Sexual violence (SV) can deeply impact victims’ physical and psychosocial well-being. Yet many healthcare providers, including registered nurses (RNs), hesitate to screen patients due to a lack of confidence and knowledge. The SATELLITE Sexual Violence Assessment and Care Guide was developed to address this gap; however, the guide’s educational effectiveness remained untested. This pilot study aimed to assess the feasibility, acceptability, and efficacy of an education program based on the SATELLITE guide among RNs in clinical settings (n = 8), using a pre- and post-test design. Results indicated that the education was not only feasible and acceptable, but also demonstrated the effects as desired with significant increases in RNs’ knowledge and confidence in SV screening and care. The program’s assessment tool was reliable, and participant recruitment was feasible. Based on these findings, it is recommended that the SATELLITE education program be further tested with a larger RN sample and extended to other healthcare providers. Additionally, exploring SATELLITE’s use in different regions, cultural contexts, and healthcare settings would enhance understanding of the program’s broader applicability and effectiveness.

Given the complex needs of the aging population, nurse educators must prepare future registered nurses to help older adults remain safe and healthy in their homes. This article describes partnerships between a school of nursing and low-income senior housing providers to develop new, high-impact community-based learning experiences. Baccalaureate nursing students conducted home visits in low-income senior housing communities and engaged in a research study to quantify activities conducted by students and the impact the home visits had on client personal health goal attainment.

Women in the United States are retiring at an unprecedented rate, with many retirements driven by recent economic downturns and social expectations, such as caregiving. Successful retirement transition is a key component of happiness during older adulthood, but many factors suggest that forced retirement may have a negative impact on health. The purpose of the current research study was to explore the lived experiences of women who were forced to retire. The current study population comprised 10 women, age ≥55, recruited from community settings to participate in individual semi-structured interviews. Participants shared common experiences, despite having different reasons for retiring. The overarching theme of Now What? Denied the Opportunity to Mentally Prepare was identified. Findings suggest opportunities for nurses to assess women for mental and physical health indicators and assist them as they transition into retirement, particularly if the retirement was unplanned. [ Journal of Psychosocial Nursing and Mental Health Services, 57 (10), 12–16.]

A record number of women are going through the major life transition of retirement. The purpose of the current study was to explore women's perceptions of retirement with the goals of better understanding important patterns of response regarding retirement transitioning and to inform nurses on how to assist clients who are anticipating or engaging in the retirement transition. A sample population of 170 retired women was recruited using convenience sampling from community settings within six southeastern U.S. states. Participants expressed their perceptions of retirement through written responses to open-ended questions. Content analysis revealed the following themes: Love It/Happy; Unhappy/Regrets; So Much Time, So Little (money, resources, etc.); Searching; Busy; Relief/Freedom; Giving: For Me and Thee; Adequate Resources; Creating Your Own Structure; and Positive Attitude. Careful assessment for health changes, promotion of positive coping skills, and provision of educational planning and therapeutic resources to women who are transitioning to retirement should assist women toward healthy and successful retirements. [Journal of Gerontological Nursing, 45(4), 31-39.].

Correction: Establishment and characterization of a primaryNew information has been obtained on the E006AA epithelial cell line which was characterized in the paper we published in the Prostate 60(2): 141-152 (2004) as having originated from an African American prostate tumor line.We now believe that this cell line is a subclone of the 786-O renal adenocarcinoma line from a white male.The STR profile of the E006AA subclone E006AA-hT, available at the American Type Culture Collection (ATCC) site has STRs which match the profile of 786-O cells (also available at the ATCC site).The analyses presented in the 2004 article are original and accurate using the techniques and methodologies that were available at the time (eg, H&E staining, cell-type and prostate-specific marker, AR expression, RT_PCR, Tumorigenicity, Karyotype, etc).We had no reason to doubt that the line we cultured did not originate from an African American prostate tumor.We now believe it may have been contaminated in its early passages with the 786-0 cell line before it was cryopreserved, as 786-0 cells were also studied in the lab from which this line originated.We urge ATCC to cease advertising this cell line, E006AA-hT, as originating from African American prostate cancer tissue.We would also like to apologize for the confusion, costs, and delays in research this mistake may have caused other researchers; and we thank the researchers who brought this error to our attention.

