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Biomedical subjects

C Bianchi

Publications and source records attributed to C Bianchi.

At least 109 records · Page 6Linked to original sources
PubMed1998

Comparative study of the sorption of clomipramine and viloxazine hydrochlorides in Stedim 6 and PVC bags.

The stability of two antidepressant drugs, clomipramine and viloxazine hydrochlorides, was studied as was their possible sorption on Stedim 6, a new multilayer polyethylene-lined film, which was considered comparatively to polyvinyl chloride (PVC) and glass surfaces. Appropriate amounts of the drugs were added to 500 ml of 5% dextrose and 0.9% sodium chloride solutions in Stedim 6 and PVC bags, and in glass flasks, in order to obtain the concentrations currently used in clinical practice. All the containers were stored at room temperature in daylight for 72 hours. Samples were taken at various times and evaluated for remaining drug concentrations by UV spectrometry. The two drugs appeared stable under the given conditions. No concentration decrease was observed in glass flasks. Viloxazine hydrochloride showed an excellent compatibility with the PVC bags, but a slight concentration decrease (about 6-7% in 72 hours) was observed for clomipramine hydrochloride, depending on the contact duration. The compatibility of the two drugs with the new material Stedim 6 was found to be perfect. The behavioral differences observed between the two drugs with regard to PVC are explained in terms of differences of lipophilicity of the drugs. Those observed for a given drug with regard to the two materials are due to the crystalline structure of polyethylene and the amorphous one of PVC.

Adsorption↗
PubMed1998

Susceptibility survey of piperacillin/tazobactam and some beta-lactam comparators in Italy.

From September 1994 to March 1995 an Italian multicenter in vitro study to evaluate the susceptibility of piperacillin/tazobactam compared with that of imipenem, ceftazidime, ceftazidime, ceftriaxone, cefotaxime and ampicillin/sulbactam against aerobic bacterial pathogens isolated in 132 different hospitals, was undertaken. In total, 26,732 isolates were collected but only 25,266 aerobic bacteria were able to be evaluated (16,863 Gram-negative and 8,403 Gram-positive). Escherichia coli was the most frequent pathogen isolated (25.9%) followed by Staphylococcus aureus (14.9%), Pseudomonas aeruginosa (13.9%), Enterococcus faecalis (8.2%) and Klebsiella pneumoniae (5.9%). Piperacillin/tazobactam had a general spectrum of activity (84.8% susceptible strains) comparable to imipenem (87.9%), and was distinctly greater than ceftazidime (71.1%).

Anti-Bacterial Agents↗
PubMed1997

Evolution of the Dmt-Tic pharmacophore: N-terminal methylated derivatives with extraordinary delta opioid antagonist activity.

The delta opioid antagonist H-Dmt-Tic-OH (2',6'-dimethyl-L-tyrosyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid) exhibits extraordinary delta receptor binding characteristics [Ki delta = 0.022 nM; Ki mu/Ki delta = 150,000] and delta antagonism (pA2 = 8.2; Ke = 5.7 nM). A change in chirality of Dmt at C alpha (1, 2, 6, 8, 10, 13) curtailed delta receptor parameters, while replacement of its alpha-amino function by a methyl group (3) led to inactivity; Tyr-Tic analogues 4 and 11 weakly interacted with delta receptors. N-Alkylation of H-Dmt-Tic-OH and H-Dmt-Tic-Ala-OH with methyl groups produced potent delta-opioid ligands with high delta receptor binding capabilities and enhanced delta antagonism: (i) N-Me-Dmt-Tic-OH 5 had high delta opioid binding (Ki delta = 0.2 nM), elevated delta antagonism on mouse vas deferens (MVD) (pA2 = 8.5; Ke = 2.8 nM), and nondetectable mu activity with guinea pig ileum (GPI). (ii) N,N-Me2-Dmt-Tic-OH (12) was equally efficacious in delta receptor binding (Ki delta = 0.12 nM; Ki mu/Ki delta = 20000), but delta antagonism rose considerably (pA2 = 9.4; Ke = 0.28 nM) with weak mu antagonism (pA2 = 5.8; Ke = 1.58 microM; GPI/MVD = 1:5640). N-Me-(9) and N,N-Me2-Dmt-Tic-Ala-OH (15) also augmented delta opioid receptor binding, such that 15 demonstrated high affinity (Ki delta = 0.0755 nM) and selectivity (Ki mu/Ki delta = 20132) with exceptional antagonist activity on MVD (pA2 = 9.6; Ke = 0.22 nM) and weak antagonism on GPI (pA2 = 5.8; Ke = 1.58 microM; GPI/MVD = 1:7180). Although the amidated dimethylated dipeptide analogue 14 had high Ki delta (0.31 nM) and excellent antagonist activity (pA2 = 9.9; Ke = 0.12 nM), the increased activity toward mu receptors in the absence of a free acid function at the C-terminus revealed modest delta selectivity (Ki mu/Ki delta = 1655) and somewhat comparable bioactivity (GPI/MVD = 4500). Thus, the data demonstrate that N,N-(Me)2-Dmt-Tic-OH (12) and N,N-Me2-Dmt-Tic-Ala-OH (15) retained high delta receptor affinities and delta selectivities and acquired enhanced potency in pharmacological bioassays on MVD greater than that of other peptide or non-peptide delta antagonists.

