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R Serra

Publications and source records attributed to R Serra.

At least 55 records · Page 3Linked to original sources
PubMed1997

A new metabolic simulator system for routine cardiopulmonary exercise test equipment: technical specifications and validation. ECSC Working Group on Standardization Stress Test Methods.

Modern stress-test instruments require non-steady-state calibration (i.e., during exercise) instead of calibration at rest (i.e., before use) in stable conditions. The purpose of the present study was to describe a new specific computer-controlled check system for stress-test instruments, which operates on the basis of physiological respiratory equations. It can produce rapid and automatic modifications of metabolic data, allowing breath-to-breath simulation. When connected to the stress-test equipment to be controlled, it makes it possible to identify discrepancies between preset and measured values. Systematic comparative measurements were performed using as reference two mass spectrometer-controlled analysers and a high-precision flow meter. Accuracy, trend and reproducibility in continuously changing conditions were very satisfactory.

Calibration↗
PubMed1997

Improved simulation system for routine cardiopulmonary exercise test equipment. Part II: A new metabolic simulator system: practical applicability. The European Coal and Steel Community (ECSC) Working Group on Standardization of Stress-test Methods.

The utilization in clinical practice of an improved metabolic calibrator was tested. The morphological characteristics and integration patterns of the signals were checked with a reference stress-test instrument and compared with physiological recordings. No significant differences were observed. Conversion formulae were developed to compare the calibrator's data with those produced by routine instruments. Simultaneous graphical representations of erroneous and reference signals and computer processing of data allowed on-line detection of even minimal sources of error in dynamic working conditions.

Calibration↗
PubMed1996

Effects of different levels of dietary zinc on the gilthead, Sparus aurata during the growing season.

Gilthead were fed three diets. Diet A was the control diet, whereas diets B and C were supplemented with 300 and 900 mg Zn/kg, respectively. Fish fed with diet C, at the end of the experiment, showed the lowest weight. Zinc concentrations presented the higher values in gills, liver, and kidney. Muscle and brain had the lower mean values and showed a tight control of zinc levels. These results reinforce the hypothesis that zinc in the CNS should be strictly controlled in order to maintain the functional role of the metal. Significant differences in tissue zinc concentrations were obtained between fish fed different amounts of zinc, the metal concentrations being higher in tissues of fish fed diet C. The tissue decrease of zinc, found at the end of the experiment, may depend on a lower feed consumption or on different zinc requirements during the cold season. These changes, even if not univocal among the three diets, may be associated with the life cycle of fish. Furthermore, copper concentrations were little affected by the different concentrations of zinc in the three diets; liver and kidney presented the highest concentrations; liver showed a significant decrease in copper content at the end of the experiment. We conclude that: zinc concentrations of the diet may affect the gilthead weights and the tissual metal content; and zinc concentrations in the diets, depending on the growth rate, may be varied depending on the season.

Animals↗
PubMed1996

Regulation of differentiation by TGF-beta.

Recent experiments in neural, skeletal, endothelial, and hematopoietic tissues have provided new insights into the way members of the transforming growth factor-beta (TGF-beta) superfamily regulate cellular differentiation. TGF-betas regulate the fate of multipotential stem cells instructively (in the neural crest) by regulating the expression or function of tissue-specific transcription factors, as well as selectively (in the mesenchyme) by regulating the expression of required growth factors and their receptors. During skeletal development, TGF-betas have unique functions and act sequentially to modulate chondrocyte and osteoblast differentiation. Responsiveness to TGF-betas changes as cells differentiate and evidence now suggests that changes in TGF-beta receptor profile may account for some of these differences. Drosophila and transgenic mouse models are now providing useful insights into mechanisms of TGF-beta action in vivo.

Animals↗
PubMed1995

Influence of age and health on immune functions and trace elements.

