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Biomedical subjects

A Sardella

Publications and source records attributed to A Sardella.

At least 37 records · Page 2Linked to original sources

Efficacy of topical mesalazine compared with clobetasol propionate in treatment of symptomatic oral lichen planus.

OBJECTIVE: To compare topically applied mesalazine (5-aminosalicylic acid) to topically applied clobetasol propionate in the treatment of patients suffering from symptomatic oral lichen planus. DESIGN: Randomized controlled longitudinal investigation. PATIENTS AND METHODS: Twenty-five out-patients suffering from oral lichen planus and referred to the Department of Oral Pathology and Oral Medicine of the University of Milan, Italy, during the period January to August 1997. Patients were randomly allocated (Group A and Group B) to treatment with mesalazine 5% or clobetasol propionate 0.05%. The drugs were topically applied twice daily for 4 weeks. Discomfort and pain were evaluated by the patient before and after treatment using a Visual Analogue Scale from zero (no pain) to 10 (extreme pain). Results were statistically evaluated by a Mann-Whitney U test. RESULTS: The two pharmacological regimens obtained partial and complete absence of symptoms. In particular, the mesalazine tested group disclosed 57% complete absence of symptoms, 21.3% partial response and 9% no response. No statistically relevant difference has been detected between the two regimens. CONCLUSIONS: The results of this preliminary study, if confirmed by further investigations, suggest that mesalazine might be considered an alternative to clobetasol propionate for treatment of symptomatic oral lichen planus.

Administration, Topical↗

Attitude towards smoking and oral cancer prevention among northern Italian dentists.

The aim of the study was to evaluate the smoking habits of Northern Italian dental practitioners and their basic skills in the prevention of oral cancer. 217 of the 250 dental practitioners (86.8%) contacted by telephone from September to December 1994, answered a simple questionnaire. One third of the sample interviewed was formed by current smokers; nevertheless 60.8% of them always advise their patients to give up smoking. Only a relatively small percentage of the questioned dental practitioners (10.6%) do not examine the oral mucosa of the patients on a regular basis and 40% of responders had made a clinical diagnosis of oral cancer in the past. The lack of a specific dental education was associated with less scrupulous examination of the oral soft tissues and minor experience of cancer diagnosis. Despite their smoking habit, Northern Italian dental practitioners self-reported encouraging behaviour towards primary and secondary oral cancer prevention.

Adult↗

Endotoxin tolerance impairs a pertussis-toxin-sensitive G-protein regulating tumour necrosis factor release by macrophages from tumour-bearing rats.

The aim of this work was to study whether a G-protein regulates lipopolysaccharide (LPS) induced TNF-alpha production in tumour-bearing rat peritoneal macrophages differently to in normal rats. We also investigated whether a state of 'early endotoxin tolerance' affects LPS induced TNF-alpha release via a G-protein-mediated phenomenon. LPS-stimulated (50 micrograms ml-1 of Salmonella enteritidis LPS) TNF-alpha release was investigated in peritoneal macrophages harvested from both normal rats and tumour-bearing rats. Cholera toxin (10, 100 and 1000 ng ml-1) did not significantly modify LPS-induced TNF-alpha release. In contrast pertussis toxin (0.1, 1.0 and 10 ng ml-1) significantly increased LPS-induced TNF-alpha release and inhibited LPS-stimulated prostaglandin E2 (PGE2) production in both normal rat macrophages and tumour-bearing rat macrophages. Pertussis toxin effects on these LPS responses were correlated with a pertussis-toxin-mediated ADP-ribosylation of a 41 kDa protein(s). The LPS-mediated responses were significantly greater in macrophages from tumour-bearing rats than in macrophages from normal rats. PGE2 (10(-9), 10(-8) and 10(-7) M) suppressed LPS-induced TNF-alpha production in a dose-dependent fashion. A state of 'early endotoxin tolerance' was then induced in tumour-bearing rats by a single intravenous injection of 125 micrograms rat-1 of LPS, and experiments were performed on peritoneal macrophages harvested 24 h after LPS injection. In tolerant macrophages pertussis toxin induced an increase in LPS-stimulated TNF-alpha release and an inhibition in LPS-stimulated PGE2 release significantly lower than in macrophages harvested from non-tolerant tumour bearing rats. Our results suggest that a pertussis-toxin-sensitive G-protein may serve to regulate the synthesis of TNF-alpha in rat peritoneal macrophages and that the activity of this pertussis-sensitive G-protein is increased in macrophages from tumour-bearing rats. Furthermore, our experiments would indicate that a 'state of endotoxin tolerance', caused by altering the function of presumably a Gi-protein, may exert beneficial effects on the functions of macrophages in tumour-bearing rats.