Animals↗
PubMed1997

The muscarinic modulation of [3H]D-aspartate efflux and [Ca2+]i levels in rat cerebellar granule cells.

The effects of ACh on [3H]D-aspartate efflux and on calcium levels ([Ca2+]i) were studied at the same time in sister cultures of rat cerebellar granule cells stimulated with electrical pulses (5-20 Hz) or depolarized with KCl (15-40 mM). ACh, 0.3-1000 nM, greatly facilitated the 10-Hz-evoked tritium efflux while its effect on 20 mM KCl-evoked efflux was significantly smaller. ACh, 10-1000 nM, enhanced [Ca2+]i levels to a limited extent under both experimental conditions. Therefore, ACh facilitation was evident above all on the electrically evoked [3H]D-aspartate efflux. The ACh-mediated responses depended on the activation of M3-muscarinic receptors since these responses were blocked by 4-DAMP. ACh, 50 microM, reduced the [Ca2+]i plateau, determined by prolonged electrical or KCl stimulation. This effect was due to its action of M2-receptors being blocked by AF-DX 116. In conclusion, at very low concentrations, ACh greatly facilitated the electrically evoked [3H]D-aspartate efflux through M3-receptors, while at a higher concentrations, it inhibited, through M2-receptors, the rise in [Ca2+]i caused by prolonged cell depolarization.

Acetylcholine↗
PubMed1997

Helix-inducing alpha-aminoisobutyric acid in opioid mimetic deltorphin C analogues.

The achiral symmetric alpha-aminoisobutyric acid (Aib) replaced the critical N-terminal residues of the amphibian skin opioid deltorphin C (H-Tyr-D-Ala-Phe-Asp-Val-Val-Gly-NH2) without detriment to the physicochemical requirements for delta opioid receptor recognition. Substitutions by the alpha, alpha-dialkyl amino acid in place of D-Ala2 or Phe3, or both, exhibited high delta receptor affinity (Ki delta = 0.12-3.6 nM) and 5-9-fold greater selectivity (Ki mu/Ki delta = 5000-8500) than the parent compound. This is the first definitive demonstration that the D-chirality of alanine and the aromaticity of phenylalanine are replaceable by an achiral alpha, alpha-dialkylated residue without detrimental effects on ligand binding. Incorporation of the mono-alpha-alkyl amino acid L- or D-Ala at the third position also produced highly selective delta ligands (Ki mu/Ki delta = 2000-3500), albeit with reduced delta affinities (Ki delta = 6-15 nM). Replacement of the anionic residue Asp4 by Aib yielded an opioid peptide that fit two-site binding models for the delta receptor (eta = 0.763; P < 0.0001) and displayed dual high affinity for both delta and mu receptors, emphasizing the repulsive effect by a negative charge at mu receptor sites and the insignificance of Asp for delta affinity. Molecular dynamics conformation analyses suggested that Aib residues caused distinct changes in deltorphin C secondary structure when substituted for D-Ala2, Asp4, and simultaneously D-Ala2 and Phe3 but not when substituted for Phe3. These conformational changes might be critical factors for the proper orientation of reactive constituents of residues in the N-terminal region of deltorphin C. Disparities between binding data and functional bioassays of [Aib3] indicated that Phe3 was required for bioactivity in mouse vas deferens but not for interaction with delta opioid receptors in rat brain membranes.

Amino Acid Sequence↗
PubMed1997

Address and message sequences for the nociceptin receptor: a structure-activity study of nociceptin-(1-13)-peptide amide.

