PP028. To assess maternal and neonatal outcomes of women on an antihypertensive agent with gestational hypertension, chronic hypertension or preeclampsia.

INTRODUCTION: There is a lack of evidence regarding antihypertensive medicine use in pregnancy. OBJECTIVES: To compare maternal and neonatal outcomes of women on an antihypertensive agent with gestational hypertension (GHTN), chronic hypertension (CHTN) and preeclampsia (preE). METHODS: The Consortium on Safe Labor electronic database from 19 hospitals across the US with 228,668 deliveries during 2002-2008 was used to extract data on gravidas with GHTN, CHTN, and preE on a calcium channel blocker, methyldopa, or beta blocker. Univariate and multivariate analyses were performed. RESULTS: There were 637 women on beta blockers, 207 on calcium channel blockers, 249 on Methyldopa, and 6869 women with hypertension on no agent (control group). Women on beta blockers had an increased risk of ICU admission, OR 3.74 (95% CI 1.8-7.6). Risk of thrombosis was increased in women on beta blockers, OR 3.6 (95% CI 1.4-9.2) and calcium channel blockers, OR 10.6 (95% CI 3.8-29.2). There was no increased risk of small for gestational age babies. There was a small, increased risk of NICU admission for babies of women on calcium channel blockers, OR 1.7 (95% CI 1.2-2.6) and methyldopa, OR 1.9 (95% CI 1.4-2.7). CONCLUSION: Beta and calcium channel blocker use was associated with significant risks of morbidity compared to Methyldopa use by gravid women with hypertensive disease.

Symptomatic fibroid uterus in a 15-year-old girl.

A 15 year-old gravida 1, abortus 1 black girl presented with chief complaints of menorrhagia, severe dysmenorrhea, and progressively worsening abdominal pain, which was caused by a very large uterine leiomyoma. The symptoms began 6 months earlier, shortly after a 10-week spontaneous abortion at age 14. A solitary 25-cm uterine leiomyoma was removed uneventfully with an abdominal laparotomy. In the English literature of the past 50 years, this case represents the sixth, and we believe, the largest, documented uterine fibroid among teenagers, which required corrective surgery.

Assessing the female sexual assault survivor.

Because sexual assault survivors often seek treatment in primary care settings, clinicians must be prepared to evaluate these patients in a nonjudgmental manner. The initial evaluation includes a medical and assault history. During the physical examination, physical injuries are noted and forensic evidence is collected. Treatment includes prophylaxis for pregnancy and sexually transmitted infections and counseling referrals. This article focuses on care of the adult female sexual assault survivor. Psychosocial support, physical examination, collection of evidence, treatment, and documentation are discussed.

Novel group of virulence activators within the AraC family that are not restricted to upstream binding sites.

Several regulators within the AraC family control the expression of genes known or thought to be required for virulence of bacterial pathogens. One of these, Rns, activates transcription from an unprecedented variety of binding-site locations. Although nearly all prokaryotic activators bind within a small region upstream and adjacent to the promoter that they regulate, Rns does not bind within this region to activate its own promoter, Prns. Instead, to activate Prns, Rns requires one binding site 224.5 bp upstream and one downstream of the transcription start site. We show in this study that several other AraC family activators recognize the same binding sites as Rns and share with it the ability to utilize a downstream binding site. Like Rns, other members of this group of activators positively regulate the expression of virulence factors in pathogenic bacteria. These regulators are also able to activate transcription from promoter-proximal upstream binding sites since they are able to substitute for Rns at Pcoo, a promoter with only upstream binding sites. Thus, Rns is the prototype for a group of regulators, which include CfaR, VirF, AggR, and CsvR and which activate transcription from locations that are more diverse than those of any other known activator.

Fundamentalism, multiculturalism and problems of conducting research with populations in developing nations.

A growing number of nurse researchers travel globally to conduct research in poor and underserved populations in developing nations. These researchers, while well versed in research ethics, often find it difficult to apply traditional ethical standards to populations in developing countries. The problem of applying ethical standards across cultures is explained by a long-standing debate about the nature of ethical principles. Fundamentalism is the philosophical stance that ethical principles are universal, while the anthropologically-based 'multicultural' model claims the philosophical position that principles are culturally bound. The authors explicate the two philosophical stances and advocate a morally sensitive but moderate position of 'ethical multiculturalism' rather than favouring either of the above philosophical positions. The final section suggests ways to promote ethical multiculturalism while planning and conducting nursing research.

