Biomedical subjects

S Milani

Publications and source records attributed to S Milani.

At least 37 records · Page 2Linked to original sources

PubMed2000

Longitudinal distance standards of fetal growth. Intrauterine and Infant Longitudinal Growth Study: IILGS.

BACKGROUND: Most ultrasonographic fetal growth norms are derived from cross-sectional data or from longitudinal data treated as coming from cross-sectional studies, although only longitudinal models may detect particular aspects of fetal growth shape, such as peak of growth velocity. MATERIALS AND METHODS: The sample included 238 singleton normal pregnancies. All the fetal traits under study (biparietal diameter, occipito-frontal diameter, head circumference, femur diaphysis length and abdomen circumference) were measured according to the classical ultrasound techniques by highly trained operators. Individual growth profiles (made up of 5 to 9 measures) were taken at regular intervals between the 12th and the 40th week. Growth norms were traced by means of a two-stage linear model: (I) a 3-constant fetal growth function was fitted to each individual growth profile, (II) growth centiles were based upon the weighted mean and covariance matrix of the individual growth constants. RESULTS: Fetal growth curves show a sigmoid shape with a maximum slope (i.e. a peak growth velocity) which occurs earlier for head diameters (about 18 weeks), later for femur diaphysis length (20 weeks) and abdomen circumference (22 weeks). During intrauterine growth, all traits show a progressive increase in interindividual variability, which is more prominent for abdomen circumference. CONCLUSION: The mathematical model applied to a large sample of growth profiles provided a satisfactory description of the individual fetal development and its biological variability, and allowed the construction of longitudinal distance standards useful for clinical purposes.

Abdomen↗

PubMed2000

The natural history of premature adrenarche.

The growth and pubertal development of patients with premature adrenarche are reported to be normal, but the effects of this condition on pubertal growth are not well documented. In the present study the growth kinetics of a group of 38 female patients with isolated premature adrenarche followed in our institution for a period of 5.77 (SD=1.7) yr were evaluated to assess whether and how premature adrenarche affects pubertal growth and final height. Birth weight and length, height, skeletal maturation, onset of puberty, age at menarche, height prognosis and final height were documented. To examine the shape of growth kinetics, growth profiles of each girl were fitted with Preece-Baines nonlinear function (PB1) and mean constant curves were obtained by a 2-stage linear model. The biokinetic constants of the patients were compared both with those obtained by Preece and Baines in normal British girls participating in the Harpenden study and by Milani et al. in normal Italian girls. Birth weight and length of premature adrenarche patients were within the normal range for a northern Italian population [+0.29 (1.57) and -0.40 (1.49) SDS, respectively]. Analysis of the biokinetic constants showed that in PA girls the prepubertal component of height velocity, ie. the one preceding the diagnosis of PA, was consistently higher than that of both normal Italian and Harpenden girls, accounting for the increased height of the patients at the beginning of puberty. In contrast, the pubertal component of height velocity was reduced with respect to control groups, leading to a final height similar to the one estimated by the PB1 model and to the target height. In conclusion, the transient acceleration of growth and bone maturation observed in girls with premature adrenarche did not negatively influence the onset and progression of puberty but modified the growth pattern of these patients. Prepubertal growth was enhanced with respect to normal controls, and this enhancement was compensated for by a reduction of the pubertal growth component leading to a final height in accordance with the target height. This abnormal growth shape is not due to an altered tempo of growth but it is rather a consequence of premature adrenarche.

Body Height↗

PubMed2000

[Neonatal anthropometry and early differentiations in embryo-fetal growth].

