Biomedical subjects

G Tringali

Publications and source records attributed to G Tringali.

At least 19 recordsLinked to original sources

PubMed2007

Therapeutic patient education in oncology: pedagogical notions for women's health and prevention.

Therapeutic patient education has been defined by the World Health Organization as a comprehensive approach to support patients and their families to better understanding of their diseases. In oncology, the contribution of therapeutic education may enable the patients to have adequate information of the illness, to actively participate in the management of the disease, to understand how to live with the illness, to learn how to face the critical moments of the clinical course, and to live in harmony with all health professionals. In addition, there may be several advantages for health professionals: a reduction in emotional labour, increased professional satisfaction, and a reduction in the potential tensions and conflicts with patients and their relatives. We suggest that therapeutic patient education in oncology may be useful for both patients and health professionals and probably lead to a reduction in the costs of healthcare delivery.

Female↗

PubMed2004

Simultaneous estimation of a Y-specific fragment, an X-specific fragment and sex determination of forensic studies in real-time PCR.

The human sex test in forensic multiplexes is based on the amelogenin gene on both the X and Y chromosomes commonly used in sex genotyping. In this work sex determination across the quantification of nuclear DNA was achieved by real-time PCR of a segment of the X-Y homologous amelogenin (AMG) gene that allowed the simultaneous estimation of a Y- and an X-specific fragment. The AMG real-time PCR design has been used to quantify a set of forensic casework samples.

Amelogenin↗

PubMed2004

Rapid and efficacious real-time quantitative PCR assay for quantitation of human DNA in forensic samples.

A reliable quantification of human DNA is necessary in the process of routine forensic human identification. When DNA is degraded, contaminated or associated with inhibitors, is important to accurately estimate the concentration of extracted DNA prior to perform an analysis based on nuclear markers amplified. In this work, a new approaches to DNA quantification employees the use of a real-time fluorescence probe system. The real-time PCR assay is highly sensitive, specific, rapid, cost-effective and flexible assay for analysis of forensic casework samples, can perform with DNA of poor quality and detect specifically amplifiable DNA rather than total DNA for STR analysis.

DNA↗

PubMed2004

Supercritical fluid extraction of polycyclic aromatic hydrocarbons from marine sediments and soil samples.

Supercritical fluid extraction (SFE) was used to extract polycyclic aromatic hydrocarbons (PAH) from a certified sample of marine sediment. This sample contains a great number of organic pollutants that are present in low concentrations. The extractions were carried out at 50 and 80 degrees C, at a pressure varying from 230 to 600 bar and using CO2 in the supercritical phase and the effect of three organic modifiers (methanol, n-hexane and toluene), added at 5%/vol, at the same temperature and pressure conditions, were then considered. PAHs were characterized by GC-MS and the recover yield was estimated for 6 PAHs that were representative of those present in the sample, according to their molecular weight and to the number of condensed rings. The analytical conditions giving the best recovery efficiency were used on an unpolluted soil sample spiked with 11 PAHs of environmental importance at a concentration similar to that certified for the sediment sample. An increase in the yield of recovered PAHs, using methanol as co-solvent, was observed while higher temperatures caused a negative effect on the quantity of recovered pollutants. The recovery yield for PAHs from the spiked soil sample was measured and found to be greater than 90%. Better recoveries were obtained for those compounds with higher molecular weight.

Chromatography, Gas↗

PubMed2004

Association of IL-1 RN*2 allele and methionine synthase 2756 AA genotype with dementia severity of sporadic Alzheimer's disease.