Adenosine Diphosphate Ribose↗

Monocytes and lymphocytes as active participants in the pathogenesis of experimental shock.

We investigated the role played by monocytes and lymphocytes in the pathogenesis of experimental shock. Splanchnic artery occlusion (SAO) shock was induced in anaesthetized rats by clamping splanchnic arteries for 45 min followed by reperfusion. Sham operated animals were used as controls. SAO shocked rats had a decreased survival time (80 +/- 11 min, while sham shocked rats survived more than 4 h), increased serum (248 +/- 21 U/ml) and macrophage (145 +/- 15 U/ml) levels of TNF-alpha, enhanced myeloperoxidase (MPO) activity in the ileum (3.38 +/- 0.2 U x 10(-3)/g tissue), decreased number of monocytes, lymphocytes and neutrophils and a profound hypotension. In addition we found an increased expression of vascular cell adhesion molecule-1 (VCAM-1) on aortic endothelium and a reduced percentage of VLA-4 positive monocytes and lymphocytes. Inhibition of TNF-alpha synthesis, reversed the increased endothelial expression of VCAM-1, increased the percentage of integrin VLA-4 positive leukocytes and improved monocyte, lymphocyte and neutrophil count. Furthermore a passive immunization with specific antibodies raised against VCAM-1 (2 mg/kg, i.v. 3 h before SAO) increased survival, reduced MPO activity in the ileum (0.034 +/- 0.04 U x 10(-3)/g tissue) and improved mean arterial blood pressure. Our data suggest that monocytes and lymphocytes participate in the pathogenesis of splanchnic ischaemia-reperfusion injury and may amplify the adhesion of neutrophils to peripheral tissues.

Animals↗

Prevalence of oral lesions in inflammatory bowel disease.

OBJECTIVE: To obtain precise data on the prevalence of oral lesions in inflammatory bowel disease (IBD). METHODS: Oral lesions were carefully sought in a consecutive series of 198 Italian IBD outpatients, 77 with Crohn's disease (CD) and 121 with ulcerative colitis (UC); 89 subjects with functional intestinal motility disorders served as controls. RESULTS: The oral lesions detected were angular cheilitis (in 7.8% of CD patients, 5% of UC patients, and 0% of controls (p < 0.05, patients vs controls), lichen (6.5, 5.8, and 3.3%, respectively, p = not significant), aphthous ulcers (5.2, 5.8, and 5.6%, respectively, p = not significant), candidiasis (5.2, 0.8, and 0%, respectively, p < 0.05, CD patients vs controls), benign tumors (5.2, 0, and 7.8%, respectively, p < 0.05, patients vs controls), leukoplakia (5.2, 11, and 3.3%, respectively, p = not significant), and, less frequently, glossitis and herpes labialis. No specific CD oral lesions were observed in this series. No correlation was found between clinical disease activity and frequency of oral lesions. CONCLUSIONS: Aphthous ulcers are not common in IBD patients. Oral candidiasis is more frequent in CD than UC patients and controls.

Adolescent↗

[Hepatitis C and dentistry. Review of the literature].

In 1988 the RNA virus responsible for the majority of cases of parenteral non A, non B hepatitis (NANBH) was isolated and designated Hepatitis C Virus (HCV). Since then, the sequence of the genome of the virus has been defined and at least 10 different types identified. Clinical studies indicate that the majority of patients who acquire HCV develop chronic hepatic disease, in particular chronic active hepatitis or cirrhosis and some of them will develop hepatocellular carcinoma. Currently, there is no effective anti-HCV therapy and no passive or active immunization protocol for HCV. Epidemiological studies indicate that HCV infection is relatively well confined to specific patient populations, in particular injecting drug users and recipients of blood and blood products. Nevertheless as HCV infection is transmitted mainly parenterally it must be regarded as a potential hazard for dental health care staff. This article reviews current knowledge concerning HCV infection with particular attention to those issues relevant to the dentists in Italy including the dental management of the HCV infected patient and the risk of HCV cross-infection in the dental environment.