Apparently healthy elderly donors were screened according to a simple protocol that included clinical examination and the determination of hematological and biochemical values. This screening was performed to detect subclinical alterations which might interfere with immune responses and trace element status. The elderly were divided into two groups. The first group consisted of 22 (age 76 +/- 1 years) positively selected elderly (PSE), i.e. healthy subjects with no hematological and laboratory alterations, the second one comprised 13 (age 75 +/- 1 years) negatively selected elderly (NSE). Data were then compared with those obtained from 40 (age 35 +/- 2 years) healthy young controls. In both groups of elderly donors, plasma zinc levels were normal, while plasma copper concentrations were increased. Intracellular values of zinc and copper in mono- and polymorphonuclear cells from both groups of elderly were within reference limits. After in vitro activation, granulocyte chemiluminescence activity was impaired only in NSE. A decrement in the number of circulating CD3 lymphocytes and an increase in CD8d, CD57 cells were found in PSE, while NSE showed an increased number of CD3,DR cells and CD8d, CD57, CD8b,CD57 and CD16,CD56 positive cells. Our results indicate that only plasma copper levels were affected by age, whereas subclinical alterations in hematological or biochemical values appear to impair immune responses in the elderly.

Adult↗
PubMed1995

pRb is necessary for inhibition of N-myc expression by TGF-beta 1 in embryonic lung organ cultures.

The beta type transforming growth factors (TGF-beta) are potent inhibitors of epithelial cell proliferation, and data suggest that growth inhibition by TGF-beta 1 is mediated through suppression of Myc family genes in certain cell types. Indirect evidence has indicated that the product of the retinoblastoma gene (pRb) may also be involved in this pathway. Previously, we have shown that TGF-beta 1 inhibits branching morphogenesis and N-myc expression in mouse embryonic lung cultures. The purpose of this study was to determine the role of pRb in the inhibition of branching morphogenesis and N-myc expression by TGF-beta 1. Treatment with TGF-beta 1 was shown to inhibit development of lungs from homozygous Rb null (Rb-/-) and heterozygous null (Rb+/-) mouse embryos to the same extent as lungs from wild-type (Rb+/+) embryos. However, TGF-beta 1 treatment did not suppress N-myc expression in Rb-/- as it did in Rb+/+ embryonic lung explants as determined by in situ hybridization and quantitative RT-PCR. The effect of TGF-beta 1 treatment on N-myc expression in lungs from Rb+/- embryos was intermediate between that seen in Rb+/+ and Rb-/- embryos. Embryonic lungs derived from transgenic mice expressing the SV40 large T-antigen in lung epithelium under the control of the surfactant protein C promoter also showed inhibition of development in response to TGF-beta 1 treatment. The data demonstrate that pRb is necessary for TGF-beta 1 suppression of N-myc expression but not for TGF-beta 1 inhibition of branching morphogenesis; therefore, suppression of N-myc is not necessary for inhibition of branching morphogenesis by TGF-beta 1.

Animals↗
PubMed1995

Heavy metals in some species of waterfowl of northern Italy.

Concentrations of heavy metals (zinc, copper, cadmium, and iron) were measured in several tissues (brain, gizzard, leg-muscle, heart, breast-muscle, intestine, liver and kidney) of moorhens (Gallinula chloropus), black-headed gulls (Larus ridibundus), and coots (Fulica atra) collected between autumn 1985 and spring 1989 in northern Italy. Cadmium concentrations in the liver and kidney of water-rails (Rallus aquaticus) and in five species of Anatidae collected also were measured. High mean (+/- SD) copper levels were detected in aerobic muscles such as heart (38 +/- 5 micrograms/g dry weight (DW)) and pectoral muscles (35 +/- 7 micrograms/g DW). Compared to other tissues, the iron content of brain was rather low and constant, with a mean value of 160 +/- 17 micrograms/g DW in moorhens, 157 +/- 60 micrograms/g DW in black-headed gulls, and 157 +/- 25 micrograms/g DW in coots. Iron concentrations in tissues of moorhens from the Reno River were significantly higher than those from the Sile River. Cadmium was detectable only in the liver and kidney; there was a linear relationship between cadmium levels in these two organs. The highest mean (+/- SD) cadmium concentrations were present in the kidney of black-headed gull (30 +/- 20 micrograms/g DW).

Animals↗
PubMed1994

TGF beta 1 inhibits branching morphogenesis and N-myc expression in lung bud organ cultures.