It is well known that the biologic variability in fetal size increases as pregnancy advances, although the embryonal and early fetal growth patterns as well as how early and how much the genetic, hormonal and environmental variables play a role in its modulation are still debated. It is accepted that growth in the first trimester of pregnancy is relatively uniform, with a minimal biologic variability; this variability may be underestimated, because the transversal studies do not permit the identification of the growth pattern. The aim of this work is to evaluate, by means of a longitudinal study, the time of embryo-fetal growth differentiation related at neonatal anthropometric measurements. We evaluated 238 neonates (123 female; 115 male) delivered at term after low risk, uncomplicated pregnancies. The subjects were divided into three tertles (low, mid and high) according to birth weight, length and head circumference. For each tertle, distance curves, velocity curves, and rate of increase were calculated by using respectively fetal abdominal circumference (for birth weight), fetal femural length (for neonatal length) and fetal head circumference (for neonatal circumference). The distance curves showed clear differences among the tertles only in the second period of pregnancy, whereas the velocity curves showed clear differences among tertles already in the first 12 weeks. The value of growth rates were similar for all the variables during the entire time considered. This study shows that the anthropometric differences between newborn subgroups exist already at the end of the first trimester of pregnancy and, in physiological conditions, until the end of pregnancy. The anthropometric differences observed early in our study, at twelve weeks of gestational age, are still present at the end of pregnancy and let us suppose a very early expression of the genetic potential for individual growth.

Anthropometry↗

PubMed1999

Neurofibromatosis type 1 growth charts.

Growth abnormalities such as macrocephaly and short stature have been described and are considered a consistent finding in neurofibromatosis type 1 (NF1), one of the most common autosomal dominant disorders in man. We present here a clinical study on the growth profile of a sample of NF1 patients collected through a population-based registry that covers three contiguous regions of North-East Italy (NEI-NF Registry). Auxometric traits of 528 NF1 patients have been measured with the aim of drawing growth charts for height, weight, and head circumference (OFC). Height velocity charts were based on a subset of 143 children who underwent multiple measurements. No differences in height were apparent between NF1 and normal subjects up to age 7 (girls) and 12 (boys) years; subsequently, the 50th centile of NF1 subjects tends to overlap with the 25th centile of normal subjects, and the 3rd centile is much lower in NF1 subjects than in normal subjects, mainly during adolescence. The negatively skewed distribution of height seems to indicate that height growth impairment affects only a proportion of NF1 subjects; height growth impairment does not seem related to disease severity. As for weight, our data suggest that slight overweight is a characteristic of adult NF1 subjects (mainly among males), independent of disease severity. Height growth velocity is normal during childhood for both sexes, whereas the pubertal spurt is slightly anticipated and reduced in NF1 boys but not in girls. Our data confirm previous observations that macrocrania affects most NF1 subjects; the shape of the head growth curve is similar in NF1 and normal girls, whereas NF1 boys present an OFC pubertal growth spurt much more pronounced and delayed than normal boys. The disproportion between OFC and height seems to be related to disease severity in boys but not in girls. Growth charts presented here can be useful in neurofibromatosis clinics for the identification of the effects of secondary growth disorders, for growth prognosis, and for the evaluation of the effects of a therapy such as GH therapy after radiotherapy for optic glioma.

Adolescent↗

PubMed1999

Functions of the fibrinolytic system in human Ito cells and its control by basic fibroblast and platelet-derived growth factor.

During liver fibrogenesis, hepatic stellate cells (HSC) proliferate and migrate under the influence of growth factors, including platelet-derived growth factor (PDGF) and basic-fibroblast growth factor (b-FGF). The plasminogen activation system regulates extracellular matrix (ECM) catabolism and cell movement. We evaluated the expression and biological functions of the plasminogen activation system in human HSC and its interaction with PDGF and b-FGF. Urokinase-plasminogen activator receptors (u-PAR) were measured by radioligand binding, cell cross-linking, immunoassay, and RNAse protection assay. u-PA and plasminogen activator inhibitors (PAIs) expression and activities were analyzed by zymography, immunoassay, and RNase protection assay. Cell migration and proliferation, studied in Boyden chambers and by microscopic counting, were evaluated after the addition of PDGF, b-FGF, and blockade with anti-u-PA, anti-u-PAR antibodies, and antisense oligodeoxynucleotides (aODN) against u-PAR mRNA. We have shown that HSC produce u-PAR, u-PA, and PAI-1. PDGF and b-FGF up-regulate u-PA and u-PAR, but not PAI-1, and exogenous addition of u-PA stimulates HSC proliferation, chemotaxis, and chemoinvasion. Inhibition of u-PA/u-PAR with antibodies against u-PA or u-PAR and with u-PAR aODN inhibit the proliferative, chemotactic, and chemoinvasive activity of PDGF and b-FGF. These findings indicate that u-PA and u-PAR are required for the mitogenic and chemoinvasive activity of PDGF and b-FGF on HSC.

