Use of skin staples for securing the mesh in the Lichtenstein repair of inguinal hernia.
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Biomedical subjects
Publications and source records attributed to J Fawcett.
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Writing research can be challenging--especially writing the conceptual model. Deciding how much to include of the conceptual model and where to place it is difficult. This experienced research author presents four steps to guide the nurse author in writing the conceptual model for research reports.
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The Comprehensive Sexual Assault Assessment Tool (CSAAT) was developed for collection of data about the victims and offenders in cases of rape and sexual assault. The CSAAT provides a systematic guide for victim assessment, evidence documentation, and initial treatment. Use of the CSAAT facilitates collection of investigative data about the victim and the offender that are critical components of victim interviews and crime investigations, as well as victim forensic data. The CSAAT can be used by health care professionals who care for the victims of sexual assault. The tool reflects the major concepts of the Roy Adaptation Model and was designed as a victim evaluation report for clinical and forensic purposes. The CSAAT can also be used to compile agency statistics, as part of the training for sexual assault nurse examiners, and to collect research data. A case study involving two victims illustrates the importance of evidence collection and use of the Federal Bureau of Investigation's Combined DNA Index System (CODIS) for linking victims by offender DNA.
A gene called deleted in colon cancer (DCC) has been identified on a region of chromosome 18, which is deleted in 70% of colorectal cancers. The DCC gene encodes a protein belonging to the immunoglobulin superfamily with similarity to the N-CAM transmembrane proteins and is a putative tumor-suppressor gene. Alternative splicing of transcripts of transmembrane proteins, including N-CAM, is known to occur, resulting in different isoforms of the protein. Using five antibodies against the DCC gene product (three monoclonal antibodies raised in our laboratory, one commercially available antibody, and a rabbit polyclonal antibody), we have demonstrated by immunostaining a DCC protein isoform in reticuloendothelial cells in human thymus, tonsil, and lymph node. This can be distinguished from another isoform described in normal colonic epithelium, because this latter is not demonstrable with the antibodies we have used. It could not be detected in normal colonic epithelium, polyps or colorectal carcinomas. This restrictive distribution suggests that not all DCC gene products are important in colonic cancer.
Dendritic cells (DC) are potent stimulators of primary T lymphocyte responses to foreign antigen. The initial DC-T lymphocyte interaction involves the binding of the adhesion molecule leukocyte function antigen-1 (LFA-1; CD11a/CD18) on the T lymphocyte to an intercellular adhesion molecule (ICAM) on the DC. Although blood and tonsil DC express ICAM-1 (CD54) and ICAM-2 (CD102) on their surface, anti-ICAM-1 and anti-ICAM-2 monoclonal antibodies (mAb) have little inhibitory activity on the DC-stimulated mixed leukocyte reaction (MLR). We therefore examined the expression of the more recently identified LFA-1 ligand, ICAM-3 (CD50), in comparison to ICAM-1 and ICAM-2 on blood DC and sought a functional role for ICAM-3 in DC-mediated T lymphocyte responses. Resting blood DC expressed significantly more ICAM-3 than ICAM-1 or ICAM-2 as assessed by flow cytometry. Treatment of resting DC with interferon-gamma led to increased expression of ICAM-1; however, ICAM-2 and ICAM-3 levels remained relatively constant. Solid-phase recombinant chimeric molecules ICAM-1-, ICAM-2- and ICAM-3-Fc were able to co-stimulate CD4+ T lymphocyte proliferation in conjunction with suboptimal solid-phase CD3 mAb 64.1. However, the anti-ICAM-3 mAb CAL 3.10 inhibited a DC-stimulated MLR to a greater extent than anti-ICAM-1 or anti-ICAM-2 reagents and appeared to act by blocking the DC ICAM-3- T lymphocyte LFA-1 interaction. As ICAM-3 is the predominant LFA-1 ligand on resting blood DC, we postulate that DC may utilize ICAM-3 for initial DC- T lymphocyte interactions, and that ICAM-1, which is up-regulated upon DC activation, and/or ICAM-2, may contribute to DC migration or later phases of the T lymphocyte activation process.