Lung buds isolated from 11.5 days post coitum mouse embryos survive and undergo branching morphogenesis in culture. This organ culture system was used to examine the role of TGF beta 1 and N-myc expression in lung branching morphogenesis. By 24 hours, TGF beta 1 reversibly inhibited branching morphogenesis in a concentration-dependent manner. N-myc is known to be expressed during embryonic development in epithelial cells involved in branching morphogenesis and homozygous null N-myc mice have defects in lung development. In the present study, TGF beta 1 was shown to inhibit the steady-state level of N-myc RNA 3- to 4-fold at 14 and 48 hours of treatment as measured by northern blot and RNase protection analysis. Suppression of N-myc expression in epithelium was confirmed by in situ hybridization. Since inhibition of N-myc occurred prior to the observed changes in morphology and previous genetic studies have demonstrated and important role for N-myc in lung development, a model is proposed in which TGF beta 1 inhibits tracheobronchial development by inhibiting expression of N-myc.

Animals↗
PubMed1994

Transforming growth factor beta 1 suppresses transformation in hepatocytes by regulating alpha 1 beta 1 integrin expression.

We previously reported that (a) treatment of the ras-transformed hepatocyte cell line NR4 with transforming growth factor (TGF) beta 1 suppresses many characteristics associated with the transformed phenotype including altered morphology, actin cytoskeleton reorganization, and anchorage-independent growth such that the cells more closely resemble the immortalized CWSV1 parent cell line; (b) transformed NR4 cells expressed significantly less alpha 1 integrin RNA than the immortalized CWSV1 cells; and (c) TGF-beta 1 treatment of NR4 cells stimulated the expression of alpha 1 and beta 1 integrin RNAs. In this report, the role of the alpha 1 beta 1 integrin in TGF-beta 1-mediated suppression of the ras-transformed phenotype was investigated. We determined that (a) the cell surface integrin that increased in response to TGF-beta 1 treatment of NR4 cells was alpha 1 integrin; (b) TGF-beta 1 altered the ability of NR4 cells to attach to collagen and laminin, the extracellular matrix components that interact with the alpha 1 beta 1 integrin receptor; (c) TGF-beta 1 treatment resulted in relocalization of the alpha 1 integrin on the NR4 cell surface; and (d) TGF-beta 1-mediated inhibition of anchorage-independent growth was blocked by the presence of alpha 1 integrin antibody. A cell line that overexpresses alpha 1 integrin was derived from NR4 cells; characterization of these cells indicated that they continued to express H-ras RNA but were less transformed than the parent NR4 cells. Specifically, they had an altered morphology, an organized actin cytoskeleton, and reduced ability to demonstrate anchorage-independent growth.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

TGF beta regulation of cell proliferation.

The beta-type transforming growth factors (TGF beta) are potent inhibitors of cell proliferation. The mechanisms of TGF beta growth inhibition have been investigated. In skin keratinocytes, TGF beta 1 rapidly suppresses c-myc expression at the level of transcriptional initiation, and expression of c-myc was shown to be necessary for proliferation of these cells. Overexpression of c-myc, using an inducible construct, blocks growth inhibition by TGF beta 1. In 11.5 day p.c. lung bud organ cultures, TGF beta 1 inhibits tracheobronchial epithelial development, including branching morphogenesis. At this stage of development, the tracheobronchial epithelia express N-myc, but not c-myc, TGF beta 1 was shown to markedly inhibit N-myc expression in epithelia of the lung bud organ cultures. N-myc gene knockout experiments by others have shown that N-myc is required for branching morphogenesis of the tracheobronchial tree. The data indicate that suppression of expression of either N-myc or c-myc may play a role in TGF beta growth inhibition. To study the role of TGF beta 1 in normal mammary development and in mammary neoplasia, we have constructed three transgenic mouse lines that express a simian TGF beta 1S223/225 mutated to produce a constitutively active product under the control of the MMTV enhancer/promoter. Expression of the transgene was associated with marked suppression of the normal pattern of mammary ductal tree development in female transgenics from all three lines. However, during pregnancy, alveolar outgrowths developed from the hypoplastic ductal tree, and lactation occurred. Unlike many other transgenic mouse models in which expression of TGF alpha or oncogenes under control of the MMTV promoter leads to mammary epithelial hyperplasia and increased tumor formation, the MMTV-TGF beta 1 transgene causes conditional hypoplasia of the mammary ductal tree. No spontaneous tumors have been detected in the MMTV-TGF beta 1 transgenic animals, indicating that overexpression of TGF beta 1 in mammary epithelia does not enhance, and may actually suppress, early stages of carcinoma development. Other studies have shown that overexpression of TGF beta 1 in carcinoma cells enhances tumorigenicity and metastatic spread. We propose that TGF beta has a bifunctional role in carcinogenesis, retarding carcinoma development but enhancing progression once neoplastic transformation has occurred and the growth inhibitory response to TGF beta has been lost.