Articulation index and hearing handicap.

This investigation examined the relationship between perceived hearing handicap and the Articulation Index (AI) and the extent to which this relationship was influenced by the variables age, gender, degree of hearing loss, and audiometric slope. Subject age, gender, pure-tone thresholds, and scores for the Self-Assessment of Communication (SAC) and the Significant Other Assessment of Communication (SOAC) were extracted retrospectively from 373 patient files (194 males, 179 females). Correlation analysis revealed a significant (p < .01) negative relationship between AI values and both measures of hearing handicap, and also indicated that SAC/SOAC total scores correlated significantly (p < .01) with each other. Partial correlation analyses revealed that degree of hearing loss was the only variable under study that had substantial influence on the strength of AI/hearing handicap correlations.

A beta and perlecan in rat brain: glial activation, gradual clearance and limited neurotoxicity.

A beta1-40 and perlecan (A beta + perlecan) were infused into rat hippocampus for 1 week via osmotic pumps. At the end of the infusion a deposit of A beta immunoreactive material was found surrounding the infusion site. No neurons could be identified within this A beta deposit. The neuron-free area resulting from A beta + perlecan was significantly larger than that found after infusions of A beta40-1 and perlecan (reverse A beta + perlecan), perlecan alone or phosphate-buffered saline vehicle. Following infusion of A beta + perlecan, the glial cells segregated in a manner similar to that associated with compacted amyloid plaques in Alzheimer's disease (AD). Activated microglia/macrophages were prevalent within the A beta deposit while the perimeter of the deposit was delimited by reactive astrocytes. Thioflavin S and Congo red staining indicated a beta-pleated sheet conformation of the A beta deposits, implying formation of fibrils. Intact, apparently healthy neurons were found immediately adjacent to the A beta + perlecan deposit. In contrast, reverse A beta peptide did not form congophilic deposits despite the presence of perlecan. Apoptotic profiles visualized with bisbenzamide or TUNEL staining of fragmented DNA were not seen at any of the infusion sites, yet were readily seen in hippocampal sections from animals treated with kainic acid. At 8 weeks, A beta immunoreactivity, Thioflavin S and Congo red staining was reduced, indicating that A beta was being cleared. There also was no evidence of neuron loss by Nissl or TUNEL staining. The zone of apparent necrosis did not expand between 1 and 8 weeks, and in some instances appeared to contract. The consistency of the A beta + perlecan infusion method in producing reliable A beta amyloid deposits permits estimates of the rate at which fibrillar A beta amyloid can be removed from the brain, and may provide a useful model to study this process in vivo. However, the absence of clearly identifiable degenerating/dying neurons at the 1 or 8 week survival times suggests that either fibrillar A beta + perlecan slowly displaced the brain parenchyma during infusion, or neurons were killed very gradually during the process of clearing the A beta.

Recombinant human thyrotropin stimulation of thyroglobulin in the follow-up of patients with stage I or II differentiated thyroid carcinoma.

OBJECTIVE: To present an approach for follow-up of low-risk patients who have undergone treatment for differentiated thyroid carcinoma. METHODS: We review our experience with monitoring of 167 patients who had undergone near-total thyroidectomy for stage I or II thyroid carcinoma and were receiving levothyroxine and discuss the advantages and disadvantages of various tests for detection of recurrent disease in this setting. RESULTS: Almost 200,000 patients who have been treated for thyroid cancer live in the United States and require monitoring for possible recurrence of their disease. Most of these patients had stage I or II well-differentiated cancer. A cost-efficient method of follow-up for these low-risk patients is needed that relies on measurement of serum thyroglobulin (Tg) rather than expensive isotope imaging procedures. The availability of recombinant human thyrotropin (thyroid-stimulating hormone) (rhTSH) allows the evaluation of Tg dynamics and provides another method, along with ultrasonography, to monitor these patients. Among our 167 patients, 10 had Tg measurements of 2.5 to 5.0 ng/mL and were thought to be at risk for recurrent cancer. Ultrasonography of the neck revealed no suspicious lymph nodes. Tg response to rhTSH stimulation disclosed that two of these patients had an exaggerated increase in Tg level, compatible with persistent or recurrent cancer. CONCLUSION: Although rhTSH stimulation testing has not yet become established in clinical practice, the finding of an exaggerated Tg response to rhTSH in patients with previously treated thyroid cancer seems to be an early indication of recurrent disease.