Nociceptin (NC) and some of its fragments as well as nociceptin-(1-13)-peptide amide [NC- (1-13)-NH2] and a series of its analogues were prepared and tested in the mouse vas deferens in an attempt to identify the sequences involved in the activation (message) and in the binding (address) of nociceptin to its receptor. The NC receptor that inhibits the electrically evoked twitches of the mouse vas deferens was demonstrated to be distinct from the delta opioid receptor, since naloxone and Dmt-Tic-OH (a selective delta opioid receptor antagonist) block the delta opioid receptor but have no effect on the nociceptin receptor. Results from structure-activity experiments suggest that (a) the entire sequence of NC may not be required for full biological activities, since NC(1-13)-NH2 is as active as NC; (b) fragments of NC have however to be amidated as in NC(1-13)-NH2 in order to be protected from degradation by proteases; (c) cationic residues (as Arg8,12, Lys9,13) appear to play a functional role, since their replacement with Ala in the sequence of NC(1-13)-NH2 leads to inactivity; (d) the N-terminal tetrapeptide Phe-Gly-Gly-Phe is essential for activity: its full length and flexibility appear to be required for NC receptor activation and/or occupation; (e) Phe4 and not Phe1 appears to be the residue involved in receptor activation, since the replacement of Phe1 with Leu has no effect, while that of Phe4 leads to inactivity. Results summarized in this paper indicate that the structural requirements of NC for occupation and activation of its receptor are different from that of opioids, particularly delta agonists.

Amino Acid Sequence↗
PubMed1997

Immediate and delayed effects of in vitro ischemia on glutamate efflux from guinea-pig cerebral cortex slices.

Immediate and delayed effects of glucose deprivation, oxygen deprivation (hypoxia) and both oxygen and glucose deprivation (in vitro ischemia) on glutamate efflux from guinea pig cerebral cortex slices were studied. Immediate effects were evaluated by measuring changes of glutamate efflux during the metabolic insults. Delayed effects were evaluated by measuring the response of the tissue to a 50 mM KCI pulse applied 60 min after the metabolic insults. Deprivation of glucose in the medium did not induce either immediate or delayed effects, while hypoxic condition produced an immediate slight stimulation of glutamate efflux without any delayed effect. Conversely, in vitro ischemia produced both immediate and delayed effects on glutamate efflux. During in vitro ischemia glutamate efflux dramatically increased in a calcium-independent and tetrodotoxin-sensitive manner; this effect was potentiated by a low sodium containing medium. The blockade of the sodium/potassium ATPase exchanger by ouabain caused a glutamate outflow similar to that induced by in vitro ischemia. On the whole, these data demonstrate the central role played by the sodium electrochemical gradient and by the membrane glutamate uptake system in the glutamate overflow induced by in vitro ischemia. Moreover, in slices previously exposed to both oxygen and glucose deprivation the effect of KCI on glutamate efflux was potentiated. This in vitro ischemia-induced delayed potentiation of neurotransmitter efflux, until now unreported in the literature, was found to be selectively restricted to glutamatergic structures and to be mainly due to an enhancement of the exocytotic component of glutamate release.

Animals↗
PubMed1997

Pleural plaques as risk indicators for malignant pleural mesothelioma: a necropsy-based study.

Pleural plaque is recognized as a reliable marker of previous exposure to asbestos. However, it is controversial whether pleural plaque is a risk indicator for asbestos-related malignancies. In the present study, the thoracic cavities were examined for pleural plaques in 3,005 necropsies performed at the Monfalcone Hospital in people aged 15 years or older. Plaques were classified into three classes: 1, small (plaques measuring 1-4 cm in major diameter); 3, large (plaques involving a major part of a hemithorax); and 2, moderate (intermediate conditions). The prevalences of pleural plaques were 70.9% among men, and 24.0% among women. The prevalences of plaques (total plaques, various classes) among subjects with pleural mesothelioma were compared with those observed in the remaining cases. The series included 92 subjects with malignant pleural mesothelioma (82 men and 10 women). Mesothelioma cases showed higher prevalences of total plaques as well as higher prevalences of classes 1, 2, and 3, when compared with controls. These differences reached the statistical significance for total plaques, and classes 2, 3. The present data are consistent with the idea that pleural plaque is a risk indicator for pleural mesothelioma.

Adolescent↗
PubMed1997

Influence of breast- and formula-feeding on plasma cholesterol precursor sterols throughout the first year of life.