Cell Division↗

PubMed1999

Clinical equivalence between deflazacort oral drops and tablets in active rheumatoid arthritis.

In order to assess the clinical equivalence between deflazacort oral drops and tablets, 18 patients with active rheumatoid arthritis were enrolled in an open, controlled, randomised ('tablets --> drops' sequence, or vice versa), two-period (21 days each) crossover trial (from tablets to drops, or vice versa). Individual dose titration of deflazacort drops or tablets was made weekly on the basis of clinical need. Primary outcome measures of efficacy were changes in the joint swelling count (JSC), erythrocyte sedimentation rate (ESR), hand-grip strength (HGS), joint pain (JP), duration of morning stiffness (MS), physician's global evaluation and patient's self-assessment. Sixteen patients were available by the end of the study. The formulations were equivalent with respect to HGS and improvement in duration of MS, and close to equivalence with respect to JSC and ESR decrease; the drops seemed to be more effective than tablets with respect to JP reduction. No differences between the two formulations were observed with respect to physician's and patient's assessment. The minimum effective dose of each preparation and the relative potency ratio were also established. Drops and tablets were found to have the same potency.

Administration, Oral↗

PubMed1999

Expression of platelet-derived growth factor in newly formed cholangiocytes during experimental biliary fibrosis in rats.

BACKGROUND/AIMS: Chronic cholestasis stimulates a fibroductular reaction which may progress to secondary biliary fibrosis and cirrhosis. Since platelet-derived growth factor has been indicated as a major fibrogenic factor in chronic liver disease, we analyzed its expression and that of its receptor beta subunit in a rat model of chronic cholestasis. METHODS: Liver tissue samples collected at 7, 10, 21, and 28 days after induction of cholestasis obtained by bile duct ligation, were analyzed by immunohistochemistry, in situ hybridization and RNase protection assay for the expression of platelet-derived growth factor (PDGF)-B chain and receptor beta subunit. Furthermore, the expression of PDGF-B chain mRNA was analyzed in highly purified cholangiocytes from normal and cholestatic rat liver. RESULTS: In cholestatic liver, platelet-derived growth factor-BB and B chain mRNA expression increased up to 4 weeks in epithelial cells of proliferating bile ducts, and periductular mesenchymal cells. The increased expression of PDGF-B chain mRNA was confirmed in highly purified cholangiocytes obtained from normal and cholestatic rat liver. The expression of the receptor beta subunit progressively increased after induction of cholestasis and was mainly localized to desmin-positive periductular hepatic stellate cells. CONCLUSIONS: These data suggest that platelet-derived growth factor-B chain can be synthesized by cholangiocytes during chronic cholestasis. The presence of its receptor on periductular hepatic stellate cells raises the possibility that, in this experimental setting, this cytokine might contribute to fibrogenesis in vivo.

Animals↗

PubMed1999

Prospective study of first-line vigabatrin monotherapy in childhood partial epilepsies.

This was a prospective open comparative pilot study to assess the efficacy and tolerability of first-line vigabatrin monotherapy in childhood partial epilepsies. Two groups of patients were recruited over the same period. The vigabatrin monotherapy group comprised 40 patients (18 male, 22 female; mean age at last visit 7.5 years); the comparative carbamazepine monotherapy group comprised 40 consecutive clinic patients (22 male, 18 female; mean age at last visit 7.8 years). Seizures disappeared in 82% of vigabatrin patients and in all carbamazepine patients with idiopathic partial epilepsy, and in 50% of vigabatrin patients and 55% of carbamazepine patients with symptomatic partial epilepsy. Interictal EEG abnormalities decreased in vigabatrin patients more than in carbamazepine patients (P < 0.05). Tolerability was good in vigabatrin patients, but four out of 37 showed mild irritability by the end of the trial. Persistent sedation was observed in eight of the 40 patients receiving carbamazepine. No patient had drug therapy discontinued because of side-effects. During vigabatrin long-term monotherapy, efficacy and good clinical tolerability were maintained. These results suggest that vigabatrin may be an alternative first-line treatment for childhood partial epilepsies. Further blinded comparative randomized trials are needed.