Female↗

G 619, a dual thromboxane synthase inhibitor and thromboxane A2 receptor antagonist, inhibits tumor necrosis factor-alpha biosynthesis.

G 619 is 3-carbamyl-(3'-picolyl)-4-methoxy-1-benzamide. The compound is structurally related to picotamide, a previously reported dual thromboxane synthase inhibitor/thromboxane A2 receptor antagonist, which displays inhibitory activity on tumor necrosis factor-alpha. The aim of the present work was to study the effect of G 619 on tumor necrosis factor-alpha synthesis both in vivo and in vitro. Salmonella enteritidis lipopolysaccharide was used to induce tumor necrosis factor-alpha production. Septic shock was produced in male rats by a single intravenous (i.v.) injection of 20 mg/kg (LD90) of Salmonella enteritidis lipopolysaccharide. Rats were pretreated with G 619 (50 mg/kg, i.v.) or vehicle (1 ml/kg, i.v.) 1 h before endotoxin challenge. Salmonella enteritidis lipopolysaccharide administration dramatically reduced survival rate (0%, 72 h after endotoxin administration), reduced mean arterial blood pressure, increased plasma levels of thromboxane B2 and 6-keto-prostaglandin F1 alpha and enhanced serum levels of tumor necrosis factor. Furthermore, endotoxic shock produced characteristic gastric damage, consisting of haemorrhagic infiltrates. Pretreatment with G 619 in vivo significantly protected against Salmonella enteritidis lipopolysaccharide-induced lethality (80% survival rate and 60% survival rate 24 h and 72 h after Salmonella enteritidis lipopolysaccharide injection, respectively), reduced hypotension, decreased plasma thromboxane B2 and serum tumor necrosis factor-alpha levels and enhanced blood levels of 6-keto-prostaglandin F1 alpha. In rat peritoneal macrophages, G 619 in vitro (25, 50 and 100 microM) significantly blunted (P < 0.001) Salmonella enteritidis lipopolysaccharide-stimulated production of tumor necrosis factor-alpha, whereas it increased 6-keto-prostaglandin F1 alpha and cyclic AMP levels. The present data indicate that G 619 may be useful during disease states characterized by elevated tumor necrosis factor-alpha levels.

6-Ketoprostaglandin F1 alpha↗

Detecting hibernated myocardium with SPECT and thallium-glucose-insulin infusion.

UNLABELLED: Because thallium kinetics, like potassium kinetics, may be affected by serum insulin levels, we performed two pilot studies to identify severely ischemic myocardium using different protocols based on the infusion of a thallium, insulin, potassium and glucose solution. Results were compared with those obtained with two currently used protocols based on rest injection or reinjection of 201Tl. METHODS: In the first study (Protocol 1) of 15 men with a previous large myocardial infarction, perfusion was evaluated by SPECT in 20 segments after a 30-min infusion of 201Tl (111 MBq), insulin (5 U) and potassium (10 mEq) in 10% glucose solution (250 ml). Imaging was repeated 30 min later and the results were compared with those obtained from stress and 3-hr reinjection images. In the second study (Protocol 2), 15 patients were evaluated randomly at rest and 3 hr later (rest-redistribution). On a separate day, the patients were then re-evaluated after infusion of 201Tl (111 MBq), potassium (10 mEq) and insulin (5 U) in 5% glucose (250 ml); images were obtained 90 and 180 min postinjection. RESULTS: In Protocol 1, radiotracer activity in segments with no uptake during stress was detected in 35% with the reinjection technique and 58% with the insulin solution protocol. In Protocol 2, 31% of segments revealed thallium activity after insulin infusion but not at rest or rest-redistribution. Serum measurements showed high insulin levels (444 +/- 138 in Protocol 1, 125 +/- 33 mU/ml in Protocol 2), although glucose levels were not significantly altered (149 +/- 32 versus 71 +/- 20 mg/dl, respectively). Potassemia was not affected and the patients tolerated the tests satisfactorily. CONCLUSION: These results confirm that continuous infusion of 201Tl with a low dose of insulin in a glucose/potassium chloride solution is safe and may enhance cellular uptake of the radiotracer in severe ischemic regions, thereby improving viable myocardium detection.

Blood Glucose↗

TCV-309, a novel platelet activating factor antagonist, inhibits leukocyte accumulation and protects against splanchnic artery occlusion shock.