We evaluated endogenous cholesterol synthesis and plasma lipid profile longitudinally from birth to 1 year old in infants who were exclusively breast-fed (n = 19) or formula-fed (n = 19) for the first 4 months of life. At 1 and 4 months of age, breast-fed infants had higher plasma total and low-density lipoprotein cholesterol and apolipoprotein B levels than formula-fed infants, whereas plasma mevalonate and lanosterol levels were not different between the two study groups.

Analysis of Variance↗
PubMed1997

Glutamate regulation of dopamine release in guinea pig striatal slices.

The effect of L-glutamic acid (L-Glu) on basal and electrically evoked [3H]-dopamine efflux in guinea pig striatal slices was studied. In the presence of magnesium, L-Glu significantly increased spontaneous [3H]-dopamine efflux. This response was unaffected by the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the non-competitive NMDA receptor antagonist, D-5-methyl-10,11, dihydro-5-H-dibenzo-[a,d]-cyclohepten-5,10-imine maleate (MK-801), the glycine antagonist 7-chlorokynurenic acid (7-CL-KYN) and by the metabotropic receptor antagonist (+)-alpha-methyl-4-carboxyphenyl-glycine (alpha-M4CPG) and L-2-amino-3-phosphonopropionic acid (L-AP3). However, the metabotropic glutamate receptor agonist, trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD), increased spontaneous [3H]-dopamine efflux, as did L-Glu, and this response was completely counteracted by alpha-M4CPG. In the absence of magnesium, L-Glu induced a concentration-dependent increase in basal [3H]-dopamine efflux, which was prevented by MK-801. In electrically stimulated striatal slices L-Glu, applied 25 min before the stimulation, concentration-dependently increased the [3H]-dopamine efflux both in the presence and in the absence of magnesium. This effect was completely prevented by CNQX, but not by MK-801 or DL-2-amino-5-phosphono-pentanoic acid (AP5). On the contrary, L-Glu, applied during electrical stimulation (2 min) in the absence of Mg2+, increased the [3H]-dopamine efflux to 200%, and this effect was partly counteracted by MK-801. These results provide evidence that different subtypes of excitatory amino acid receptors modulate [3H]-dopamine efflux depending on the functional state (rest or activity) of the nerve endings. The spontaneous [3H]-dopamine efflux appears to be controlled by metabotropic receptors in the presence of Mg2+ and by NMDA receptors in its absence. Conversely, the AMPA/kainate receptors facilitate the electrically evoked [3H]-dopamine efflux in the presence of Mg2+, whereas the NMDA receptors appeared to be operative, in the absence of Mg2+, as long as L-Glu was applied simultaneously with the electrical stimulation.

Animals↗
PubMed1997

Characterization of glutamate and [3H]D-aspartate outflow from various in vitro preparations of the rat hippocampus.

The characteristics of high-K+ and electrically evoked endogenous glutamate and [3H]D-aspartate release have been studied in multiple in vitro preparations of the rat hippocampus (transverse slices, granule cells cultures, synaptosomes and mossy fibre synaptosomes) under similar experimental conditions. High external K+ concentrations evoked [3H]D-aspartate and endogenous glutamate overflow in a concentration-dependent manner in all preparations (except it was not possible to measure endogenous glutamate outflow from granule cells). This effect was tetrodotoxin-insensitive but partially calcium-dependent. In slices, field electrical stimulation evoked an overflow of endogenous glutamate, but not of [3H]D-aspartate, in a frequency-dependent manner. This effect was concentration-dependently amplified by the glutamate uptake inhibitor L-trans-pyrrolidine-2,4-dicarboxylic acid (t-PDC). The electrically evoked glutamate overflow in the presence of t-PDC was tetrodotoxin-sensitive and calcium-dependent. In primary dentate gyrus cell cultures, electrical stimulation evoked an overflow of [3H]D-aspartate in a frequency-dependent manner, while endogenous glutamate outflow was not detectable. This effect could be inhibited by tetrodotoxin and by the N-type calcium channel blocker omega-conotoxin GVIA. Finally, the effect of adenosine has been studied in order to assess the pharmacological modulability of [3H]D-aspartate and endogenous glutamate stimulation-induced overflow. Adenosine was found to inhibit 35 mM K(+)- and 20 Hz electrical stimulation-induced [3H]D-aspartate and endogenous glutamate overflow. These effects were all prevented by the A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT). These data are in line with the hypothesis that reuptake plays a role in regulating glutamate release, and that [3H]D-aspartate represents a valid marker of endogenous glutamate under most (but not all) experimental conditions.