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In their response to Draper's (1993) critique of Fawcett's (1992) paper 'Conceptual models and nursing practice: the reciprocal relationship', the authors argue that Draper's critique is flawed. They point out that Draper fails to acknowledge the diversity within the positivist movement, makes logical leaps, and fails to acknowledge Fawcett's long-standing distinction between middle-range theories and conceptual models and her discussions of the differences in the criteria to be used when evaluating conceptual models and theories.
CD31 is a member of the immunoglobulin superfamily consisting of six Ig-related domains. It is constitutively expressed by platelets, monocytes, and some lymphocytes, but at tenfold higher levels on vascular endothelial cells. CD31 has both homotypic and heterotypic adhesive properties. We have mapped the homotypic binding sites using a deletion series of CD31-Fc chimeras and a panel of anti-CD31 monoclonal antibodies. An extensive surface of CD31 is involved in homotypic binding with domains 2 and 3 and domains 5 and 6 playing key roles. A model consistent with the experimental data is that CD31 on one cell binds to CD31 on an apposing cell in an antiparallel interdigitating mode requiring full alignment of the six domains of each molecule. In addition to establishing intercellular homotypic contacts. CD31 binding leads to augmented adhesion via beta 1 integrins. The positive cooperation between CD31 and beta 1 integrins can occur in heterologous primate cells (COS cells). The interaction is specific to both CD31 and beta 1 integrins. Neither intercellular adhesion molecule-1 (ICAM-1)/leukocyte function-associated antigen-1 (LCAM-1) nor neural cell adhesion molecule (NCAM)/NCAM adhesion leads to recruitment of beta 1 integrin adhesion pathways. Establishment of CD31 contacts have effects on the growth and morphology of endothelial cells. CD31(D1-D6)Fc inhibits the growth of endothelial cells in culture. In addition, papain fragments of anti-CD31 antibodies (Fab fragments) disrupt interendothelial contact formation and monolayer integrity when intercellular contacts are being formed. The same reagents are without effect once these contacts have been established, suggesting that CD31-CD31 interactions are critically important only in the initial phases of intercellular adhesion.
It is now well established that in kidney, as in liver, endosomes participate in the degradation of insulin. Degradation in this compartment involves the action of the insulin-degrading enzyme or a similar enzyme with the formation of large intermediate products. The role of lysosomes is less clear, for although earlier studies suggested that they are the major or sole site of degradation, this has been increasing questioned. More recently, it has been concluded that endosomes, at least in liver, are the major site of insulin degradation and that classic lysosomes are only involved in the latter stages of degradation if at all. As intracellular insulin processing varies among cell types, we set out to examine directly the processing of insulin within cultured proximal-like opossum kidney cells. By means of analytical subcellular fractionation and reverse phase HPLC analysis of products, we established the following sequence of events. After internalization, [125I]A14-insulin is partially degraded in endosomes. The formed products together with intact insulin, which accounts for most of the radioactive material in the endosomes, are then directed to the lysosomal compartment, where degradation proceeds rapidly to completion. Bacitracin inhibited degradation in both compartments and, although not eliminating insulin trafficking, may impair the transfer of insulin from endosomes to lysosomes. This study establishes a major role for lysosomes in kidney cell insulin degradation.
