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Biomedical subjects

J Russo

Publications and source records attributed to J Russo.

At least 91 records · Page 5Linked to original sources
PubMed1998

Antiproliferative effect of synthetic resveratrol on human breast epithelial cells.

Resveratrol (3,5,4'-trihydroxy-trans-stilbene), a phytoalexin, is a constituent of the human diet that has been shown to inhibit cellular processes associated with tumor initiation, promotion and progression. In this study, we examined the effect of synthetic resveratrol on the proliferative capacity of immortal and neoplastic human breast epithelial cells in culture. MCF-7, an estrogen receptor-positive breast cancer cell line, MCF-10F, an immortal estrogen receptor-negative breast epithelial cell line, and MDA-MB-231, a malignant estrogen receptor-negative breast epithelial cell line, were treated with 5, 10, 20 or 40 microg/ml resveratrol, and their proliferative activities were determined with the WST-1 colorimetric assay after periods of time ranging from 24 to 144 h of treatment. Our results showed that this phytoalexin inhibited the proliferation of human breast epithelial cells in a dose- and time-dependent manner. Treatment of cells with resveratrol reduced the number of viable cells and prevented the exponential growth of the three cell lines examined. These observations indicate that resveratrol has a direct antiproliferative effect on human breast epithelial cells that is independent of the estrogen receptor status of the cells. Thus, this dietary compound is a potential chemopreventive agent for both hormone responsive and non-responsive breast cancers.

Anticarcinogenic Agents↗
PubMed1998

Identification of new genes differentially expressed in breast carcinoma cells treated with human chorionic gonadotropin.

Human chorionic gonadotropin (hCG) inhibits the growth of human breast epithelial cells MCF-7. Differential display was utilized for analyzing RNA of hCG-treated MCF-7 cells in order to determine whether this effect was mediated by specific gene activation or repression. Three cDNA clones, 19, 29 and 44, were differentially expressed in treated cells. Clone 44, whose sequence matched a gene expressed in dexamethasone-treated T-cell hybridoma, was increased by approximately 4-fold, while clones 19 and 29 were markedly reduced by hCG treatment. These latter ones were considered to be novel genes, since no homology was found in the gene-bank. Our results indicate that hCG influences gene expression in mammary epithelial cells, supporting its potential role in breast cancer prevention and therapy.

Blotting, Northern↗
PubMed1997

Cloning and gene mapping of the chromosome 13q14 region deleted in chronic lymphocytic leukemia.

Frequent deletions and loss of heterozygosity in a segment of chromosome 13 (13q14) in cases of B-cell chronic lymphocytic leukemia (CLL) have suggested that this malignancy is caused by inactivation of an unknown tumor suppressor gene located in this region. Toward the identification of the putative CLL tumor suppressor, we have constructed a high-resolution physical map of YAC, PAC, and cosmid contigs covering 600 kb of the 13q14 genomic region. In addition to densely positioned genetic markers and STSs, this map was further annotated by localization of 32 transcribed sequences (ESTs) using a combination of exon trapping, direct cDNA selection, sample sequencing of cosmids and PACs, and homology searches. On the basis of these mapping data, allelic loss analyses at 13q14 using CLL tumor samples allowed narrowing of the genomic segment encompassing the putative CLL gene to <300 kb. Twenty-three ESTs located within this minimally deleted region are candidate exons for the CLL-associated tumor suppressor gene.

Alleles↗
PubMed1997

Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues.

Tamoxifen (TAM) exerts a long-term suppressive effect on human breast cancer cell proliferation. To determine whether the effects of TAM are mediated by specific gene activation or repression, normal and tumoral human breast tissues obtained before and during TAM treatment were analyzed by differential display technique. Total RNA for differential display analysis was obtained from breast tissues from two women with the diagnosis of estrogen receptor-positive stage II (T2N1M0) infiltrating ductal carcinoma, made by incisional biopsy, followed by modified radical mastectomy performed after a 30-day treatment with TAM (20 mg/day). One 202-bp cDNA band, AP5-1, was present in normal and tumoral biopsy samples, but was absent in breast tissue obtained during TAM treatment, and was confirmed by Northern hybridization, which showed a 2.7-kb band in both patients. The differentially expressed cDNA fragment showed 99% homology to Homo sapiens CD36 gene, a glycoprotein that acts as a receptor for the extracellular matrix proteins thrombospondin-1, collagen types I and IV, and oxidized low-density lipoprotein. These results indicate that the down-regulation of CD36 induced by TAM might represent alternative or additional mechanisms of action of this drug affecting the functions of thrombospondin-1, which is involved in hematogenous tumor spread, invasion and angiogenesis, and oxidized low-density lipoprotein, playing a role in inhibition of arteriosclerosis. The multiple functions affected by the down-regulation of CD36 by TAM warrant the need for additional studies.