Adenosine↗
PubMed1997

Post-ischemic recovery of acetylcholine release in vitro: influence of different excitatory amino acid receptor subtype antagonists.

The release of endogenous acetylcholine was measured in electrically (5-20 Hz) stimulated guinea pig cerebral cortex and caudate nucleus slices under ischemic (hypoxic and glucose-free) conditions. Ischemia reduced acetylcholine release by 40-90%; the inhibition depended on the duration of ischemia (10-30 min) while the extent of post-ischemic recovery was inversely related to it. Caudate nucleus slices displayed a higher sensitivity to ischemia than did cortical slices. To test the effects of excitatory amino acid receptor antagonists on the ischemia-induced reduction of acetylcoline release and on its post-ischemic recovery, the following drugs were used: 5-methyl-10,11-dihydro-5-H-dibenzo-[a,b]-cyclohepten-5,10-imine (MK-801,-a blocker of the N-methyl-D-aspartate [NMDA] receptor-linked channel), 7-chloro-kynurenic acid (7-Cl-KYN) and (E)-3-[2(phenylcarbamoyl)ethenyl]-4,6-dichloroindole-2-carboxylic acid sodium salt (GV150526A, blockers of the glycine site of the NMDA receptor), eliprodil, (an antagonist at the polyamine site of the NMDA receptor), and 6-cyano- 7-nitro-quinoxalin-2,3-dione (CNQX, a D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid [AMPA] receptor antagonist). These did not modify the time-course and the extent of ischemia-induced inhibition but improved post-ischemic recovery in a concentration dependent manner. GV 150526A and CNQX appeared to be more effective in the cerebral cortex. Only eliprodil was devoid of any effect in both areas. The evaluation of acetylcholine release from brain slices represents a suitable in vitro model to quantify the effectiveness of drugs in favouring recovery from the cholinergic presynaptic failure induced by ischemic conditions. The different effects of the excitatory amino acid receptor antagonists cited above, depending on the brain areas considered and the receptor subtypes involved, may be of interest in view of their therapeutic potential.

Acetylcholine↗
PubMed1997

Inhibitory cholinergic control of endogenous GABA release from electrically stimulated cortical slices and K(+)-depolarized synaptosomes.

In the present study we characterize the optimal experimental conditions under which to investigate the cholinergic regulation of endogenous electrically evoked gamma-aminobutyric acid (GABA) release from guinea pig cortical slices. Superfusion with the neuronal GABA reuptake inhibitor, SKF89976A (10 microM) caused cortical GABA release to be linearly correlated with the frequency of electrical stimulation (5, 10, 20 Hz). Electrically evoked GABA release (10 Hz) was tetrodotoxin-sensitive and Ca(2+)-dependent and was under GABAB autoreceptor control. Under these experimental conditions, acetylcholine (0.1-10 microM) and physostigmine (30 microM) decreased the electrically evoked GABA release while the M2 receptor antagonist AFDX-116 (0.01-0.1 microM) counteracted these effects. Similar results were also observed in a cortical synaptosomal preparation stimulated with K+ (10 mM). These findings demonstrate an inhibitory cholinergic regulation of electrically evoked GABA release via M2 receptors located on cortical GABAergic terminals.

Acetylcholine↗
PubMed1997

Laparoscopic cholecystectomy and gallbladder cancer: a diagnostic and therapeutic dilemma.

The correct treatment strategy of patients with unsuspected gallbladder cancer undergoing laparoscopy, and the prevention of delayed diagnosis are current issues. We report a case of late diagnosis with umbilical metastasis and poor survival. A policy of careful inspection of the gallbladder and a cautious strategy in the case of gross alteration of its external morphology seems advisable during laparoscopic cholecystectomy. Although no agreement exists concerning the best treatment in the event of delayed diagnosis, the adopted strategy is contingent on patient status, disease stage and the possibility of performing appropriate follow-up.

Aged↗
PubMed1997

Bone turnover in neonates: changes of urinary excretion rate of collagen type I cross-linked peptides during the first days of life and influence of gestational age.