Adolescent↗

PubMed1999

Success and failure in periradicular surgery: a longitudinal retrospective analysis.

The objective of the present study was to compare the success rates of 2 different periapical surgical techniques, the traditional technique with rotary instruments and the ultrasonic technique, which uses ultrasonic retrotips. A longitudinal retrospective study was carried out on 302 apices (181 teeth) that had undergone periapical surgery. Surgical outcome was evaluated by 2 independent operators using standardized periapical radiographs. Each radiographic finding was classified into 1 of 4 groups: complete healing, incomplete healing, uncertain healing, and unsatisfactory outcome (failure). An SAS statistical analysis system was used for data management and analysis. Prognostic factors were determined by means of the Fisher exact test. Complete healing after 4.6 years (the average follow-up period) was observed in 68% of the teeth treated through the use of the standard technique and 85% of those treated through the use of the ultrasonic technique. The success rate increased as the follow-up period lengthened (68.4% at 2 years vs 80% at 6 years). The success rate was higher in maxillary (77.9%) than in mandibular (66.1%) teeth. A comparison between the retrofilling materials was not feasible because all teeth in the standard technique group were retrofilled with amalgam and all teeth in the ultrasonic group were retrofilled with Super-EBA.

Adult↗

PubMed1999

School-administered weekly iron-folate supplements improve hemoglobin and ferritin concentrations in Malaysian adolescent girls.

BACKGROUND: Iron deficiency and its consequent anemia constitute the commonest micronutrient deficiency in the world. OBJECTIVE: We investigated whether long-term, weekly iron-folate supplements administered at school would improve hemoglobin and ferritin concentrations in adolescent girls, including those with mild-to-moderate anemia and hemoglobin concentrations indicating borderline anemia. DESIGN: Subjects were 266 girls with hemoglobin concentrations of 80-119.9 g/L (group A) and 358 girls with hemoglobin concentrations of 120-130 g/L (group B) who were otherwise healthy. Two hundred sixty-six girls in group A and 268 girls in group B were randomly assigned to receive either 60 or 120 mg Fe plus 3.5 mg folic acid weekly for 22 wk. Ninety of the girls in group B were randomly assigned to receive only 5 mg folic acid weekly. Capillary hemoglobin and plasma ferritin were measured at baseline and after 12 and 22 wk of supplementation. RESULTS: By the end of the study, 2% of the girls had dropped out and > 96% had taken > or = 20 of the 22 tablets; side effects were minimal. Mean plasma ferritin increased significantly in all iron-supplemented groups, independently of initial hemoglobin values and iron doses. Ferritin concentrations decreased in the girls supplemented with folic acid only. As expected, hemoglobin responses to iron were higher in group A than in group B and increases were positively correlated with initial plasma ferritin. Hemoglobin failed to respond to folate supplementation if initial plasma ferritin concentrations were low. Mean hemoglobin increased significantly and consistently in relation to the length of treatment. CONCLUSION: Long-term, weekly iron-folate supplementation was found to be a practical, safe, effective, and inexpensive method for improving iron nutrition in adolescent schoolgirls.

Adolescent↗

PubMed1999

Expression of monocyte chemotactic protein-1 precedes monocyte recruitment in a rat model of acute liver injury, and is modulated by vitamin E.

BACKGROUND: Increased expression of monocyte chemotactic protein-1 (MCP-1) has been indicated as a mechanism underlying leukocyte recruitment after liver injury. In this study we examined the temporal relationship between MCP-1 expression and the appearance of monocyte infiltration during acute liver injury. In addition, we tested the effects of vitamin E, a well known antioxidant, on these parameters. Rats were intoxicated with a single intragastric administration of CCl4 with or without pretreatment with vitamin E (atocopherol). METHODS: Monocyte chemotactic protein-1 expression was analyzed by northern blotting and in situ hybridization and monocyte infiltration was determined by ED-1 immunostaining. The results were quantitated by computerized image analysis. Expression of MCP-1 mRNA was significantly increased as early as 12 hours following injury, and progressively increased thereafter. In contrast, a significant increase in the number of ED-1 positive cells, an index of monocyte infiltration, was observed only 24 and 48 hours after injury. RESULTS: Vitamin E markedly reduced MCP-1 expression at the mRNA and protein levels, and caused a significant reduction in the number of monocyte/macrophages, indicating a role for oxidative stress in the induction of MCP-1 expression in vivo. Accordingly, in cultured hepatic stellate cells, different oxidative stress-related molecules increased MCP-1 mRNA. CONCLUSIONS: These data suggest the existence of a direct relationship between MCP-1 expression and monocyte infiltration after acute liver injury, and that preventing the generation of oxidative stress-related molecules results in decreased expression and release of this chemokine.