The aim of this study was to evaluate: (1) the accumulation of leukocytes in the ileum and the lung during splanchnic artery occlusion (SAO) shock; (2) the role of platelet-activating factor (PAF) and tumor necrosis factor (TNF-alpha) in this phenomenon. Untreated anesthesized rats subjected to total occlusion of the celiac, superior and inferior mesenteric arteries for 45 min, followed by reperfusion, uniformly died within 90 min after reperfusion. The mean survival time was 93 +/- 7 min. The neutrophilic infiltrate was quantitated in the ileum and in the lung using a myeloperoxidase (MPO) assay. MPO activity in the ileum and in the lung averaged 0.05 +/- 0.03 and 0.4 +/- 0.02 U x 10(-3)/g protein in animals killed before occlusion. MPO activity did not change in rats killed immediately before reperfusion and was significantly elevated (0.11 +/- 0.02 and 1.7 +/- 0.6 U x 10(-3)/g protein in the ileum and the lung, respectively) in those killed 80 min after the beginning of the reperfusion. The histological examination confirmed the accumulation of leukocytes in the mucosa of the ileum and the lung over the 80 min. SAO shocked rats exhibited leukopenia and increased serum levels of TNF-alpha. In order to evaluate the role of PAF and TNF-alpha in SAO shock, a powerful PAF receptor antagonist, TCV-309 (5 micrograms/kg i.v.), was injected 5 min after reperfusion. TCV-309 increased survival time, lowered serum TNF-alpha, reduced MPO activity in both the ileum and the lung and ameliorated leukopenia induced by SAO shock.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Protective effects of L-659,989, a platelet-activating factor receptor antagonist, in myocardial ischemia and reperfusion in rats.

The cardioprotective effects of L-659,989, a specific platelet-activating factor (PAF) receptor antagonist, were investigated in an ischemia/reperfusion model in rats. Pentobarbital-anesthetized rats were subjected to left main coronary artery occlusion (1 h) followed by reperfusion (1 h) (MI/R); Sham-operated rats were used as controls (Sham MI/R). Rats receiving vehicle showed reduced survival rate (60%), marked myocardial injury (necrotic area/total area = 54.5 +/- 6%; necrotic area/area at risk 76.6 +/- 6.7%), high serum creatine phosphokinase (CPK) activity (150 +/- 10 U/ml), and increased myocardial myeloperoxidase (MPO) activity in the area at risk (AR, 6.2 +/- 0.5 U x 10(-3)/g protein) and in the necrotic area (6.6 +/- 0.7 U x 10(-3)/g protein). PAF plasma levels increased significantly during reperfusion and peaked at 15 min of reperfusion. Administration of L-659,989 enhanced survival rate (80%), reduced myocardial damage (necrotic area/total area 25.6 +/- 3.5%; necrotic area/AR 34.6 +/- 5.4%), attenuated the increase in serum CPK (50 +/- 6 U/ml) and decreased MPO activity both in the AR (2.8 +/- 0.3 U x 10(-3)/g tissue) and in the necrotic area (2.3 +/- 0.5 U x 10(-3)/g tissue). Our results suggest that PAF-inducing adhesion and activation of polymorphonuclear leukocytes (PMN) plays a significant role in the injury associated with ischemia/reperfusion.

Animals↗

Beneficial effects of BAY u3405, a novel thromboxane A2 receptor antagonist, in splanchnic artery occlusion shock.