Antineoplastic Agents, Hormonal↗
PubMed1997

Differential expression of human ferritin H chain gene in immortal human breast epithelial MCF-10F cells.

Subtractive hybridization was used to isolate genes expressed uniquely in the immortalized human breast epithelial cell (HBEC) line MCF-10F and not in the mortal HBEC line S-130, from which MCF-10F cells were derived. We identified a 233-bp cDNA that was expressed in MCF-10F cells and not in their mortal counterpart S-130 cells. Sequence comparison with the GenBank database revealed that the cDNA was identical to the gene encoding human ferritin heavy H chain. Northern blot analysis using the isolated cDNA as a probe showed a differentially expressed 1.1-kb transcript of ferritin H in total RNA from the immortal MCF-10F cells, MCF-10F cells treated with the chemical carcinogens 7,12-dimethylbenz[a]anthracene and benzo[a]pyrene, and the breast cancer cell lines MCF-7, HBL-100, T-47D, and BT-20. No ferritin H transcript was detected in the mortal line S-130 or in other primary HBEC cultures. Increased levels of mRNA transcript signals were also detected in total RNA from breast cancer tissue samples. Tissue with ductal hyperplasia had higher expression levels than normal adjacent mammary tissue. In situ hybridization showed high levels of ferritin H transcript in mammary tissue areas with ductal hyperplasia, carcinoma in situ, and infiltrating ductal carcinoma. This is the first report of the differential expression and upregulation of human ferritin H chain gene in immortal HBECs. It may be an important factor in the process of immortalization, possibly an early stage of malignant transformation of HBECs, providing cells with iron necessary for growth and clonal expansion. Also, ferritin iron, once released, may increase the level of reactive iron, leading to an increase in oxygen free-radical generation, oxidative DNA damage, and mutation.

Base Sequence↗
PubMed1997

The relationship of patient-administered outcome assessments to quality of life and physician ratings: validity of the BASIS-32.

The reliability and validity of a patient-administered version of the Behavior and Symptom Identification Scale (BASIS-32) was compared to the original interviewer-administered version. The construct validity of BASIS-32 subscales was assessed by examining their relationship with functional and satisfaction quality of life and physician ratings of functional and clinical status. A total of 361 acute psychiatric inpatients were given a self-administered BASIS-32, nurse-administered Lehman's Quality of Life Interview (QOLI), and Psychiatrist Assessment Form at admission and discharge. The original factor structure, internal consistency reliability, discriminant validity, and sensitivity to change were replicated. The patient-administered BASIS-32 is equally as reliable and valid as the interview. Construct validity analyses revealed that functional and satisfaction QOLI indices were moderately related to the BASIS-32 in the hypothesized directions. All satisfaction scales were associated with significantly less severity. Physician ratings were only mildly related to the subscales. The BASIS-32 used in outcome assessments with inpatients provides important and unique perspectives on functional and clinical status that are not tapped by clinician-rated assessments.

Inpatients↗
PubMed1997

Hostility, social support, and perceptions of work.

The aim of this study was to determine whether hostility and perceived availability of social support are related to perceptions of the work environment. The W.W. Cook and D.M. Medley (1954) Hostility (Ho) scale; the Interpersonal Support Evaluation List (S. Cohen, R. Mermelstein, T. Kamarck, & H. Hoberman, 1985); and measures of collegiality, time pressure, and job dissatisfaction were completed by 204 attorneys (159 men and 45 women). After controlling for age, gender, and other job characteristics, high Ho scores were related to lower perceived supportive collegiality at work. Low perceived availability of social support was related to greater job dissatisfaction. Neither hostility nor social support was associated with perceptions of time pressure at work. These findings suggest that hostility and availability of social support may be an important pathway linking certain job characteristics to cardiovascular disease and other illnesses.