Animals↗

PubMed1998

Expression of the thrombin receptor in human liver: up-regulation during acute and chronic injury.

Thrombin is generated during tissue damage in several organs, including the liver, and participates in the process of tissue repair through proteolytic activation of a specific thrombin receptor (TR). The aim of this study was to investigate TR expression in human liver by immunohistochemistry and in situ hybridization. In normal liver, immunostaining for TR was present in the endothelial lining of the hepatic sinusoids. During chronic hepatitis, several cells expressing the TR were detected in the inflammatory infiltrate of portal tracts. In cirrhosis with chronic active hepatitis, expression of the TR was also present in mesenchymal cells of fibrous septa. TR expression was markedly up-regulated during fulminant hepatitis, with the highest expression in mesenchymal cells in areas of regeneration. Up-regulation of TR expression was associated with increased levels of TR messenger RNA (mRNA), as assessed by in situ hybridization and RNAse protection assay of liver RNA. Immunostaining of serial sections using specific cellular markers showed that different nonparenchymal cells contribute to TR expression during liver injury. TR expression was also shown in cultured human hepatic stellate cells, with increasing signal comparing activated versus quiescent cells. Because thrombin is rapidly generated after tissue damage, regulated TR expression may be involved in tissue remodeling and/or scarring during liver damage.

Acute Disease↗

PubMed1998

A histomorphometric long-term longitudinal study of trabecular bone loss in glucocorticoid-treated patients: prednisone versus deflazacort.

Administration of a corticosteroid with minor osteopenic effects is considered an effective prevention of glucocorticoid osteoporosis. Deflazacort, an oxazolinic derivative of prednisolone, is reported to be less harmful to cancellous bone mass than other equally effective corticosteroids. However, comparative long-term studies, particularly on trabecular bone, are needed before a smaller detrimental effect on bone of deflazacort can be unequivocally confirmed. We conducted such a prospective long-term study using histomorphometric analysis of iliac bone. For the study, 18 pairs of nonimmobilized patients, matched for age, sex, menopausal state, corticosteroid dose, and type and severity of the disease, were randomly submitted to treatment with therapeutically equivalent doses of prednisone or deflazacort. Bone biopsies from iliac crest were taken before and at various times during treatment. In order to represent the time-related trabecular bone loss and find out possible differences between patients on prednisone or deflazacort, a previously described model of bone loss kinetics was applied. No significant differences in biochemical indices of bone turnover or in histomorphometric variables between prednisone- and deflazacort-treated patients were recorded before treatment. The mean duration of treatment at the final biopsy was similar for prednisone and deflazacort (15.8 and 15.2 months, respectively). Patients showed evident clinical improvement with both treatments. Osteoid and resorption surfaces showed no significant differences throughout the observation period in any of the 18 pairs. On the contrary, both steroids induced a significant decrease in trabecular bone, although the bone loss rate induced by prednisone was significantly higher than that induced by deflazacort (P < 0.05). The kinetics of bone loss and the different osteopenic effects of the two drugs are described by the negative exponential function fitted to data from patients never previously given glucocorticoids; the model yields highly significant difference (P approximately equal to 0.01) between the two drugs and allows estimation of the difference even 3 years after the beginning of treatment (-3.0%/year versus -1.1%/year for prednisone and deflazacort, respectively). This prospective long-term study confirms that an exponential model accurately describes the trabecular bone loss induced by long-term corticosteroid treatment and demonstrates that deflazacort, at therapeutically effective doses, induces less trabecular bone loss than prednisone.