Splanchnic artery occlusion shock was induced in male anaesthetized rats by clamping the splanchnic artery for 45 min. The arteries were then released and survival rate, mean survival time, mean arterial blood pressure, plasma levels of thromboxane B2 and 6-keto-PGF1 alpha, macrophage phagocytosis activity and plasma levels of myocardial depressant factor were evaluated. In addition, the neutrophilic infiltrate was quantified in the ileum and lung using a myeloperoxidase (MPO) assay. Sham splanchnic-artery-occlusion-shocked rats were used as controls. Splanchnic-artery-occlusion-shocked rats died within 93 +/- 7 min, while all sham-shocked animals survived more than 3 h. Splanchnic artery occlusion shock caused changes in mean arterial blood pressure, significantly increased the plasma levels of thromboxane B2 (7.5 +/- 1.3 ng/ml; p < 0.001 vs. sham), 6-keto-PGF1 alpha (8.9 +/- 1.7 ng/ml; p < 0.001 vs. sham) and myocardial depressant factor (114 +/- 11 U/ml), and reduced macrophage phagocytosis. Furthermore, MPO activity was significantly elevated (0.12 +/- 0.03 x 10(-3) and 1.8 +/- 0.5 x 10(-3) U/g protein in the ileum and lung, respectively) 70 min after starting reperfusion. Administration of BAY u3405, a novel thromboxane A2 receptor antagonist (30 mg/kg i.v., 30 min before occlusion), significantly increased survival time (187 +/- 3.7 min) and survival rate, improved mean arterial blood pressure, reduced the plasma levels of myocardial depressant factor (54 +/- 3 U/ml), partially restored macrophage phagocytosis and lowered MPO activity in both the ileum and the lung. Our data are consistent with an involvement of thromboxane A2 in splanchnic artery occlusion shock and suggest that BAY u3405 might be of benefit in low-flow states such as circulatory shock.

6-Ketoprostaglandin F1 alpha↗

Anorectic activity of NG-nitro-L-arginine, an inhibitor of brain nitric oxide synthase, in obese Zucker rats.

We investigated the effects of NG-nitro-L-arginine (L-NO Arg) administration (12.5, 25 and 50 mg/kg i.p.) on food consumption and body weight of male obese Zucker rats (fa/fa) and in their lean age-matched controls (FA/?; FA/FA), both groups aged 14 weeks. Acute or repeated administration of L-NO Arg reduced food intake and body weight in both obese and lean rats. However the lean rats showed tolerance to the L-NO Arg effects after 5 days of treatment. L-NO Arg anorexia was suppressed by pretreatment with metergoline. These results suggest that L-NO Arg may represent a new anorectic drug.

Amino Acid Oxidoreductases↗

Protective effects of G 619, a dual thromboxane synthase inhibitor and thromboxane A2 receptor antagonist, in splanchnic artery occlusion shock.

Splanchnic artery occlusion (SAO) shock was induced in anesthetized rats by clamping the celiac trunk and the superior mesenteric artery for 45 min. The arteries were then released and survival rate, mean survival time, mean arterial blood pressure (MAP), plasma levels of thromboxane B2 (TxB2) and 6-keto-PGF1 alpha, and the phagocytotic activity of peritoneal macrophages were evaluated. Shocked animals died within 89 +/- 10 min, while all sham-shocked rats survived greater than 3 h. SAO shock produced relevant changes in MAP, significantly increased plasma levels of TxB2 and 6-keto-PFG1 alpha, and decreased peritoneal macrophage phagocytotic activity. The administration of G 619, a dual thromboxane synthase inhibitor/thromboxane A2 receptor antagonist (50 mg/kg, 15 min before SAO shock) significantly increased survival time (190 +/- 13 min) and survival rate, reduced plasma levels of TxB2, and partially restored the impairment in peritoneal macrophage phagocytosis. Finally, the administration of G 619 had beneficial effects on changes in MAP-induced bay SAO shock. These data further confirm the involvement of TxA2 in SAO shock and suggest that G 619 may have positive effects in low-flow states.

6-Ketoprostaglandin F1 alpha↗

[An assessment of the proliferative activity in oral lichen planus].

The author's aim was to evaluate the cell proliferation of oral lichen planus, by an in vitro labelling technique using tritiated thymidine (TLI). For this purpose six patients with oral lichen planus and six control volunteers with oral mucosa clinically sound were studied. The cell kinetic parameter was investigated by counting cells from autoradiographs on histological sections of the biopsies. Significant differences were found between the basal TLI of the two group (p = 0.002) but no between the epithelial TLI (Wilcoxon test).

Biopsy↗

[Study of cellular kinetics in oral leukoplakia].

The Authors aim was to study the Labeling Indices (LI) of 12 subjects with oral leukoplakia, using an in vitro labeling technique with tritiated thymidine (Silvestrini-Kit, Ribbon spa, Milan). Twelve volunteers of our Dental Clinic were enrolled in this study as a control group. The kinetic parameter was investigated by counting cells from autoradiographs on histological selections of the biopsies. By a Wilcoxon test, significant differences were found between the LI of the two groups: p = 0.00003. Finally, a comparison has also been made between LI of these lesions and the LI of oral squamous cell carcinomas.

Adult↗