The aim of the current study was to examine mental health outcomes in retired women and determine whether relationships existed among mental health outcomes, sociodemographic characteristics, and type of retirement (i.e., voluntary or forced). A cross-sectional study was conducted with 80 women ages 55 and older residing in five southeastern states. Women had retired at least part-time from working outside of the home. Sociodemographic variables, diagnosis of depression, diagnosis of cognitive impairment, and health-related quality of life were assessed. Women with forced retirement had worse mental health compared to those who retired voluntarily. Minority women had higher rates of forced retirement compared with White women. Poorer mental health outcomes for women with forced retirement suggest the need for careful consideration of this transition as a socially determined health factor for retired women, especially minority women. Clinicians need to assess women for mental health indicators during the transition to retirement and provide educational and therapeutic resources to promote mental health during the transition from working life to retirement. [Journal of Psychosocial Nursing and Mental Health Services, 56(7), 37-45.].

Problem: The large number of aging retirees is changing the landscape of US healthcare and economic systems. Many nurses will be among these retirees. While retirement has been studied in many fields, it has been explored considerably less in nursing science. Retirement as a concept is complex, not well-defined across disciplines, and the impact of this important transition on health and well-being is not well-understood. Purpose: The purpose of this article is to explore the concept of retirement as a transition that may be related to health and well-being in aging individuals. Findings: Conceptual exploration supports that retirement is defined by two identified attributes: (a) It is a transitional period surrounding stopping or changing full or part-time, paid or unpaid employment status, and (b) it occurs at a time when a person self-identifies as being retired. Identified antecedents and consequences of retirement are closely related to health. Conclusion: Many life changes often occur during the transition of retirement. As a concept, retirement is linked to healthy, transitional aging. Nursing's holistic perspective of addressing client needs can be better understood when caring for individuals who have retired or are planning to retire.

You have accessJournal of UrologyDiscussed Poster, Sunday, May 21, 2006, 1:00 - 4:00 pm1 Apr 2006415: Cross-Talk between Androgen Receptor and Prosaposin in Prostate Cancer and Stromal Cells Supports a Potential Mechanism for Antiandrogen Withdrawal Syndrome Shahriar Koochekpour, Francine Hebert, Tae-Jin Lee, Oliver Sartor, Milena Z. Garcia, Luis Marrero, Ruoxiang Wang, Ying Sun, Gregory A. Grabowski, Sorena Kafai, Jennifer Aguirre, Ardalan Minokadeh, and David Y. Pattan Shahriar KoochekpourShahriar Koochekpour More articles by this author , Francine HebertFrancine Hebert More articles by this author , Tae-Jin LeeTae-Jin Lee More articles by this author , Oliver SartorOliver Sartor More articles by this author , Milena Z. GarciaMilena Z. Garcia More articles by this author , Luis MarreroLuis Marrero More articles by this author , Ruoxiang WangRuoxiang Wang More articles by this author , Ying SunYing Sun More articles by this author , Gregory A. GrabowskiGregory A. Grabowski More articles by this author , Sorena KafaiSorena Kafai More articles by this author , Jennifer AguirreJennifer Aguirre More articles by this author , Ardalan MinokadehArdalan Minokadeh More articles by this author , and David Y. PattanDavid Y. Pattan More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)32671-5AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "415: Cross-Talk between Androgen Receptor and Prosaposin in Prostate Cancer and Stromal Cells Supports a Potential Mechanism for Antiandrogen Withdrawal Syndrome." The Journal of Urology, 175(4S), p. 135 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 175Issue 4SApril 2006Page: 135 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Shahriar Koochekpour More articles by this author Francine Hebert More articles by this author Tae-Jin Lee More articles by this author Oliver Sartor More articles by this author Milena Z. Garcia More articles by this author Luis Marrero More articles by this author Ruoxiang Wang More articles by this author Ying Sun More articles by this author Gregory A. Grabowski More articles by this author Sorena Kafai More articles by this author Jennifer Aguirre More articles by this author Ardalan Minokadeh More articles by this author David Y. Pattan More articles by this author Expand All Advertisement Loading ...