Animals↗
PubMed1993

Stimulation of DNA synthesis and protooncogene expression in primary rat hepatocytes in long-term DMSO culture.

We have previously described the use of a chemically defined medium (CDM) supplemented with epidermal growth factor (EGF) and dimethylsulfoxide (DMSO) to maintain long-term cultures of rat hepatocytes in a highly differentiated state. In this study, conditions necessary to stimulate high levels of DNA synthesis in hepatocytes in long-term DMSO culture were defined. Hepatocytes were maintained in culture for 20 days in CDM containing DMSO and EGF, insulin, and glucagon. EGF, insulin, and glucagon were then removed for 7 days. Readdition of EGF, insulin, and glucagon at day 27 (shiftup) was accompanied by a three- to sixfold increase in labeling index. If DMSO or dexamethasone (dex) + DMSO were removed at time of shiftup, the labeling index increased by 18- to 54-fold. TGF beta inhibited DNA synthesis stimulated by EGF shiftup, TGF alpha shiftup, or EGF shiftup in combination with removal of dex + DMSO. Stimulation of DNA synthesis was accompanied by a specific, sequential induction of protooncogene mRNA levels; c-fos mRNA was induced 23-fold at 0.5 h after readdition of EGF; c-myc mRNA was induced three- to four-fold by 0.5 h; TGF alpha mRNA was induced sevenfold by 8 h; K-ras mRNA was induced fourfold by 26 h. Changes in protooncogene expression paralleled changes seen in regenerating liver. When DMSO was removed for greater than 48 h, the cells flattened and spread out, chords of cells were no longer well defined, albumin mRNA levels decreased, and fibronectin, beta 1 integrin, and TGF beta transcripts increased.

Animals↗
PubMed1993

Percutaneous neurolysis of the celiac plexus via the anterior approach with sonographic guidance.

OBJECTIVE: The purpose of this study was to evaluate the usefulness of sonographically guided percutaneous neurolysis of the celiac plexus in patients with abdominal tumors or chronic pancreatitis in whom systemic analgesics were ineffective. SUBJECTS AND METHODS: Neurolysis of the celiac plexus was performed in 38 patients, 34 with neoplastic disease and four with chronic pancreatitis. Under sonographic guidance, a 22-gauge needle was advanced by the anterior route to the area above the celiac plexus, and 30-40 ml of 50% alcohol was injected. Pain relief was assessed 1 week, 6 months, and 1 year after the procedure. Patients subjectively rated the pain after treatment as totally relieved, partially relieved, or unchanged. RESULTS: At 1 week and at 6 months after treatment, pain was totally relieved in 61% of patients, partially relieved in 31%, and unchanged in 8%. After 1 year, pain was totally relieved in 39%, partially relieved in 52%, and unchanged in 9%. The complications observed were five cases of mild diarrhea and one case of retroperitoneal pain, which subsided with conservative treatment. CONCLUSION: The anterior, sonographically guided approach appears to be as successful as other percutaneous techniques for neurolysis of the celiac plexus.

Abdominal Neoplasms↗
PubMed1992

Transforming growth factor beta 1 partially suppresses the transformed phenotype of ras-transformed hepatocytes.