BACKGROUND: Genetic polymorphisms of APO-E, homocysteine, and the IL-1 gene cluster (IL-1A, IL-1B, receptor antagonist IL-1RN) are associated with sporadic Alzheimer's disease and may involve interdependent pathways of neuronal toxicity. OBJECTIVE: To determine whether these polymorphisms and the genetic determinants of homocysteine (methylenetetrahydrofolate reductase, MTHFR; methionine synthase, MTR; transcobalamin, TC) are associated with an increased risk of severe dementia in Alzheimer's disease. METHODS: 152 patients with Alzheimer's disease and 136 controls were studied. The association of occurrence and dementia severity (Reisberg score <6 and >or=6) of Alzheimer's disease with APO-E, IL-1A, IL-1B, IL-1RN, MTHFR677 C-->T and 1298A-->C, MTR 2756 A-->G, and TC 776 C-->G polymorphisms was evaluated by multivariate logistic regression analysis after adjustment for age, sex, and age of onset of Alzheimer's disease. RESULTS: IL-1A TT and IL-1B CT/TT associated genotypes were at risk of Alzheimer's disease (odds ratio 4.80 (95% confidence interval, 1.32 to 17.40), p = 0.017); the MTR 2756 AA genotype was at risk of severe dementia (OR 2.97 (1.23 to 7.21), p = 0.016); IL-1 RN*2 was protective (OR 0.28, (0.11 to 0.69), p = 0.006). Allele epsilon4 of the APO-E and IL-1B CC genotypes increased the risk of severe Alzheimer's disease associated with the MTR 2756 AA genotype by 3.3-fold and 1.5-fold, respectively. CONCLUSIONS: Distinct determinants of the IL-1 gene cluster are related to the generation and progression of Alzheimer's disease. MTR only influences progression of the disease, which may be enhanced by carriage of allele epsilon4 of APO-E.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

PubMed2003

Ghrelin is released from rat hypothalamic explants and stimulates corticotrophin-releasing hormone and arginine-vasopressin.

Ghrelin and synthetic growth hormone secretagogues have diverse effects on the hypothalamus including effects on appetite and the growth hormone axis as well as on the hypothalamus-pituitary-adrenal (HPA) axis. We previously studied the effect of synthetic growth hormone secretagogues on CRH and AVP release from rat hypothalami in vitro, and now report on the effects of ghrelin on CRH and AVP release. The ghrelin protein content and ghrelin output from rat hypothalamic explants was measured using a specific novel ghrelin enzyme immunoassay. The effect of 10(-8) M to 10(-6) M ghrelin on CRH and AVP release was studied in the rat hypothalamic explants, where stimulation with des-octanoyl ghrelin was used as control. The presence of both ghrelin mRNA and protein could be shown in the rat hypothalamus. Ghrelin output was detected in the incubation fluid of rat hypothalamic explants and could be stimulated with high potassium concentrations. Our data also demonstrated a dose-dependent effect of ghrelin on both CRH and AVP release, while des-octanoylated ghrelin showed no effect on either peptide. In summary, the current data suggest that ghrelin is expressed in the hypothalamus both at RNA and the protein levels. Ghrelin stimulates the HPA axis in the rat via stimulation of both CRH, and particularly, AVP release from the hypothalamus. The local autocrine/paracrine and endocrine effects of ghrelin in the hypothalamus could influence all the hormonal systems involved in ghrelin effects, including growth hormone release, the HPA axis and appetite.

Animals↗

PubMed2002

Evaluation of oxidative stress in diabetic patients after supplementation with a standardised red orange extract.

Diabetes mellitus is associated with a high oxidative stress level, resulting from an imbalance between free radicals or reactive oxygen species production and the antioxidant systems. Inhibition of these oxidative processes by co-adjuvant therapy could therefore prevent, or at least delay, the onset and/or the development of long-term diabetic complications. Dietary supplementation with plant biophenols may be a successful strategy to decrease this risk of pathological complications. The Red Orange Complex (ROC) is a standardized red orange extract containing, as its main active principles, phenolic compounds (anthocyanins, flavanones and hydroxycinnamic acids) as well as ascorbic acid. The aim of the present preliminary study was to evaluate the effects of short-term (2 mo) dietary supplementation with ROC (50 mg/d, orally) on some serum non-invasive biomarkers of oxidative stress (total antioxidant status, or TAS, levels of thiol groups and levels of free radicals) in a group of 33 patients with Type 2 diabetes, in comparison with a group of 28 healthy volunteers. The results obtained demonstrate that in diabetic patients supplementation with ROC can improve blood levels of thiol groups on proteins (an indirect measurement of glutathione activity in serum); furthermore, it can elicit a marked decrease in serum free radical levels, in patients with high blood oxidative stress status. However, ROC supplementation appeared unable to modify serum TAS. Finally, the glycemic profile remained stable during the study period in all subjects, and no unpleasant side effects were reported. In conclusion, the treatment of diabetic patients with ROC might be of therapeutic benefit in order to protect against diabetes complications that are partially due to uncontrolled lipid oxidation. D

Aged↗

PubMed2001

HIV-1 Gp120 protein modulates corticotropin releasing factor synthesis and release via the stimulation of its mRNA from the rat hypothalamus in vitro: involvement of inducible nitric oxide synthase.