A Delphi survey to identify activities of nurse practitioners in primary care.

The practice activities of nurse practitioners (NPs) in primary care have not been well delineated. The purpose of this study is to identify the activities of NPs in the provision of primary care. Patient, practitioner, and healthcare system variables were collected to describe the sample and determine if these factors influenced the activities of NPs. Primary care NPs (n = 139) representing the practice areas of pediatrics (n = 12), family (n = 75), adult (n = 15), and women's health (n = 37) responded to serial questionnaires using Delphi technique asking them to identify activities they perform routinely in their practices. Using frequency analysis, activities common to the practice of all NPs were identified, and using Chi-square, activities of specialty NP practice were identified. Regression analysis was used to correlate NP, patient, and healthcare system variables with the activities performed as part of NP practice. Three lists of activities of NP practice were developed: core activities of all NP practice, specialty activities, and other activities. Initial analyses of variables that might influence NP practice were examined. These results can be useful to healthcare consumers choosing providers, as well as legislators, educators, employers of NPs, and other interested healthcare professionals.

Behavioral changes in transgenic mice expressing both amyloid precursor protein and presenilin-1 mutations: lack of association with amyloid deposits.

Mutations in the amyloid precursor protein (mAPP) and in presenilin 1 (mPS1) have both been linked to increased production of the beta-amyloid peptide (A beta). Doubly transgenic mice produced by mating of a parental line carrying the "Swedish" (K670N/M671L) APP mutation with a FAD4 (M146L) mutant presenilin 1 line developed numerous fibrillar A beta deposits by 6 months of age. Prior work demonstrated that mAPP and doubly transgenic (mAPP/mPS1) mice have deficits in Y-maze alternation behavior as early as 3 months of age. Increased activity was also apparent in the mAPP/mPS1 mice at this time point. These changes in Y-maze performance persisted in mAPP/mPS1 mice at 6 and 9 months of age. The mPS1 singly transgenic mice were not impaired on this task at any age. Six- and nine-month-old mice were also tested for spatial navigation behavior in the Morris water maze. In training trials, no differences in escape latency were detected among the four genotypes. In probe trials, no differences were detected in either the time spent in the trained quadrant or the number of platform crossings among the four groups. Histological staining for A beta amyloid deposits indicates that all doubly transgenic mice have amyloid deposits by 6 months of age (roughly 25 mice examined thus far), yet no 3-month-old mice have been found with deposits. A beta immunostaining confirmed that the 9-month-old mice tested behaviorally also have A beta deposits. Thus, doubly transgenic mice exhibited changes in Y-maze performance prior to the formation of amyloid deposits, which are essentially unchanged as the deposits increase in number and size to 9 months of age. Yet these mice fail to reveal impairments in spatial navigation at 6 or 9 months in spite of the increasing plaque burden. These data indicate that A beta deposits alone are not sufficient to cause robust spatial memory impairment in mice of this mixed background lineage and age.

The Client Encounter Form: conceptual development, reliability analysis, and clinical applications.

This descriptive correlational study investigated the reliability of a new measure of client-nurse practitioner interaction, the Client Encounter Form (CEF), and used the CEF to describe the domains of client-nurse practitioner interaction that occurred during problem and preventative visits at a primary care clinic. The CEF is based on Cox's Interactional Model of Client Health Behavior. Data were collected from a convenience sample of 41 primary care clinic visits. Descriptive data on all clients and the patterns of use characterized by the CEF were collected using retrospective chart review (n = 60). Reliability testing showed the CEF has high interrater reliability; Cohen's Kappas for its dimensions ranged from 0.78-1.0. The CEF was also shown to be useable in a primary care clinic. Health information, affective support, goal setting, and technical procedures were consistently part of the nurse-client interactions in this sample, demonstrating they are part of the nurse practitioner model of care. Analysis revealed different patterns of interaction for preventative and problem-oriented visits. Preventative visits had higher levels of health promotion information, psychological affective support, and health promotion goal-setting behaviors. Problem visits included more information regarding the client's diagnosis, medications, and treatments, and more affective support related to the client's physical condition.

Acute carbon tetrachloride feeding induces damage of large but not small cholangiocytes from BDL rat liver.