The effect of transforming growth factor beta type 1 (TGF-beta 1) on DNA synthesis, anchorage-dependent and anchorage-independent proliferation, cytoskeletal organization, and gene expression in ras-transformed simian virus 40 (SV40)-immortalized hepatocyte cell lines was measured. An SV40-immortalized cell line (CWSV1), a control neo-transfected and selected cell line (N1), and neo+ras-transfected and selected cell lines (NR3 and NR4) were used for this study. CWSV1 and N1 cells do not grow in soft agarose and are not tumorigenic. The ras-transformed hepatocytes NR3 and NR4 grow in soft agar and are tumorigenic. TGF-beta 1 treatment did not inhibit DNA synthesis or anchorage-dependent growth in the SV40-immortalized hepatocyte cell line CWSV1 or in the ras-transformed hepatocytes. TGF-beta 1 treatment inhibited anchorage-independent growth, increased actin cytoskeleton organization, and altered the morphology of ras-transformed hepatocytes; that is, with regard to all three of these properties, TGF-beta 1-treated ras-transformed hepatocytes more closely resembled the immortalized parent cell line. c-Ha-ras and c-myc RNA levels were not altered in TGF-beta 1-treated NR4 cells. TGF-beta 1 treatment did alter expression of some genes in NR4 cells. The level of expression of alpha 1 integrin RNA was higher in CWSV1 cells than in NR4 cells and increased in NR4 cells when they were treated with TGF-beta 1. Similarly, the levels and profiles of integrins on the cell surface of CWSV1 cells compared to NR4 cells, as determined by cell surface protein iodination, differed and in TGF-beta 1-treated NR4 cells more closely resembled the surface integrin profile for CWSV1 cells.

Actins↗
PubMed1992

Functional analyses of albumin expression in a series of hepatocyte cell lines and in primary hepatocytes.

A series of simian virus 40-immortalized hepatocyte cell lines which are heterogeneous with regard to expression of albumin protein and RNA were characterized for their ability to transcribe the albumin gene. Nascent chain extension assay showed that albumin RNA levels in these cells were determined predominantly at the transcription level. The albumin promoter and enhancer sequences were fused to the bacterial chloramphenicol acetyltransferase gene; the ability of the resulting expression constructs to drive chloramphenicol acetyltransferase expression after transfection into these hepatocyte cell lines was measured. The activity of the albumin promoter and enhancer constructs in primary hepatocytes was also measured. The albumin promoter was expressed differentially in these cells; however, no correlation was found between the transcriptional efficiency of the transfected albumin promoter and endogenous albumin transcription. The albumin enhancer was functional in some but not all albumin-positive cells. The minimal albumin enhancer was mapped to a 330-base pair fragment extending from -9.94 kilobases (kb) to -10.27 kb; three elements within this fragment recently shown to be necessary for enhancer function in a murine hepatocyte cell line were also essential for albumin enhancer function in the rat hepatocyte cell line CWSV1. A transcriptional silencer was identified which could suppress the expression of the homologous albumin promoter and the heterologous herpes simplex virus thymidine kinase promoter. Preliminary analysis localized the albumin silencer between -11 and -12 kb. Our results suggest that multiple regulatory sequences may act cooperatively to determine efficient tissue-specific expression of the albumin gene.

Albumins↗
PubMed1992

[Intraoperative microbiological monitoring in abdominal aortic aneurysms in elective surgery. A review of the literature and the authors' personal experience].

Thirty-one patients, ranging in age from 57 to 78 years (mean 66), with the exclusion of cases with doubtful possible results, underwent abdominal aortic aneurysmectomy for asymptomatic AAA and had cultures from the aneurysmal wall and endovascular thrombus to identify possible microbiological source of future graft infection; 5 (16%) of 31 cultures yielded bacterial growth and the most common organism isolated was staphylococcus epidermidis. During an average follow-up of 15.4 months no graft infection was noted in patients with positive or negative aortic cultured. A literature review stresses the same disparity between positive cultures obtained at the aneurysmectomy and subsequent low graft-infection rate. It is concluded that the aneurysm wall itself does not represent an important source of early or late graft infection and it's suggested that the bacterial presence both in the wall and thrombus could be explained by an exogenous contamination at the operation time.

Aged↗