Proc Amer Assoc Cancer Res, Volume 45, 2004 1818 In prostate cancer, as in other malignancies, the complex multi-step process of cancer invasion and metastasis involves both tumor and stromal cells interacting in a complex microenvironment. Migration and invasion are cellular events that require the participation of proteolytic enzymes such as matrix metalloproteinases (MMPs), urokinase plasminogen activator (uPA), and Cathepsin D. Identification and characterization of molecular regulators of these proteases, and their pathways, are of critical importance in developing strategies designed to better control prostate cancer in the patient. Using a novel cloning strategy in our laboratory, we identified prosaposin as a secreted protein in a poorly differentiated androgen-independent prostate cancer cell line (PC-3). The studies reported herein continue our efforts to characterize the role of saposin C/prosaposin in prostate carcinogenesis and in the metastatic process. Prosaposin is the lysosmal precursor of four homologous sphingolipid activator proteins (saposin A-D) and also functions as a secretory protein with neurotrophic activities. The neurotrophic activity of prosaposin has been located at the amino-terminal portion of saposin C. We found a higher expression of prosaposin or saposin C in prostate stromal cells and androgen-independent prostate cancer cells-(PC-3 and DU-145) than in androgen-dependent LNCaP cells or normal prostate epithelial cells. Using in vitro invasion assay, saposin C stimulates migration and invasion of prostate cancer and stromal cells. To understand the underlying molecular mechanisms, we evaluated saposin C’s effects on the expression or activity of matrix-degrading enzymes (MMPs, uPA, and Cathepsins). Saposin C upregulated the uPA/uPAR and Cathepsin D mRNA and protein (both cellular and secreted forms) expression in these cells. In contrast, using immunoblotting and gelatin zymography, the expression or enzymatic activities of MMP-2 and –9 were not affected. Prostate stromal cell response in the above assays suggests that saposin C, acting via paracrine loops, may act as a potential mediator of tumor-stromal interaction in prostate cancer. Normal prostate epithelial cells were not responsive to saposin C treatment in this study. Our findings for the first time documented a novel regulatory role for saposin C (or prosaposin) in motility, invasion, and expression of uPA/uPAR/Cathepsin D in prostate cancer and stromal cells. Through these effects, saposin C may contribute to the invasive or metastatic potential of prostate cancer. Supported by Stanley S. Scott Cancer Center, Louisiana State University-Health Sciences Center.

You have accessJournal of UrologyDiscussed Poster, Sunday, May 9, 2004, 1:00 - 5:00 pm1 Apr 2004580: Prosaposin is a Novel AR-Target Gene and Upregulates AR/PSA Expression in Prostate Stromal and Cancer Cells Shahriar Koochekpour, Oliver Sartor, Tae Jin Lee, Francine Hebert, David Y. Patten, and Ardalan Minokadeh Shahriar KoochekpourShahriar Koochekpour More articles by this author , Oliver SartorOliver Sartor More articles by this author , Tae Jin LeeTae Jin Lee More articles by this author , Francine HebertFrancine Hebert More articles by this author , David Y. PattenDavid Y. Patten More articles by this author , and Ardalan MinokadehArdalan Minokadeh More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)37842-XAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "580: Prosaposin is a Novel AR-Target Gene and Upregulates AR/PSA Expression in Prostate Stromal and Cancer Cells." The Journal of Urology, 171(4S), p. 154 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 171Issue 4SApril 2004Page: 154 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Shahriar Koochekpour More articles by this author Oliver Sartor More articles by this author Tae Jin Lee More articles by this author Francine Hebert More articles by this author David Y. Patten More articles by this author Ardalan Minokadeh More articles by this author Expand All Advertisement PDF DownloadLoading ...