Adaptation, Psychological↗
PubMed1997

Microsatellite instability and loss of heterozygosity in chromosomes 9 and 16 in human breast epithelial cells transformed by chemical carcinogens.

Microsatellite instability (MSI) and loss of heterozygosity (LOH) in chromosomes 9 and 16 have been reported in human breast cancers. In order to determine whether changes in these chromosomes play a role in the initiation and progression of this disease, we performed microsatellite polymorphism analyses in human breast epithelial cells (HBEC) transformed by chemical carcinogens, an in vitro system that recapitulates various stages of neoplastic transformation. In this experimental system we studied the mortal HBEC MCF-10M, immortal MCF-10F cells, derived from MCF-10M cells, and clones derived from MCF-10F cells treated with benzo[a]pyrene (B[a]P) (BP1 and BP1E) and 7,12-dimethylbenz[a]anthracene (DMBA) (D3 and D3-1). The four clones of transformed cells were injected into severe combined immunodeficient (SCID) mice. Only BP1-E cells induced the formation of tumors, designated BP1E-Tp cells. These cells originated six additional tumors, designated BP1E-Tf no. 1 through Tf no. 6. Microsatellite analyses were carried out using five markers for chromosome 9 and 20 for chromosome 16. There was no evidence of MSI or LOH in clones BP1 and BP1E when compared with the MCF-10M and MCF-10F cells, whereas BP1E-Tp cells and Bp1E-Tf no. 1-Tf no. 6 tumors exhibited MSI at loci p23 and p21, and LOH at p21-22 of chromosome 9. They also exhibited MSI and LOH at multiple loci of both the short and long arms of chromosome 16, i.e. p13.13, p13.3, p12, q12.1, q12.2, q23 and q24, to which putative tumor suppressor genes have been localized. Clones D3 and D3-1 exhibited no genomic changes in chromosome 9, but did show MSI at locus q12.1 of chromosome 16 using marker D16S285. Although the cells treated with DMBA expressed early phenotypes of neoplastic transformation, they were not tumorigenic, and also manifested fewer changes than the tumorigenic BP1E-Tp cells and the tumors BP1E-Tf. The changes in chromosomes 9 and 16 observed in these latter ones indicated an association with the expression of tumorigenesis, which represents a late event in the progression of the neoplastic transformation of HBEC. Of interest was the observation that HBEC transformed by chemical carcinogens in vitro express genomic changes similar to those found in spontaneous breast carcinomas.

Animals↗
PubMed1997

Chorionic gonadotropin inhibits rat mammary carcinogenesis through activation of programmed cell death.

Human chorionic gonadotropin (hCG) inhibits the progression of 7,12-dimethylbenz[a]anthracene (DMBA) induced mammary carcinomas. In order to determine whether this phenomenon was mediated by induction of programmed cell death or apoptosis, 45-day-old virgin Sprague-Dawley rats received 8 mg DMBA/100 g body weight; 20 days later they were injected daily with 100 IU hCG for 40 days (DMBA + hCG group). Age-matched untreated, hCG- and DMBA + saline treated rats were used as controls. Tissues were collected at the time of DMBA administration and at 5, 10, 20 and 40 days of hCG injection. RNA from mammary glands, adenocarcinomas and ovaries was probed for transforming growth factors (TGF) alpha and beta, and the apoptotic genes TRPM2, ICE, bcl2, bcl-XL, bcl-XS, p53 and c-myc. The mammary glands of hCG-treated animals with or without DMBA exhibited elevated expression of TRPM2, ICE, bcl-XS, c-myc and p53; and elevation in the apoptotic index. Mammary adenocarcinomas developed in those animals treated with hCG showed an elevation in the expression of p53, c-myc and ICE genes in comparison with the levels detected in the adenocarcinomas developed by the animals treated with DMBA alone. No significant alterations in the expression of any of the genes tested was observed in ovarian RNAs. These results led us to conclude that hCG induces programmed cell death in the mammary gland initiated in the carcinogenic process, that this process is p53 dependent, and is modulated by c-myc expression. Our data also indicate the possibility that a cell death program dependent on the bcl2 family exists, because of the potential involvement of p53, bcl-XS and Bax in apoptosis. This additional mechanism of tumor inhibition makes hCG treatment a useful approach for the prevention and therapy of breast cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

Longitudinal assessment of quality of life in acute psychiatric inpatients: reliability and validity.