New markers have been used to monitor the changes of bone turnover occurring during growth. Data on bone turnover rate during the perinatal period are, however, very scarce. In the present study we evaluated bone turnover rate, assessed by the measurement of urinary N-terminal telopeptide of type I collagen (NTx) concentrations, at different gestational ages, and we documented the trend of bone turnover rate occurring in the first days after birth. Urine samples were obtained from 83 healthy full term newborn infants, 16 preterm, and 17 infants of diabetic mothers (IDMs). The first miction after birth was collected. Urine samples were also collected 24 and 48 h after birth. NTx was measured by an enzyme-linked immunosorbent assay (Osteomark, Ostex International, Inc. Seattle, WA). The relationship between NTx at birth and all the other variables has been evaluated using multiple regression analysis. The changes of NTx excretion over time and the effect of the groups were studied by multivariate analysis of variance (MANOVA) for repeated measures. We found a remarkable association between gestational age and NTx concentrations at birth (R = 0.56; p < 0.00001). NTx concentrations showed a progressive decrement, reaching a nadir between the 38th and the 42nd week of gestation. The NTx concentrations changed significantly during the first 48 h of life in the three groups. Moreover, preterm infants had NTx excretion values at birth significantly higher than full term infants (p < 0.001), whereas NTx excretion rates of IDMs were not different from those of the other two groups of subjects. In conclusion, gestational age seems to be the major determinant of bone turnover in neonates; NTx excretion rate is higher before term, it slows in proximity of delivery, and it increases significantly during the first 48 h of life. Preterm infants have higher bone turnover rate than full term infants. NTx excretion rate of IDMs was comparable with those of the control subjects.

Biomarkers↗
PubMed1997

Opioid diketopiperazines: synthesis and activity of a prototypic class of opioid antagonists.

Discovery of high affinity and ultraselective delta opioid dipeptide antagonists composed of 2',6'-dimethyl-L-tyrosyl (Dmt) and 1,2,3,4-tetrahydroisoquinoline-3-carboxylic (Tic) served as the basis for the conformationally restricted diketopiperazine cyclo(Dmt-Tic) and related open chain analogues. These peptides primarily bind to delta opioid receptors: c(Dmt-Tic) displayed 30- to 50-fold higher delta affinity (Ki delta) than its diastereo-isomeric analogues and more than 4000-fold greater than its Tyr cognate; all of the c(Tyr-Tic) analogues were essentially inactive; c[(N-methyl)Dmt-Tic] lost 5-fold in Ki delta, while Ki mu increased 10-fold to yield a nonselective peptide; and the c(Dmt-Phe) series exhibited considerably reduced binding which indicated a synergism between Dmt and Tic in the binding mechanism. Whereas acetyl-Dmt-Tic linear peptides weakly interacted with opioid receptors, Ac-Dmt-Tic-NH2, exhibited better delta antagonist activity than c(Dmt-Tic) and greater delta receptor selectivity (Ki mu/Ki delta = 570). A three point attachment hypothesis for the interaction between c(Dmt-Tic) and the delta receptor was proposed: hydrophobicity imparted by the aromatic rings and the methyl groups of Dmt, hydrogen bonding through the tyramine hydroxyl group, and cation-pi interactions were suggested as contributing factors in binding the diketopiperazine in the receptor pocket. Although c(Dmt-Tic) exhibited a weak antagonist activity with mouse vas deferens, this diketopiperazine may provide a scaffolding for the formation of more potent antagonists for potential therapeutic applications.

Animals↗
PubMed1997

Latency periods in asbestos-related mesothelioma of the pleura.

Latency periods (time intervals elapsing between first exposure to asbestos and death) were examined in 421 cases of malignant pleural mesothelioma, diagnosed in the Trieste-Monfalcone area, Italy. Occupational data were collected from the patients or from their relatives by personal or telephone interviews. Routine lung sections were examined for asbestos bodies in 370 cases. Latency periods, calculated in 312 cases, ranged from 14 to 72 years (mean 48.7, median 51). Latency periods differed significantly from one occupational group to another. Mean latency periods were 29.6 among insulators, 35.4 among dock workers, 43.7 in a heterogeneous group defined as various, 46.4 in non-shipbuilding industry workers, 49.4 in shipyard workers, 51.7 among women with a history of domestic exposure to asbestos, and 56.2 in people employed in maritime trades. The ANOVA test indicated a correlation between latency periods and occupational groups. Latency periods in people with asbestos bodies visible in routine lung sections did not differ from those seen in cases with no evidence of asbestos bodies. These data suggest that intensity of exposure is a relevant, but not the only, factor in determining the duration of latency periods.

Adult↗