Adult↗

PubMed1998

Human hepatic stellate cells express class I alcohol dehydrogenase and aldehyde dehydrogenase but not cytochrome P4502E1.

BACKGROUND/AIMS: Alcohol dehydrogenase, cytochrome P4502E1 (CYP2E1), and aldehyde dehydrogenase are known to play an important role in alcohol metabolism in the liver. Although the ethanol oxidation pathways are mainly localized in hepatocytes, we examine whether human hepatic stellate cells might also metabolize ethanol and acetaldehyde. METHODS: Hepatic stellate cells were isolated from normal human livers and exposed in vitro to 50 mmol/l ethanol or 85 micromol/l acetaldehyde for different periods of time. Alcohol dehydrogenase/aldehyde dehydrogenase activity and CYP2E1 protein expression were measured in hepatic stellate cells. Moreover, alcohol dehydrogenase and aldehyde dehydrogenase mRNA expression were evaluated in hepatic stellate cells. RESULTS: Exposure of hepatic stellate cells to ethanol for 24 h resulted in a 5-fold increase in cell alcohol dehydrogenase activity. The effect of ethanol on alcohol dehydrogenase activity was paralleled by a significant increase in the alcohol dehydrogenase mRNA expression in hepatic stellate cells. Acetaldehyde significantly increased the activity of high affinity aldehyde dehydrogenase in hepatic stellate cells, whereas ethanol was devoid of any effect. Acetaldehyde also induced high affinity aldehyde dehydrogenase mRNA expression in hepatic stellate cells. CYP2E1 was not expressed in hepatic stellate cells either in basal condition or after ethanol/acetaldehyde exposure. CONCLUSIONS: This study shows that human hepatic stellate cells have the capacity to metabolize both ethanol and acetaldehyde through a class I alcohol dehydrogenase- and an aldehyde dehydrogenase-oxidizing pathway. Conversely, no detectable levels of CYP2E1-associated proteins are expressed in these cells.

Acetaldehyde↗

PubMed1998

Evaluation of acute ischemic stroke using quantitative EEG: a comparison with conventional EEG and CT scan.

The sensitivity of quantitative electroencephalogram (EEG) was compared with that of conventional EEG in patients with acute ischaemic stroke. In addition, a correlation between quantitative EEG data and computerized tomography (CT) scan findings was carried out for all the areas of lesion in order to reassess the actual role of EEG in the evaluation of stroke. Sixty-five patients were tested with conventional and quantitative EEG within 24 h from the onset of neurological symptoms, whereas CT scan was performed within 4 days from the onset of stroke. EEG was recorded from 19 electrodes placed upon the scalp according to the International 10-20 System. Spectral analysis was carried out on 30 artefact-free 4-sec epochs. For each channel absolute and relative power were calculated for the delta, theta, alpha and beta frequency bands and such data were successively represented in colour-coded maps. Ten patients with extensive lesions documented by CT scan were excluded. The results indicated that conventional EEG revealed abnormalities in 40 of 55 cases, while EEG mapping showed abnormalities in 46 of 55 cases: it showed focal abnormalities in five cases and nonfocal abnormalities in one of six cases which had appeared to be normal according to visual inspection of EEG. In a further 11 cases, where the conventional EEG revealed abnormalities in one hemisphere, the quantitative EEG and maps allowed to further localize abnormal activity in a more localized way. The sensitivity of both methods was higher for frontocentral, temporal and parieto-occipital cortical-subcortical infarctions than for basal ganglia and internal capsule lesions; however, quantitative EEG was more efficient for all areas of lesion in detecting cases that had appeared normal by visual inspection and was clearly superior in revealing focal abnormalities. When we considered the electrode related to which the maximum power of the delta frequency band is recorded, a fairly close correlation was found between the localization of the maximum delta power and the position of lesions documented by CT scan for all areas of lesion excepting those located in the striatocapsular area.

Acute Disease↗

PubMed1998

Serologic detection of CagA positive Helicobacter pylori infection in a northern Italian population: its association with peptic ulcer disease.