This study examined the reliability, validity, and responsiveness of Lehman's Quality of Life Interview (QOLI) as an outcome measure on 981 acutely ill psychiatric inpatients assessed longitudinally at admission and discharge. Patients were stratified into five diagnostic (DX) (depressed bipolar, depressed unipolar, schizophrenia, mania, and other diagnoses) and two substance use disorder (SA) strata (with and without concurrent substance abuse/dependence) based on DSM-III-R criteria. There was good replication of the factor structure, excellent internal consistency, overall and within DX and SA groups. Intercorrelations showed that the functional and satisfaction indices measure unique aspects of the quality of life. The construct consistency of the QOLI was dependent upon psychiatric diagnosis and life domain. Intercorrelations of functional and satisfaction indices for patients with depression were greater than for manic patients. We demonstrated strong consistency of construct validity for family and social relation domains, but not safety or leisure activities. Construct validity was shown to hold longitudinally. Analyses of DX and SA group differences on satisfaction and functional indices of the 8 life domains supported discriminative validity: Depressed patients reported the most dissatisfaction, followed by schizophrenic patients, and manic patients reported the greatest satisfaction in most life domains. Patients with concurrent substance abuse generally reported less satisfaction and lower quality of life than patients without a dual diagnosis. Examination of longitudinal changes in satisfaction indicated the QOLI is responsive to changes in global life, leisure activities, living situation, and social relations from hospital admission to discharge (an average of 2 weeks). This study supports the use of the QOLI as an outcome measure to assess quality of life in acutely ill hospitalized psychiatric patients.

Activities of Daily Living↗
PubMed1997

Are aluminium potroom workers at increased risk of neurological disorders?

OBJECTIVE: To determine whether long term potroom workers in an aluminium smelter are at increased risk of neurological disorders. METHODS: Cross sectional study of 63 current and former aluminium potroom workers first employed before 1970 and with at least 10 years of service. A group of 37 cast house and carbon plant workers with similar durations of employment and starting dates in the same smelter were used as controls. The prevalence of neurological symptoms was ascertained by questionnaire. Objective tests of tremor in both upper and lower limbs, postural stability, reaction time, and vocabulary were conducted. All subjects were examined by a neurologist. RESULTS: No significant differences in age, race, or education were found between the two groups. Although the potroom group had higher prevalences for all but one of the neurological symptoms, only three odds ratios (ORs) were significantly increased; for incoordination (OR 10.6), difficulty buttoning (OR 6.2), and depression (OR 6.2). Tests of arm or hand and leg tremor in both the visible and non-visible frequencies did not show any significant differences between the two groups. Testing of postural stability showed no definitive pattern of neurologically meaningful differences between the groups. There were no significant differences between the two groups in reaction time, vocabulary score, or clinical neurological assessment. CONCLUSIONS: The objective measures of neurological function provided little support for the finding of increased neurological symptom prevalences in the potroom workers, although increased symptoms may be an indicator of early, subtle neurological changes. The results provide no firm basis for concluding that neurological effects among long term potroom workers are related to the working environment, in particular aluminium exposure, in potrooms. These findings should be treated with caution due to the low participation of former workers and the possibility of information bias in the potroom group.

Adult↗
PubMed1997

Psychiatric status, quality of life, and level of care as predictors of outcomes of acute inpatient treatment.