The proximal renal tubule is a common site of peptide hormone metabolism, including that of insulin-like growth factor-I (IGF-I). To further explore the renal uptake and processing of IGF-I, a study was carried out with the proximal-like cultured opossum kidney (OK) cell line. [125I]IGF-I associated with these cells in a specific manner. Association was competitively inhibited by IGF-I. Des(1-3)-IGF-I was equally effective, insulin had only a small effect, and the unrelated peptides, glucagon and GH, were without effect. Degradation was inhibited in similar manner. Comparisons of [125I]IGF-I with [125I]insulin revealed comparable cell association, but degradation of internalized IGF-I was several-fold slower. Furthermore, IGF-I degradation was less sensitive, by half, to the inhibitory effect of chloroquine. When OK cells were exposed to [125I]IGF-I in the presence of IGF-binding protein-3 (IGFBP-3) cell association (binding and internalization) was reduced significantly. Of note, total cell degradation was reduced (P < 0.01), but the IGF-I that was internalized was degraded more rapidly than in control cells. Gel filtration and reverse phase HPLC revealed that the products of IGF-I degradation included large IGF-I-size intermediates in addition to trichloroacetic acid-soluble material. This product profile was not altered by IGFBP-3. Thus, as previously described for insulin, cultured OK cells possess specific IGF-I receptors and degrade internalized IGF-I. However, IGF-I processing differs from that of insulin, in that degradation is slower and relatively insensitive to competition by insulin. This study also shows that IGFBP-3 inhibits the binding and uptake of [125I]IGF-I by these kidney cells. However, once IGF-I is internalized, IGFBP-3 enhances degradation. Although the mechanism of this paradoxical action requires further study, analysis of the products of degradation suggests that the same enzymes are involved in IGF-I degradation regardless of whether IGFBP-3 is present.
The relationships of the WISC-III Performance scale with the WISC-R Performance scale and the WRAT-R subscales were investigated for a sample of 47 students who are deaf and hard of hearing. Over a three year time period, the relationships between the WISC-III and WISC-R Performance IQs was high, r(43) = +.93. As anticipated, the WISC-III and WISC-R Performance IQ. A Varimax rotation revealed the presence of two factors, Perceptual Organization and Processing Speed, which accounted for 76.5% of the variance in the WISC-III performance IQ. Of the six WISC-III Performance subtests, only Coding did not contribute to the Performance IQ. Students who communicated via Total Communication (M = 92.5) exhibited higher Performance IQ means than did students who communicated orally (M = 82.6). The WISC-III Performance IQ was moderately related to the WRAT-R subscales, having the strongest association with the Arithmetic subscale. Implications of these findings for practitioners are discussed.
BACKGROUND: Treatment-resistant depression is a common clinical challenge that often requires the use of innovative pharmacologic treatments. Recent reports suggest the efficacy of the combination of a serotonin selective reuptake inhibitor and a heterocyclic antidepressant (HCA) in depressed patients who fail monotherapy with either agent alone. We present our clinical experience with the use of fluoxetine combined with an HCA in a group of 25 treatment-resistant depressed subjects. METHOD: Twenty-five depressed subjects who failed to adequately respond to at least 4 weeks of open-label fluoxetine treatment (mean dose = 73 mg/day) had an HCA added to their fluoxetine. The dose of the HCA was increased to maximize efficacy and minimize side effects. Efficacy was measured using the 21-item Hamilton Rating Scale for Depression (HAM-D-21) score and the Clinical Global Impressions-Global Improvement (CGI) scale. RESULTS: Response to treatment was defined as a 50% or greater drop in the HAM-D-21 score and a CGI of either very much improved or moderately improved from the start of the HCA. Seven (35%) of 20 subjects who demonstrated a poor or partial response to fluoxetine responded when an HCA was added to the fluoxetine. Five (71%) of the responders had previously failed to respond to monotherapy with the HCA that they responded to when used with fluoxetine. Additionally, 5 subjects who demonstrated significant improvement with fluoxetine but who had mild, residual depressive symptoms experienced at least partial further improvement with the addition of an HCA. CONCLUSION: The results suggest that the addition of an HCA to fluoxetine may be an effective treatment in treatment-resistant depressed patients who have failed to adequately respond to monotherapy with fluoxetine. Additional controlled trials are warranted to further explore the efficacy of this treatment combination in patients who demonstrate a poor or partial response to monotherapy. When using this drug combination, the clinician is cautioned to prescribe low doses of the HCA and monitor serum levels closely since fluoxetine can raise serum HCA levels.