BACKGROUND: About 60-70% of Helicobacter pylori strains possess cagA (cytotoxin associated gene A) gene and express its product CagA, a highly immunogenic 128-140 kD protein. Patients infected with CagA positive strains develop serum IgG anti-CagA. A serologic response to CagA has been detected in Helicobacter pylori infected patients with peptic ulcer more frequently than in those with gastritis alone. It is nuclear whether this finding is consistent in different geographical populations. We investigated the relationship between anti-CagA seropositivity and peptic ulcer disease in a Northern Italian population. MATERIALS AND METHODS: We studied 135 H. pylori infected patients: 65 with duodenal ulcer (DU), 28 with gastric ulcer (GU) and 42 with non ulcer dyspepsia (NUD). Sera from these patients were assayed by EIA (enzyme immunoassay) for anti-CagA IgG. RESULTS: A high prevalence of anti-CagA was found associated with DU (86.1%) and GU (96.4%), while NUD patients showed anti-CagA seropositivity of 52.4% (Odd ratio, 5.66; 95% confidence interval, 2.23 to 14.32; p < .001, DU vs. NUD; Odd ratio, 24.5; 95% confidence interval, 3.05 to 197.6; p = .003, GU vs. NUD). DU patients showed anti-CagA seropositivity titer (1.15 (0.61 OD, mean (SD) higher than that of NUD patients (0.78 (0.60 OD, mean (SD) (p < .05). CONCLUSIONS: These data demonstrate in a Northern Italian population that anti-CagA seropositivity is strongly associated with peptic ulcer disease and suggest that CagA might play an important role in ulcer pathogenesis.

Adult↗

PubMed1998

Eradication of Helicobacter pylori reduces the rate of duodenal ulcer rebleeding: a long-term follow-up study.

OBJECTIVES: The long-term efficacy of Helicobacter pylori eradication to reduce the rate of recurrence of peptic ulcer bleeding is still uncertain. We evaluated the rate of duodenal ulcer rebleeding for 48 months after H. pylori eradication. METHODS: Thirty-two male patients with H. pylori infection and duodenal ulcer bleeding were treated with omeprazole (40 mg/day for 4 wk), colloidal bismuth (480 mg/day for 2 wk), amoxicillin (2 g/day for 1 wk), and metronidazole (750 mg/day for 1 wk), and followed up for 48 months. Endoscopy and tests for H. pylori infection were repeated every year. RESULTS: Ulcer healed in all patients, but H. pylori infection persisted or recurred in 11 patients. Within 48 months, rebleeding occurred in nine (81.8%) of these patients, whereas the 21 patients who were persistently negative for H. pylori infection remained asymptomatic without rebleeding (0/ 21 = 0%, p < 0.002) during the whole follow-up. CONCLUSIONS: Eradication of H. pylori can reduce the rate of duodenal ulcer rebleeding for at least 4 yr, thus potentially modifying the natural history of the disease.

Adult↗

PubMed1998

Expression and cellular localization of keratinocyte growth factor and its receptor in human hyperplastic prostate tissue.

It is well recognized that the actions of androgens alone do not explain the hyperplastic development of the gland that occurs in elderly men. The increasing number of reports confirming the lack of mitogenic activity of androgens coupled with the powerful mitogenic activity of growth factors and the discovery of growth factor receptors led to an increased interest in the putative role of growth factors in prostate physiopathology. We have previously demonstrated the presence and the cellular localization of epidermal growth factor and of the related peptide, transforming growth factor-alpha, together with their common receptor in the epithelial compartment of the human hyperplastic prostate tissue (BPH). In the present study we examined the expression and cellular localization of messenger ribonucleic acid (RNA) encoding keratinocyte growth factor (KGF) and its receptor in human hyperplastic prostate tissue. RT-PCR of total RNA extracted from BPH tissues documented the presence of transcripts for KGF and its receptor. In situ hybridization with specific RNA probes synthesized from the respective complementary DNA demonstrated that KGF mRNA was mainly localized in the stromal cells, whereas its receptor was mainly localized in the prostate epithelium. Moreover, the mitogenic activity of KGF on cultured BPH cells compared to that of other growth factors has been tested. Our findings clearly indicate that KGF has the ability to function as a potent mitogen in BPH cells. Our data support the hypothesis that KGF plays an important role in prostate growth and that in human prostate it seems to act in a paracrine fashion.

Cell Division↗