OBJECTIVE: The study examined the role of five types of variables--demographic characteristics, psychiatric status, functional quality of life, satisfaction with quality of life, and level of care--in predicting key outcomes of inpatient treatment. METHODS: Multivariate canonical regression and univariate multiple regression models were constructed using data from 1,053 inpatients at a public hospital in Washington State. The models were used to predict length of stay, change in symptom severity during hospitalization, psychiatrists' ratings of patients' insight into their illness at discharge, patients' global satisfaction with life, and rehospitalization within 18 months. Hierarchical stepwise procedures were used to select variables that were significant predictors of outcomes. RESULTS: All five classes of predictors were related to the outcomes. The roles of demographic characteristics and diagnoses were minimal. Previous hospitalization and severity of symptoms at admission were strong predictors of psychiatric status. Indicators of functional quality of life and satisfaction with quality of life explained significant variance in all models after accounting for the other classes of predictors. Frequency of family visits was the strongest functional quality-of-life predictor, relating to positive outcomes. Pretreatment satisfaction with life was a significant predictor of most outcomes, and increased satisfaction was associated with positive outcomes. CONCLUSIONS: Patients' quality of life before psychiatric inpatient treatment predicted treatment outcomes independently of psychiatric status, demographic characteristics, and level-of-care variables. Prospective studies are needed to predict outcomes using multidimensional constructs.

Adolescent↗
PubMed1997

Periodontal laser surgery.

A gingivectomy performed with a laser is a short, easy procedure that produces an immediately dramatic effect. Compared to a scalpel gingivectomy, there is excellent hemostasis, which improves visualization, requires less need for periodontal packing, and results in minimal postoperative discomfort. Tissue rebound also is minimal. Use of lasers requires specific training. The only approved function in periodontics at this time according to the American Academy of Periodontology is soft tissue surgery. Some periodontal applications include frenectomy, soft tissue crown lengthening, distal wedge procedures, soft tissue tuberosity reductions, gingivectomy, gingivoplasty, stage II of implants, operculectomies, biopsies, coagulation of graft donor sites, hemorrhage disorder patients, and stripping procedures for various leukoplakias.

Aged↗
PubMed1997

Differentiation and breast cancer.

The mammary gland is an organ whose size, shape and function undergo fundamental changes during the various phases of a woman's growth. Although the development of the mammary gland begins during infancy, the most dramatic changes occur with the initiation of puberty. Pregnancy and lactation complete the functional development of the organ, which regresses during menopause. Epidemiological and experimental studies have demonstrated that certain hormonal influences, especially those related to reproduction, modify the risk of developing breast cancer. Thus, a full term pregnancy completed before the age of 24 years significantly reduces the lifetime incidence of breast cancer. Although the mechanism through which pregnancy protects the breast from breast cancer has not been clearly established, experimental models of mammary carcinogenesis have allowed researchers to determine that pregnancy inhibits the initiation of the neoplastic process through the induction of a complete differentiation of the mammary gland. This process activates specific genes, which in turn modify the response of the organ to ulterior hormonal changes. It is postulated that the same mechanism might be responsible for the protective effect of a woman's early first full term pregnancy. The greater incidence of breast cancer observed in nulliparous women correlates well with the greater susceptibility of the virgin rat to develop mammary carcinomas when exposed to chemical carcinogens. The successful induction of malignant transformation in the virgin animal mammary epithelium is due to the presence of undifferentiated structures with a high rate of cell proliferation. These structures are eliminated by pregnancy. The breast of nulliparous women retains those undifferentiated structures, which increase the predisposition of the organ to undergo malignant transformation, which will manifest itself clinically several years after its initiation. The correlation of human epidemiological, clinical and experimental data with those data obtained in rodent experimental models lends support to this hypothesis.

Animals↗
PubMed1996

Experimentally induced mammary tumors in rats.