BACKGROUND. Establishment of human prostate cancer cell lines is essential to advance our understanding of complex processes associated with the initiation and progression of the disease. In the present study, we report the establishment of a primary African-American prostate cancer cell line (E006AA) as well as its associated stromal cells (S006AA).METHODS. E006AA cell line was established as a spontaneously immortalized cells from a patient with a clinically localized prostate cancer. Extensive characterization of the cells was accomplished using androgen-dependent growth and sensitivity assays, Western analyses, RT-PCR/real-time PCR, cytogenetic analyses, and tumorigenicity in nude mice.RESULTS. E006AA cell line shows androgen-dependent growth, expresses PSA and the androgen receptor (AR) with 26 CAG repeats in exon 1 of AR. Cytogenetic analyses revealed a hypertriploid karyotype with additional numerical gains in chromosomes 5, 6, 8, 10, 17, 20, 21 and a marker chromosome of unknown origin as well as structural abnormalities in chromosomes 4,5,8,9, 11-14, 18, and 20. This cell line is not tumorigenic in nude mice. S006AA cell line, isolated from the same tumor specimen, also expresses AR and shows the morphological characteristics of smooth muscle cells of prostatic stroma.CONCLUSIONS. These cell lines are the first available primary epithelial and stromal cells derived from an African-American patient with organ-confined prostate cancer and in conjunction with other established cell lines, could provide an in vitro model system to investigate early transforming events in prostate cancer. Prostate 60: 141-152, 2004. (C) 2004 Wiley-Liss, Inc.

Recent studies show that antagonists of growth hormone-releasing hormone (GH-RH) inhibit proliferation of various cancers indirectly through blockage of the endocrine GH-insulin-like growth factor (IGF) I axis and directly by an action on tumor cells involving the suppression of autocrine/paracrine IGF-I, IGF-II, or GH-RH. The effectiveness of therapy with GH-RH antagonist JV-1-38 and its mechanisms of action were investigated in NCI-H838 non-small cell lung carcinoma (NSCLC) xenografted s.c. into nude mice and in vitro. Treatment with GH-RH antagonist JV-1-38 significantly (P < 0.05-0.001) inhibited tumor growth as demonstrated by a 58% decrease in final tumor volume, 54% reduction in tumor weight, and the extension of tumor-doubling time from 8.5 +/- 1.38 to 12 +/- 1.07 days as compared with controls. Using ligand competition assays with (125)I-labeled GH-RH antagonist JV-1-42, specific high-affinity binding sites for GH-RH were found on tumor membranes. Reverse transcription-PCR revealed the expression of mRNA for GH-RH and splice variant 1 (SV(1)) of GH-RH receptor in H838 tumors. Reverse transcription-PCR analysis also demonstrated that H838 tumors express IGF-I and IGF-I receptors. Tumoral concentration of IGF-I and its mRNA expression were significantly decreased by 25% (P = 0.05) and 65% (P < 0.001), respectively, in animals receiving JV-1-38, whereas serum IGF-I levels remained unchanged. In vitro studies showed that H838 cells secreted GH-RH and IGF-I into the medium. The growth of tumor cells in vitro was stimulated by IGF-I and inhibited by GH-RH antagonist JV-1-38 and a GH-RH antiserum. Our results extend the findings on the involvement of IGF-I in NSCLC and suggest that GH-RH may be an autocrine growth factor for H838 NSCLC. The antitumorigenic action of GH-RH antagonists could be partly direct and mediated by SV(1) of tumoral GH-RH receptors. The finding of GH-RH and SV(1) of GH-RH receptors in NSCLC provides a new approach to the treatment of this malignancy based on the use of antagonistic analogues of GH-RH.