In the present study, we examined whether the human immunodeficiency virus type I (HIV-I) gp120 coat protein can modulate corticotropin releasing factor (CRF) secretion by using the incubation of rat hypothalamic explants as an in vitro model. Treatment of the hypothalamic fragments with recombinant gp120 resulted in a time- and concentration-dependent increase in CRF release. The maximal dose of 10 nM gp120 increased CRF release by 56.4% after 1 h, and 78.4% after 3 h, as compared with their respective controls. The intra-hypothalamic amount of CRF was also increased by 54.7% and 77.3% vs. controls after 1 and 3 h, respectively. Moreover, the action of gp120 was blocked by pretreatment with cycloheximide, suggesting that the viral protein modulates CRF secretion via an increase in its synthesis. We also investigated the effects of gp120 on CRF gene expression. RNase protection analyses of total RNA isolated from the explants indicated that 10 nM gp120 significantly increases CRF mRNA in a time-dependent manner. Furthermore, gp120 did not modify CRF mRNA stability, suggesting that the viral protein modulates CRF gene expression at the transcriptional level. Analysis of the mechanisms that mediate gp120-induced CRF synthesis was conducted. The incubation of the explants with recombinant interleukin-1 (IL-1) type I receptor antagonist (hrIL-1 ra) did not antagonize the actions of gp120 at 1 and 3 h, indicating that the effect of the latter is independent of IL-1 mediated mechanisms. The involvement of some second messenger pathways was also investigated. Specific inhibitors of cAMP-PKA, cyclo-oxygenase or heme oxygenase pathways failed to antagonize the gp120-induced increase in CRF production. By contrast, incubation with nonselective inhibitors of nitric oxide synthase (NOS), L-NAME and L-NNA, or aminoguanidine (AG), a selective inhibitor of inducible NOS (iNOS), blocked CRF release and, AG, its mRNA accumulation, stimulated by gp120, whereas selective inhibitors of endothelial and neuronal NOS had no effect. In addition, only L-NAME, L-NNA and AG were able to inhibit the gp120-stimulated production of nitrites. These results indicate that gp120 directly stimulates CRF gene expression and peptide synthesis from the rat hypothalamus in vitro via the activation of iNOS. Therefore, the actions of this viral protein on the HPA axis may, in part, reflect its ability to modulate CRF synthesis.

Animals↗

PubMed2001

A functional link between heme oxygenase and cyclo-oxygenase activities in cortical rat astrocytes.

Recent evidence shows that the activation of heme oxygenase (HO) within the CNS is associated with increased prostanoid production. In this study, we investigated whether changes in HO activity induced by pharmacological manipulation are associated with parallel variations in cyclo-oxygenase (COX) activity and prostaglandin production in an in vitro paradigm of CNS cells, i.e. primary cultures of rat cortical astrocytes. Pharmacological tools commonly used to induce changes in HO activity, namely the HO enhancers hemin and CoCl(2) as well as the HO inhibitor Sn-mesoporphyrin-9 (SnMP9), were tested in our model, and the variations in COX activity associated with the above treatments were monitored by measuring a COX end product, prostaglandin E2 (PGE2), released into the incubation medium. We found that the increase in HO activity induced by hemin and/or CoCl(2) was not consistently associated with increases in prostaglandin production, whereas HO inhibition by SnMP9 was normally followed by a decrease in PGE2 release. The above effect was observed after both acute (30 min) and prolonged (24 hr) incubations, suggesting that baseline HO activity contributes to the maintenance of normal PG production in this model. Experiments with the stable HO end products biliverdin and bilirubin suggest that these products may play a role in mediating HO-induced COX activation.

Analysis of Variance↗

PubMed2001

Evidence for a functional link between the heme oxygenase-carbon monoxide pathway and corticotropin-releasing hormone release from primary cultures of human trophoblast cells.