Among the multiple experimental animal models employed for analyzing the various aspects of mammary carcinogenesis, the induction of mammary tumors in rats by chemical carcinogens is one of the models most utilized. Experimentally-induced mammary tumors in rodents have proven to constitute useful tools for the study of the pathogenesis of cancer and of the molecular mechanisms involved in the initiation and progression of the neoplastic process. In vivo experimental animal models provide information not available in human populations; they are adequate for hazard identification, dose-response modeling, exposure assessment, and risk characterization, the four required steps for quantifying the estimated risk of cancer development associated with toxic chemical exposure. Using the DMBA rat mammary model, we have been able to demonstrate that the carcinogen acts on the intermediate cell of the terminal end bud (TEB), and that this structure is the one that evolves to intraductal proliferation, carcinoma in situ, and invasive carcinoma. There are several factors that regulate the susceptibility of the TEB; some of them are: a) topographic location of the mammary gland, b) age of the animal, and c) reproductive history. The understanding of the mechanisms that modulate tumorigenesis will further our knowledge and understanding in the prevention of the disease, as a result of the development of strategies for stopping the progression of the initiated cells.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

Cathepsins D, B, and L in transformed human breast epithelial cells.

To investigate the regulation of lysosomal enzymes during carcinogenesis, we measured cathepsins (Cats) D, B, and L in MCF-10F, which is a human breast epithelial cell line, and cells evolved after treatment with carcinogen and transfected with c-Ha-ras oncogene. The clones used in this study, MCF-10FTras, D3, D3-1, and D3-1Tras, expressed no estrogen receptors and gradually increased invasive potential, while oncogene-transfected lines were also tumorigenic in SCID mice [16, 19]. Cats D, B, and L were determined in the cells and in cell media using enzyme-linked immunosorbent assay (ELISA), specific enzyme activity measurements, and immunocytochemistry. The major intra- and extracellular lysosomal proteinase in these cells was Cat D (30-180 pm/mg), followed by Cat B (2-10 pm/mg) and Cat L (1-5 pm/mg). An inverse relationship between intracellular Cat D levels and invasive potential of carcinogen-treated and c-Ha-ras oncogene-transfected cell lines was observed. No significant changes in extracellular concentration of Cat D precursor in this series of cell lines was observed. Intracellular levels of Cats B and L were unchanged or slightly lower in carcinogen-treated D3 and D3-1 cells, as well as in MCF-10FTras. On the other hand, in D3-1Tras cell line, evolving from c-Ha-ras transfected D3-1 line, 3.5 fold and 4.4 fold increases in Cat B and Cat L, respectively, but a 2 fold decrease in Cat D, were observed compared to the parental cell line. Immunocytochemical staining showed a granular, polarized perinuclear and cytoplasmic staining of cathepsins in all cell lines. Cysteine proteinases stained more frequently and more intensely in D3-1Tras compared to other lines, confirming the immunochemical assays. We hypothesize that several molecular events, caused by a carcinogen and an oncogene such as c-Ha-ras, are needed to increase Cat B and Cat L, but not Cat D, expression. Therefore, the cysteine and aspartic lysosomal proteinases are differentially expressed in the breast cell lines with more invasive phenotype.

Breast↗
PubMed1996

Insect immunity: early events in the encapsulation process of parasitoid (Leptopilina boulardi) eggs in resistant and susceptible strains of Drosophila.

Eggs of an immune suppressive strain (= virulent) of the parasitoid Leptopilina boulardi are encapsulated neither in resistant nor in susceptible strains of Drosophila melanogaster but are encapsulated in Drosophila yakuba. Eggs of a nonimmune suppressive strain (= avirulent) of the same parasitoid are encapsulated in a resistant strain of D. melanogaster and in D. yakuba but are not encapsulated in a susceptible strain of D. melanogaster. Egg chorion in the 2 parasitoid strains showed the same morphology and the same modifications after egg laying whatever the host strain. When a capsule is built, a small dotted dense layer was first spread on the chorion, followed by accumulation layers of cells (plasmatocytes and lamellocytes) and lastly necrosis of the inner haemocytes. The encapsulated eggs darken only at the time of necrosis of haemocytes. In susceptible hosts, neither the tiny dense layer nor haemocyte accumulation occurred. We concluded that (1) this tiny dense layer was present before the deposition of the first haemocytes, (2) inhibition of deposition of this dense layer was the initial event of the induced immunosuppression, (3) haemocytes other than lamellocytes were engaged in capsule formation, (4) the immunosuppressive factors did not target only the lamellocytes but also the plasmatocytes, (5) darkening of the encapsulated eggs was due to cell necrosis rather than to extracellular melanin deposition.

Animals↗