The accumulation of radioactive somatostatin analog [111In]pentetreotide in non-small cell lung cancer (non-SCLC) during scintigraphy of patients provides a rationale for investigating the efficacy of somatostatin receptor-based chemotherapy in non-SCLC. Consequently, in this study, we evaluated the antitumor effects of cytotoxic somatostatin analog AN-238 on H838 human non-SCLC xenografted into nude mice in comparison with its cytotoxic radical, 2-pyrrolinodoxorubicin (AN-201). The expression of messenger RNA (mRNA) for human somatostatin receptor subtypes 2 (hsst2) and 5 (hsst5) in H838 cells, and tumors was also investigated using reverse-transcription polymerase chain reaction (RT-PCR). Somatostatin receptors on H838 tumors were characterized by ligand competition assay using radiolabeled somatostatin analog, RC-160. Three i.v. injections of AN-238 at 150 nmol/kg, given on days 1, 7 and 21, resulted in a significant (p<0.05) tumor growth inhibition, the final tumor volume being 60% smaller than in the controls. The tumor doubling time was also extended significantly (p<0.05) from 9.65+/-0.56 days in the controls to 17.52+/-3.3 days. Only one of 8 mice died due to toxicity. In contrast, cytotoxic radical AN-201 was ineffective and more toxic, killing 2 of 7 animals. mRNA for hsst2 was found in H838 xenografts, but not in H838 cells from which the xenografts originated. Interestingly, H838 cells grown in a special, serum-free medium did express mRNA for hsst2. mRNA for hsst5 was not found in any samples tested. Binding studies demonstrated the presence of high affinity (K(d) = 7.3+/-1.2 nM) binding sites for RC-160 with a mean maximal binding capacity (B(max)) of 953.3+/-45.3 fmol/mg protein. AN-238 at 3.14+/-0.93 nM concentration displaced 50% of radiolabeled RC-160 binding to somatostatin receptors in H838 tumors. Our results indicate that patients with inoperable non-SCLC may benefit from chemotherapy targeted to somatostatin receptors based on AN-238.

Previous studies showed that antagonists of bombesin (BN)/gastrin-releasing peptide (GRP) inhibit the growth of various cancers by interfering with the growth-stimulatory effects of BN-like peptides and down-regulating epidermal growth factor receptors on tumors. Because the overexpression of the human epidermal growth factor receptor-2 (ErbB-2/HER-2/neu) oncogene plays a role in the progression of many breast cancers, we investigated whether BN/GRP antagonists can affect HER-2 in mammary tumors. Female nude mice bearing orthotopic xenografts of MDA-MB-435 human estrogen-independent breast cancers were treated daily with BN/GRP antagonists RC-3095 (20 μg) or RC-3940-II (10 μg) for 6 weeks. The expression of BN/GRP receptors on tumors was analyzed by reverse transcription–PCR and immunoblotting. We also evaluated whether the mRNA expression for the c- jun and c- fos oncogenes is affected by the therapy. Both BN/GRP antagonists significantly inhibited growth of MDA-MB-435 cancers; RC-3095 reduced tumor volume by 40% and RC-3940-II by 65%. The GRP receptors (subtype 1) were detected in MDA-MB-435 tumors, showing that they mediate the inhibitory effect of the antagonists. Tumor inhibition was associated with a substantial reduction in the expression of mRNA and protein levels of the ErbB/HER receptor family as well as with a decrease in the expression of c- jun and c- fos oncogenes. BN/GRP antagonists RC-3940-II and RC-3095 could be considered for endocrine therapy of estrogen-independent breast cancers that express members of the ErbB/HER receptor family and the c- jun and c- fos oncogenes.

The resistance of advanced colorectal cancers to therapy is often related to mutations in the p53 tumor suppressor gene. Because somatostatin (SRIF) receptors (ssts) are present in colorectal carcinomas, the treatment with targeted cytotoxic SRIF analogue AN-238, consisting of 2-pyrrolinodoxorubicin (AN-201) linked to octapeptide SRIF carrier RC-121, may overcome this resistance by producing a higher concentration of the cytotoxic agent in the tumors. Four colon cancer cell lines, HCT-116 and LoVo expressing wild-type p53, and HCT-15 and HT-29 with mutated p53, were investigated. HCT-116, HCT-15, and HT-29, but not LoVo possess functional ssts. We analyzed changes in p53, p21, and proliferating cell nuclear antigen (PCNA) concentrations in these cells in vitro by immunoblotting after exposure to AN-238, its radical AN-201, or doxorubicin (DOX). Equitoxic doses of AN-238, AN-201, or DOX affected p53, p21, and PCNA differently. Analysis of the p21:p53 ratios revealed that DOX increased p53 levels, but most of p53 was mutated and inactive, whereas AN-238 produced smaller changes in p53 concentrations but enhanced its activity. In HCT-15 cells, PCNA:p21 ratios, which are indicators of proliferation and repair processes, remained unchanged after exposure to AN-238 but were increased by DOX. In vivo studies in nude mice demonstrated that AN-238, AN-201, and DOX were equally effective on HCT-116 tumors that express wild-type p53. However, AN-238 also inhibited the growth of HCT-15 and HT-29 cancers that express mutant p53, whereas AN-201 and DOX showed no effect. None of the compounds could suppress the proliferation of LoVo tumors that lack functional ssts. In conclusion, cytotoxic SRIF analogue AN-238 inhibits the growth of experimental colon cancers that express ssts, regardless of their p53 status.