A meta-analysis of six randomized, placebo-controlled, double-blind trials was carried out to evaluate the effectiveness of the new antidepressant nefazodone in relieving symptoms of anxiety and agitation associated with major depression. Nefazodone blocks serotonin2 (5-HT2) receptors and selectively inhibits serotonin (5-HT) reuptake. This pharmacologic profile may confer clinical benefits that differ from those of other antidepressants, such as tricyclics (TCAs) and serotonin selective reuptake inhibitors (SSRIs). The data base included 817 patients with major depression and baseline 17-item Hamilton Rating Scale for Depression (HAM-D-17) scores > or = 18; 345 received placebo, 288 imipramine, and 184 nefazodone. Both nefazodone and imipramine exhibited antidepressant efficacy compared with that of placebo, irrespective of baseline anxiety levels. Statistically significant improvement in Hamilton Rating Scale for Anxiety (HAM-A), HAM-D anxiety factor, HAM-D psychic anxiety item, and HAM-D agitation item scores was observed with both active treatments. Nefazodone-treated patients showed significantly greater improvement in somatic anxiety (HAM-D item 11) ratings than placebo-treated patients from Week 4 through end of treatment (p < or = .01), while imipramine-treated patients did not differ from placebo patients on this item. Nefazodone-treated patients improved more rapidly (as early as Week 1) than imipramine- and placebo-treated patients on agitation (HAM-D item 9) (p < or = .01). Nefazodone was found to have an excellent safety profile and was well tolerated, with 5% of nefazodone patients prematurely discontinuing treatment for adverse experiences compared with 17% for imipramine and 5% for placebo treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: We report the results from a multicenter, double-blind, randomized, fixed-dose study designed to evaluate the relationship between daily dose and efficacy of adinazolam-SR in patients with panic disorder with agoraphobia. METHOD: Patients (N = 315) were randomized to one of four treatment groups (placebo, N = 83; 30-mg group, N = 79; 60-mg group, N = 81; and 90-mg group, N = 72) and then treated twice daily for 4 weeks. All treatment groups were comparable demographically. Primary efficacy measures included total number of panic attacks, global improvement score using the Clinical Global Impressions (CGI) scale, phobic anxiety dimension of the Symptom Checklist-90 phobic cluster, overall phobia state using the Phobia Scale, and severity of illness on the CGI. RESULTS: The 60- and 90-mg/day adinazolam-SR treatment groups showed superior results when compared with the placebo group at Week 4 while the 30-mg group did not. Treatment with adinazolam-SR was well tolerated, with sedation the only treatment-emergent symptom that occurred more frequently in patients treated with adinazolam-SR than placebo. CONCLUSION: These results suggest that adinazolam-SR at doses of 60-mg/day or greater administered twice daily is a safe and effective treatment in selected patients with panic disorder with agoraphobia.
Issues surrounding treatment compliance can be considered for a number of clinical situations. For clinicians, compliance usually means "the extent to which the patient takes the medications as prescribed." Instead of "compliance," it has been suggested that the term adherence be used, which puts more of a burden on the clinician to form a therapeutic alliance with the patient, which thereby increases behavioral compliance and possibly enhances the therapeutic effect of the medication administered. The trend toward placing more responsibility on the clinician to obtain compliance or adherence to the prescribed treatment has resulted in several strategies. These include explaining the illness and the rationale for the use of medication for its treatment, inquiring into the patient's hesitation and fears concerning medication, and using various educational approaches with the patient and the patient's significant other concerning possible side effects. Different clinical settings and situations also may modify the emphasis needed to maximize compliance. The situation of continuation and maintenance treatment may require a different treatment procedure for maximum success. The emphasis must vary quite a bit from the patient who improves and needs education to be convinced to continue maintenance treatment to the patient who has a treatment-resistant depression and needs close support and maintenance of hope to continue treatment that, up until the present, has not yielded positive results. Shifting the focus of compliance from the patient to the skill of the clinician refocuses the issue from a patient variable back to the art and science of good medicine.(ABSTRACT TRUNCATED AT 250 WORDS)
Function, which encompasses functional ability and functional status, is discussed within the context of three conceptual models of nursing. Functional ability is the person's capacity to perform biological, psychological, and social activities, whereas functional status is the actual performance of those activities. Comprehensive assessment of function encompasses instrumental and expressive elements of functional ability and functional status, with attention given to the internal, external, and cultural factors that influence function. The goal of nursing interventions is to help the individual attain the highest possible and most desirable level of function.
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