The gene expression and synthesis of both constitutive and inducible heme oxygenase (HO) isoforms have been recently described in human placental cells, but the functional role(s) of this biochemical pathway in placental physiology and pathology is still unclear. In the present study, we have investigated whether HO activity is involved in the control of CRH secretion from trophoblast cells. Fluctuations in HO activity were induced in primary cultures of human trophoblast cells using well-known activators and inhibitors of HO, and the subsequent changes in CRH secretion were monitored measuring CRH immunoreactivity released into the incubation medium. It was found that the increase in HO activity induced by hemin or cobalt chloride (CoCl(2)) was associated with parallel significant increases in CRH release. This effect was probably caused by the gaseous HO end-product, carbon monoxide (CO), because it was blocked by the HO inhibitor tin-mesoporphyrin-9, but it was not mimicked by stable HO end-products, biliverdin and bilirubin. We have also investigated whether stimulation of CRH release induced by HO was mediated by the cyclooxygenase (COX) pathway. Indeed, hemin also caused significant increases in PGE2 release in this experimental paradigm. However, CoCl(2), which also enhances CRH release, had no stimulatory effect and actually inhibited PG secretion; moreover, a nonselective COX inhibitor, indomethacin, failed to counteract hemininduced CRH release. Taken collectively, these findings suggested that modulation of CRH secretion by the HO-CO system occurs through a mechanism independent of COX activity.

Carbon Monoxide↗

PubMed2000

Evidence that hydrogen sulphide can modulate hypothalamo-pituitary-adrenal axis function: in vitro and in vivo studies in the rat.

The gas hydrogen sulphide (H2S) is normally produced in large amounts in the central nervous system during the metabolism of sulphur-containing aminoacids. H2S was recently shown to influence long-term potentiation in the rat hippocampus; this finding suggested that the gas may act as a neuromodulator in the brain. We therefore tested the effect of the gas on the release of corticotropin-releasing hormone (CRH) from rat hypothalamic explants. CRH immunoreactivity in the incubation media was taken as a marker of peptide release. We found that the addition of NaHS to incubation media was consistently associated with a concentration-dependent decrease in KCl-stimulated CRH release, whereas basal secretion was unaffected. Increased endogenous H2S production may be also obtained using an indirect precursor of H2S formation, S-adenosyl-L-methionine (SAMe). The latter mimicked the effects of NaHS, since it reduced potassium-stimulated CRH release. In vivo, SAMe showed no effect on hypothalamo-pituitary-adrenal (HPA) function under resting conditions, but inhibited stress-related glucocorticoid increase.

Adrenal Glands↗

PubMed2000

Circulating interleukin-1-beta levels after acute and prolonged exposure to low temperatures: human and rat studies.

In this study we have investigated whether IL-1 acts as a mediator of stress responses elicited by exposure to low temperatures. We also sought whether IL-1 is released from the adrenal gland under basal conditions or after exposure to low temperatures. Normal and adrenalectomized (ADX) rats were used for acute studies, whereas the effects of a prolonged exposure were investigated in a group of human subjects during a 45-day stay in Antarctica. Circulating levels of interleukin-1beta (IL-1beta) were taken as a marker of systemic IL-1 production both in humans and rats. In the latter, serum corticosterone (Cort) was also estimated. In intact rats, exposure to low temperatures (-25 or -35 degrees C) for 30 or 90 min did not modify circulating IL-1beta levels with respect to controls taken at +20 degrees C. Adrenalectomy was associated with an increase in cytokine levels only in the group exposed to -35 degrees C for 90 min; such increase is statistically significant compared to all groups of normal rats, whatever the experimental condition, as well as to ADX rats exposed to +20 degrees C and -25 degrees C for 30 and 90 min. In normal rats, the increase in circulating Cort levels was already maximal after exposure to -25 degrees C for 30 min. In humans, circulating IL-1beta levels after 45 days in Antarctica were significantly lower than those measured on arrival in the same subjects. Thus, no change in circulating IL-1beta was associated with acute low-temperature stress in rats, whereas a marked decrease in serum cytokine was observed in humans after prolonged exposure to a cold environment. Experiments with ADX rats indicated that the contribution of the adrenal glands to total-body IL-1beta production is negligible or absent.

