction in feed intake and a 47% reduction in body weight gains. Alkaline phosphatase and plasma glutamic oxaloacetate transaminase activities increased in calves receiving the high Al diets. A negative balance of P and Ca was noted in the calves fed high concentrations of Al. Apparent absorption of 32P was reduced (37%) in calved fed diets high in Al (44% of dose vs. 69%). Urinary excretion of 32P was not affected by dietary Al concentrations. Calves fed the low P (deficient) diet showed significant reductions in feed intake, weight gain, serum inorganic P, bone ash, and P content of bone. Dietary P did not significantly affect 32P absorption. Adding .20% dietary Al severely affects P metabolism and performance of young growing calves.

The families of patients with somatization disorder.

This pilot study was undertaken to better understand the families of patients with somatization disorder. Two complementary methods were used to study six patients with somatization disorder and six control patients. The first method was a semistructured clinical family interview which was videotaped and independently reviewed by five raters. The second method was by the PAFS-Q, a standardized family questionnaire. The clinical interview distinguished cases from controls both in terms of individual relationships and behavior of the family as a whole. The PAFS-Q also distinguished cases from controls, showing significantly more dysfunction for the cases on five of its eight subscales. These two methods overlap in the content areas of intimacy and individuation, with correlation coefficients between the two methodologies ranging from 0.45 to 0.79. The authors conclude that the families of patients with somatization disorder are different than their unaffected counterparts.

Long-term feeding of high zinc sulfate diets to lactating and gestating dairy cows.

Thirty dairy cows, fed a control diet consisting of silage and concentrates, were given either 0, 1000, or 2000 ppm of supplemental Zn (DM basis), from zinc sulfate monohydrate (ZnSO4.H2O) for most of a lactation. Feeding 2000 ppm Zn decreased milk yield and feed intake after several weeks. Some cows were affected more severely than others. Generally, primiparous animals were more tolerant of the high Zn diet than multiparous cows. Milk Zn was materially higher for cows fed 1000 ppm added Zn than controls. With 2000 ppm Zn, milk Zn was elevated further but returned to control values when the high Zn diet was discontinued. Plasma Zn was higher in cows fed supplemental Zn with the increase from 1000 to 2000 greater than that for the first addition. Plasma Cu was lower in cows feed 2000 ppm Zn but milk Cu was not reduced. Milk fat content was not affected, but protein and SNF were reduced by the 12th wk with the 2000 ppm Zn diet. There was no apparent effect on long-term health or performance after the cows were removed from the 2000 ppm Zn diet. Except for lower calf weights with 2000 ppm Zn, reproductive performance was not measurably affected by the dietary treatments. The 1000 ppm added Zn diet had no adverse effect on the cows in any parameter measured.