Bile duct damage and/or loss is limited to a range of duct sizes in cholangiopathies. We tested the hypothesis that CCl4 damages only large ducts. CCl4 or mineral oil was given to bile duct-ligated (BDL) rats, and 1, 2, and 7 days later small and large cholangiocytes were purified and evaluated for apoptosis, proliferation, and secretion. In situ, we measured apoptosis by morphometric and TUNEL analysis and the number of small and large ducts by morphometry. Two days after CCl4 administration, we found an increased number of small ducts and reduced number of large ducts. In vitro apoptosis was observed only in large cholangiocytes, and this was accompanied by loss of proliferation and secretion in large cholangiocytes and loss of choleretic effect of secretin. Small cholangiocytes de novo express the secretin receptor gene and secretin-induced cAMP response. Consistent with damage of large ducts, we detected cytochrome P-4502E1 (which CCl4 converts to its radicals) only in large cholangiocytes. CCl4 induces selective apoptosis of large ducts associated with loss of large cholangiocyte proliferation and secretion.

Bile acid feeding induces cholangiocyte proliferation and secretion: evidence for bile acid-regulated ductal secretion.

BACKGROUND & AIMS: We have shown that taurocholate (TC) and taurolithocholate (TLC) interact in vitro with normal cholangiocytes, increasing DNA synthesis, secretin receptor (SR) gene expression, and adenosine 3',5'-cyclic monophosphate (cAMP) synthesis. To further extend these in vitro studies, we tested the hypothesis that bile acids (BAs) directly stimulate cholangiocyte proliferation and secretion in vivo. METHODS: After feeding with TC or TLC (1% for 1-4 weeks), we assessed the following in vivo: (1) ductal proliferation by both morphometry and immunohistochemistry for proliferating cell nuclear antigen (PCNA) and measurement of [3H]thymidine incorporation; and (2) the effect of secretin on bile secretion and bicarbonate secretion in vivo. Genetic expression of H3-histone and SR and intracellular cAMP levels were measured in isolated cholangiocytes. RESULTS: After BA feeding, there was an increased number of PCNA-positive cholangiocytes and an increased number of ducts compared with control rats. [3H]Thymidine incorporation, absent in control cholangiocytes, was increased in cholangiocytes from BA-fed rats. In BA-fed rats, there was increased SR gene expression (approximately 2.5-fold) and secretin-induced cAMP levels (approximately 3.0-fold) in cholangiocytes, which was associated with de novo secretin-stimulated bile flow and bicarbonate secretion. CONCLUSIONS: These data indicate that elevated BA levels stimulate ductal secretion and cholangiocyte proliferation.

Impaired spatial navigation learning in transgenic mice over-expressing heme oxygenase-1.

Transgenic mice expressing heme oxygenase-1 (HO-1) using the neuron-specific enolase promoter were impaired in learning the Morris water maze compared to nontransgenic littermates. The memory of the HO-1 mice for the location of the platform was similarly impaired when tested using a probe trial after 7 training blocks, but performance on visible platform trials was similar for both groups of mice. Importantly, both HO-1 and nontransgenic mice had normal sensorimotor function, and performed the same on a Y-maze alternation task, highlighting the specificity of memory deficit in the spatial navigation task. These results suggest that carbon monoxide, one product of HO-1 activity, interferes in the development of spatial navigation memory, and may play a role in normal memory function.

Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes.

Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes. The mutant APP(K670N,M671L) transgenic line, Tg2576, shows markedly elevated amyloid beta-protein (A beta) levels at an early age and, by 9-12 months, develops extracellular AD-type A beta deposits in the cortex and hippocampus. Mutant PS1 transgenic mice do not show abnormal pathology, but do display subtly elevated levels of the highly amyloidogenic 42- or 43-amino acid peptide A beta42(43). Here we demonstrate that the doubly transgenic progeny from a cross between line Tg2576 and a mutant PS1M146L transgenic line develop large numbers of fibrillar A beta deposits in cerebral cortex and hippocampus far earlier than their singly transgenic Tg2576 littermates. In the period preceding overt A beta deposition, the doubly transgenic mice show a selective 41% increase in A beta42(43) in their brains. Thus, the development of AD-like pathology is substantially enhanced when a PS1 mutation, which causes a modest increase in A beta42(43), is introduced into Tg2576-derived mice. Remarkably, both doubly and singly transgenic mice showed reduced spontaneous alternation performance in a "Y" maze before substantial A beta deposition was apparent. This suggests that some aspects of the behavioral phenotype in these mice may be related to an event that precedes plaque formation.

Exaggerated astrocyte reactivity after nigrostriatal deafferentation in the aged rat.