Adrenalectomy↗

PubMed2000

Signaling pathways involved in lipopolysaccharide stimulation of prostaglandin production by rat hypothalamic astroglial cells.

The aim of this study was to investigate the mechanisms through which bacterial lipopolysaccharide (LPS) stimulates prostaglandin (PG) production in rat hypothalamic astroglial cells in vitro. The latter were treated with LPS alone or LPS plus antagonists of the interleukin-1 (IL-1) and nitric oxide (NO) pathways, and the subsequent changes in cyclooxygenase (COX) activity were monitored by measuring a COX end-product, prostaglandin E2 (PGE2), released into the incubation medium. LPS produced a concentration-dependent increase in PGE2 release from astroglia after 24 h incubation; experiments with selective antagonists showed that the increase in PGE2 release induced by LPS may be, at least in part, mediated by IL-1 and NO.

Animals↗

PubMed1999

Depolarization and a NO-donor stimulate interleukin-1beta release from the rat hypothalamus via a mechanism involving caspase 1.

Previous in vitro studies showed that rat hypothalamic explants release interleukin-1beta (IL-1beta); such release is significantly increased by several stimuli including 56 mM KCl and NO-donors in 20-min experiments. Here we tested the hypothesis that the above stimuli act via a mechanism involving cleavage of the IL-1beta precursor by interleukin-1beta converting enzyme (ICE, also referred to as caspase-1). A cell-permeable form of the caspase-1 inhibitor I and two different stimuli, 56 mM KCl and sodium nitroprusside (SNP), were used. The inhibitor was able to counteract the increase in IL-1beta release induced by both K+ and SNP, while having no effect on basal release.

Animals↗

PubMed1999

Inhibition of heme oxygenase in the central nervous system potentiates endotoxin-induced vasopressin release in the rat.

Previous in vitro studies have shown that increases in endogenous carbon monoxide (CO) generation via activation of the enzyme heme oxygenase (HO) within the rat hypothalamus are associated with the reduced release of the neuropeptides, vasopressin (AVP) and oxytocin, while evidence concerning corticotrophin-releasing hormone (CRH) is controversial. The present study investigated whether there is also a functional relationship between the HO-CO pathway and AVP and corticosterone (Cort) in vivo. Male Wistar rats were challenged with bacterial lipopolysaccharide (LPS) at doses producing significant activation of the hypothalamo-pituitary-adrenal (HPA) axis. LPS was given alone or after pretreatment with the HO inhibitor Sn-protoporphyrin-9 (SnPP9). The latter was injected either intraperitoneally (i.p.) or by intracerebroventricular (i.c.v.) route. SnPP9 given i.p. failed to modify either basal or LPS-stimulated levels of AVP and Cort. On the contrary, i.c.v. SnPP9 strongly potentiated LPS-induced AVP release and significantly enhanced basal serum Cort levels, although it failed to potentiate stimulation by LPS. The LPS + i.c.v. SnPP9 also significantly reduced the hypothalamic stores of AVP compared to controls, correlating with increased circulating levels of AVP. Taken collectively, these data are in concordance with previous in vitro observations showing that the HO-CO pathway acts centrally to attenuate endotoxin-stimulated AVP release, while having less effects on the pituitary-adrenal axis.

Animals↗

PubMed1999

Bacterial lipopolysaccharide increases prostaglandin production by rat astrocytes via inducible cyclo-oxygenase: evidence for the involvement of nuclear factor kappaB.

This study was set to investigate the mechanisms through which bacterial lipopolysaccharide (LPS) stimulates prostaglandin (PG) production in rat astrocytes. Primary cultures of rat hypothalamic astrocytes were established. Cells were treated with LPS alone or LPS plus antagonists of various pathways, and the subsequent changes in cyclo-oxygenase (COX) activity were monitored by measuring a COX end product, PGE2, released into the incubation medium. It was found that (i) LPS produced a concentration-dependent increase in PGE2 release from astrocytes. The potency of LPS was significantly increased by the addition of serum into the incubation medium; (ii) after 24 h of incubation, inducible COX (COX-2) accounts for most of the LPS-stimulated PG production, as the latter was markedly reduced by dexamethasone and the specific COX-2 inhibitor NS 398; and (iii) nuclear factor kappaB appears to play a role in the activation of COX-2 induced by LPS, since certain inhibitors of this transcription factor were able to antagonize, at least in part, the effects of LPS on PGE2 release.