Antagonists of growth hormone–releasing hormone (GHRH) such as JV‐1‐38 can inhibit androgen‐independent prostate cancer directly by several mechanisms and/or indirectly by suppressing growth hormone/insulin‐like growth factor‐I (GH/IGF‐I) axis. To shed more light on the mechanisms involved, the effects of JV‐1‐38 on PC‐3 human prostate cancer were compared with those of somatostatin analog RC‐160 in vivo and in vitro.

We evaluated the effects of the bombesin/gastrin-releasing peptide (GRP) antagonist RC-3095, and the luteinizing hormone-releasing hormone (LH-RH) antagonist Cetrorelix, administered singly or in combination, on the growth of human ovarian carcinoma cell line ES-2, xenografted into nude mice. RC-3095 at a dose of 20 microg/day and Cetrorelix (100 microg/day), significantly reduced the volume of ES-2 tumors by 63.0% (P<0.01) and 38.0% (P<0.05) respectively, after 44 days of treatment, as compared with controls. The combination of RC-3095 with Cetrorelix inhibited the growth of ES-2 tumors by 66.2% (P<0.01). Serum levels of LH were significantly decreased in the groups treated with Cetrorelix alone and/or in combination with RC-3095. RT-PCR analyses revealed that the expression of mRNA for receptors of GRP (GRPR/BRS-1) and Neuromedin B (NMBR/BRS-2) on tumors was significantly decreased in all the treated groups. The expression of mRNA for epidermal growth factor receptors (EGFR) on tumors was reduced by 36.5 % (P<0.05) in the animals treated with Cetrorelix and by 72.5% (P<0.05) in the group that received the combination of RC-3095 with Cetrorelix. Our results indicate that the bombesin antagonist RC-3095 and the LH-RH antagonist Cetrorelix inhibit effectively the growth of ES-2 ovarian cancers in nude mice. These antagonists and their combination could be considered for the therapy of patients with ovarian cancer.

The involvement of IGF-I in mammary carcinogenesis is well established, but the role of GH, as an autocrine growth factor for breast cancers is poorly understood. The goal of our study was to investigate whether antagonists of GHRH can interfere with the effects of GH and IGF-I in MXT mouse mammary cancers. GHRH antagonists JV-1-36 and JV-1-38 inhibited growth of estrogen-independent MXT mouse mammary cancers in vivo, producing about 50% reduction in tumor volume (P < 0.05). This growth inhibition was associated with a decrease in cell proliferation and an increase in apoptosis in MXT cancers. RIA and RT- PCR analyses showed that the concentrations of GH and IGF-I and the levels of mRNA for GH and IGF-I in MXT tumors were reduced by the therapy with GHRH antagonists. Messenger RNA for GH receptors was also decreased. In vitro, the proliferation of MXT cancer cells was strongly stimulated by GH and less effectively by IGF-I, indicating that both GH and IGF-I may act as growth factors for this mammary carcinoma. GHRH antagonist JV-1-38 inhibited the autonomous growth of MXT cells and the proliferation induced by IGF-I or GH and diminished (3)H-thymidine-incorporation stimulated by IGF-I and GH. These findings and a sustained increase in cyclin B2 concentrations in the cells shown by immunoblotting indicate that JV-1-38 causes a block at the end of the G(2) phase of cell cycle. Our results demonstrate that GHRH antagonists decrease the local production of both GH and IGF-I in MXT mouse mammary cancers, the resulting growth inhibition being the consequence of reduced cell proliferation and increased apoptosis.