Although clinical experience suggests that brain injury in the aged is associated with a poor prognosis, little research has examined this phenomenon at a cellular or molecular level. Unilateral 6-hydroxydopamine lesions of the nigrostriatal system were produced in 6-, 15- or 24-month-old rats. In the deafferented neostriatum, the time-dependent induction of glial fibrillary acidic protein (GFAP) was larger and persisted longer in the aged rats. The response of middle-aged rats was intermediate. In contrast, no induction of S-100 or glutamine synthetase was observed in any age group. In a second series of rats with stab wounds in the neostriatum, there were substantially larger GFAP inductions than after deafferentation, but fewer effects of age. However, in both lesion paradigms, GFAP staining increased in the contralateral striatum of old rats, but not in young rats. These data support and extend our earlier work describing larger GFAP RNA inductions after fornix transections in aged mouse hippocampus. The consistency of this exaggerated glial reactivity in the aged brain after modest injury suggests the following: 1) aged astrocytes are more sensitive to gliotrophic factors released by terminal degeneration, 2) larger quantities of such factors are produced after injury, 3) clearance of these factors is delayed in old rodents, and/or 4) aged astrocytes are less able to terminate GFAP inductions after activation. Given the potential role of inflammatory reactions as pathogenic mechanisms in Alzheimer's dementia, these data suggest that age-related glial hypersensitivity may independently increase the risk for some degenerative diseases.

Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1.

Mutations in the genes encoding amyloid-beta precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) are known to cause early-onset, autosomal dominant Alzheimer's disease. Studies of plasma and fibroblasts from subjects with these mutations have established that they all alter amyloid beta-protein (beta APP) processing, which normally leads to the secretion of amyloid-beta protein (relative molecular mass 4,000; M(r) 4K; approximately 90% A beta1-40, approximately 10% A beta1-42(43)), so that the extracellular concentration of A beta42(43) is increased. This increase in A beta42(43) is believed to be the critical change that initiates Alzheimer's disease pathogenesis because A beta42(43) is deposited early and selectively in the senile plaques that are observed in the brains of patients with all forms of the disease. To establish that the presenilin mutations increase the amount of A beta42(43) in the brain and to test whether presenilin mutations act as true (gain of function) dominants, we have now constructed mice expressing wild-type and mutant presenilin genes. Analysis of these mice showed that overexpression of mutant, but not wild-type, PS1 selectively increases brain A beta42(43). These results indicate that the presenilin mutations probably cause Alzheimer's disease through a gain of deleterious function that increases the amount of A beta42(43) in the brain.

Haitian Americans: implications for nursing care.

Each year a number of Haitians enter the United States and may become part of the U.S. health care system. Nurses need to be sensitive to cultural differences and should assess clients for special needs that may arise because of cultural diversity. This article provides strategies for interacting with the Haitian American client in a clinical setting to ensure success in providing nursing care.

Effects of neuropeptide Y (NPY) and NPY agonists on lordosis in the female guinea pig.

We have previously shown that an NPY antagonist decreases lordosis behavior and that this decrease can be reversed with NPY administration. The present experiments examined whether intracerebroventricular (icv) administration of NPY would facilitate lordosis behavior and whether it would increase feeding behavior in the female guinea pig. Additionally, we examined whether icv administration of a more specific NPY Y1 and/or Y2 receptor agonist would facilitate lordosis behavior. Although NPY (1 µg) increased feeding behavior when it was administered to the lateral ventricle of ovariectomized (ovx) estrogen (i.e., estradiol benzoate; EB) and progesterone- (P) treated guinea pigs, it had no facilitatory effect on lordosis behavior at any of the doses tested (0.5, 1, 5, or 10µg). In fact, the lower doses had a small, delayed inhibitory effect. NPY also had no effect on lordosis in females treated with EB alone. In contrast, the NPY Y1 agonist (Leu(31)Pro(34)) NPY significantly facilitated lordosis in ovx EB- and P-treated females. It had no effect in ovx females treated with EB alone. The NPY Y2 agonist NPY (13-36) had a slight, delayed inhibitory effect in ovx EB- and P-treated females. These data are consistent with the hypothesis that NPY can act at a number of receptor subtypes to affect lordosis behavior, and that NPY can facilitate lordosis behavior by acting at Y1 receptors. Furthermore, it appears that this facilitatory effect of Y1 receptors is an effect on some progesterone-mediated component of lordosis, as the Y1 agonist facilitated EB- and P-induced lordosis, but not that induced with EB alone.