Animals↗

PubMed1999

The effect of growth hormone secretagogues and neuropeptide Y on hypothalamic hormone release from acute rat hypothalamic explants.

Growth hormone (GH) secretagogues (GH-releasing peptides and their non-peptide analogues) stimulate growth hormone release via specific G-protein coupled receptors both directly from the pituitary gland and through stimulation of the hypothalamus. The exact mechanism of action in the hypothalamus is not known. The presence of endogenous GH releasing hormone (GHRH) seems to be necessary for the in-vivo actions of growth hormone secretagogues (GHSs), but data suggest that further factors must be involved as well. The effect of GHSs is not entirely specific for the GH axis; they release prolactin and stimulate the hypothalamo-pituitary-adrenal axis causing elevations in circulating ACTH and cortisol levels in both animal and human studies. Recently, it has also been suggested that GHSs stimulate hypothalamic neuropeptide Y (NPY) neurones. In the present study, we have therefore investigated the direct effect of several GHSs (GHRP-6, hexarelin and the non-peptide analogues L-692, 429 and L-692, 585) on GHRH, somatostatin (SS), corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) release in vitro in an acute rat hypothalamic incubation system. We also assessed the effect of NPY on GHRH, SS and AVP release. Freshly removed hypothalami were incubated in control media for 20 min and then in 1-4 consecutive 20-min periods in each of the test substances at different concentrations. There was no significant change in either the basal or potassium-stimulated release of GHRH or SS at low concentrations of any of the secretagogues; however, at millimolar doses a paradoxical inhibition of GHRH was observed with GHRP-6, hexarelin and L-692 585 (data are expressed as the ratio of treated to preceding basal release; at 20 min control group: 0.97+/-0.02, GHRP-6: 0.55+/-0.04, P<0.001 compared to control group; hexarelin: 0. 56+/-0.06, P<0.001, L-692,585: 0.70+/-0.03, P<0.001), while SS was stimulated after 60 or 80 min (at 80 min control: 0.80+/-0.03, hexarelin: 1.23+/-0.07, P<0.05 and L-692,585: 1.37+/-0.11, P<0.05). GHSs stimulated hypothalamic AVP release (at 20 min control: 0. 99+/-0.06 ratio to basal release, 10-4 M concentration of GHRP-6: 6. 31+/-1, P<0.001, hexarelin: 1.88+/-0.4, P<0.01, L-692,429: 1.90+/-0. 5, P<0.05 and L-692,585: 2.34+/-0.96, P<0.01), while no stimulatory effect was found on CRH release. NPY significantly stimulated SS and inhibited basal and potassium-stimulated GHRH release, while potentiating potassium-evoked AVP secretion. The Y1 receptor antagonist BIBP 3226 did not inhibit the effects of NPY on SS, GHRH or AVP release. We therefore conclude that, in this in-vitro rat hypothalamic incubation model, growth hormone secretagogues stimulate the release of AVP but have no effect on either GHRH, SS or CRH at low doses; at high doses paradoxically they inhibit the hypothalamic GH axis similar to in-vivo data in the rat. We speculate that these effects might be mediated by NPY.

Animals↗

PubMed1998

Hypothalamic interleukin-1 in physiology and pathology.

The occurrence of interleukin-1 (IL-1) in the brain is usually associated with pathological events of the central nervous system (CNS), although there is evidence that the cytokine may also play a role in physiological processes. The ability of IL-1 to induce a damage in the CNS is dependent on the type of cell producing the cytokine and the length of exposure; on this regard, it is possible to distinguish between the minutes-to-days and the days-to-years time-frames. While the long-term action of IL-1 in the CNS is unambiguously associated with the activation of glial cells as well as the occurrence of chronic disorders such as Alzheimer's disease and AIDS-related dementia, it remains to be established whether glial cells, 'interleukinergic' neurons or both cell types are involved in CNS responses to acute noxiae, such as physical stress (restrain stress, nociceptive stimulation) or immune-inflammatory challenges.

AIDS Dementia Complex↗