Biomedical subjects
Publications and source records attributed to F Carinci.
A hibernoma is a rare, benign, soft-tissue tumor composed of cells similar to those of brown adipose tissue. Only nine cases in the cervical area have been reported. Typically, hibernomas are asymptomatic and slow growing. Adequate treatment consists of complete excision. We describe an additional case of neck hibernoma and review the literature to clarify a pathologic condition rarely included in the differential diagnosis of cervical masses.
To evaluate the best surgical strategy in cases of parotid gland carcinoma, local risk factors (T, N, histology, and treatment) were analyzed in a series of 134 patients. The efficacy of the facial nerve sacrifice in case of macroscopic tumor infiltration was tested by means of survival analyses (Kaplan-Meier and Cox algorithms). This study demonstrated that nerve preservation resulted in a better prognostic value when compared with resection only in the group of patients having a T1 or T2. In patients affected by T3 and T4, the different treatment did not show any difference in survival rate. In conclusion, the sacrifice of the facial nerve is not always able to improve the survival rate.
A study regarding patients with primary and previously untreated advanced histologically proven squamous cell carcinoma of the head and neck was performed to compare two treatment modalities: neck dissection followed by chemoradiotherapy (Group I) versus chemoradiotherapy alone (Group II). Fifty-four patients were randomly chosen to receive Group I or II treatment. Our results demonstrate that Group I treatment has a higher and statistically significant disease-specific survival rate. We suggest that an association of neck dissection plus chemoradiotherapy can be useful in the event of unresectable advanced carcinomas.
Malignant myoepithelioma is a rare tumor of salivary origin, preferentially located in the parotid and submandibular glands and in the palate. We report the first case involving the tongue base in a 30-year-old man. The histopathological and clinical features and therapeutic options are discussed.
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PURPOSE: To verify the correlation to survival of 1987 and 1997 Union Internationale Contre le Cancer (UICC; International Union Against Cancer) supraglottic tumour categories. MATERIALS AND METHODS: Two hundred and sixty patients seen at the ENT Clinic at the University of Ferrara from 1970 to 1990 had a complete follow-up and met the criteria of enrolment in this study. Data were analyzed by means of survival analyses (Kaplan-Meier and Cox algorithms). RESULTS: Multivariate analysis (adjusted for number and patient's age) of 1997 UICC supraglottic tumour categories (T1 vs. T4) showed a significant correlation with the survival rate, whereas 1987 UICC categories did not reach any significant statistical value. CONCLUSION: The 1997 UICC tumour categories represent an improvement in supraglottic cancer classification.
The present study provides the first evidence that fibroblasts obtained from patients affected by Crouzon syndrome, a rare craniosynostosis, despite mutations in the high-affinity bFGF receptor retain their capacity to respond to bFGF. The growth factor reduces IL-1 secretion, downregulates biglycan and procollagen alpha(1)(I), and increases betaglycan expression. Since betaglycan is a co-receptor for bFGF signalling, an alternative signal transduction pathway is suggested in Crouzon fibroblasts, to explain the documented changes in ECM macromolecule production.
There is good evidence from linkage analysis and mouse model knockouts that the endothelin-1 gene (EDN1) is a good candidate for non-syndromic orofacial cleft (OFC) disease. EDN1 maps to the chromosomal region of the OFC1 locus in 6p23. Therefore we have examined three other candidate genes in the endothelin pathway (ECE1, EDNRA and EDNRB, which map to chromosomes 1, 4 and 13 respectively) in a linkage study of 9 families with OFC, where the disorder is not linked to chromosome 6p23. The total lod score for these 9 multiplex families never exceeded -2.00 and thus our data suggest that EDN1 and related genes are not involved in non-syndromic familial OFC.
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A schwannoma (or neurilemmoma) of the parapharyngeal space is a rare tumor in the head and neck region arising from the sheath of cranial nerves and/or the sympathetic chain. In the early stages of growth, there is usually a lack of symptoms because of the anatomical localization and slow growth of the tumor. The large dimension of the mass at presentation makes it difficult to perform a functional surgery, and in many cases the operation worsens the nerve status. The choice of surgical approach is of paramount importance in both preserving nerve function and achieving vascular control. The authors report a case and discuss the English literature.
The aims of this review are (1) to illustrate current knowledge of the mode of inheritance and the loci involved in the cleft lip and palate and (2) to summarize the results of our investigations, which were carried out in Italy. It is well established that nonsyndromic cleft of the lip with or without the palate (CL+/-P) and cleft palate only (CPO) are separate entities. Genetic heterogeneity has been observed in CL+/-P, which involves different chromosome regions, mainly 6p23 (OFC1), 2q13 (OFC2), and 19q13.2 (OFC3), as well as other loci, such as 4q25-4q31.3 and 17q21. Furthermore, an interaction between different genes has been suggested in the oligogenic model. In one case at least, an OFC1 and OFC2 interaction has been demonstrated. The mode of inheritance of CPO is compatible with a recessive single major gene model, while an association with a candidate gene, mapping on the chromosome region 2q13/TGFalpha, remains to be confirmed.
(3)H-thymidine incorporation was studied in cultured human nasal and articular chondrocytes exposed to low-energy, low-frequency pulsed electromagnetic fields (PEMFs) (75 Hz, 2.3 mT). The reverse transcriptase polymerase chain reaction (RT-PCR) analysis shows that human secondary chondrocytes derived from both nasal and articular cartilage express collagen type II mRNA, which is a specific marker of the chondrocyte phenotype. In a preliminary series of experiments, cells were exposed to PEMF for different time periods ranging from 6 to 30 hours (time-course), in medium supplemented with 10% or 0.5% fetal calf serum (FCS) and in serum-free medium. The ratios between the (3)H-thymidine incorporation in PEMFs and control cultures show an increase of the cell proliferation in cultures exposed to PEMFs when serum is present in the culture medium, whereas no effect was observed in serum-free conditions. The increase in DNA synthesis, induced by PEMFs, was then evaluated only at the times of maximum induction and the results were analyzed by the three-factor analysis of variance (ANOVA). The data presented in this study show that even if (3)H-thymidine incorporation is higher in nasal than in articular chondrocytes, PEMF induce an increase in the proliferation of both cell types. Moreover, the concentration of FCS in the culture medium greatly influences the proliferative response of human chondrocytes to the PEMF exposure. Though normal human osteoblast cells increase their proliferation when exposed to PEMFs if only 10% FCS is present in the medium, human chondrocytes are able to increase their cell proliferation when exposed to PEMFs in the presence of both 0.5% and 10% of FCS in the medium. The results obtained may help to explain the basic mechanisms of PEMF stimulation of fracture healing.
OBJECTIVE: To assess the efficacy, safety and extent of perceived indications of acarbose, a new antidiabetic agent, under routine clinical practice conditions in an unselected Northern Italian population of type II diabetic patients. METHODS: The study population was assigned to three different groups according to the physician's clinical judgement: group A (acarbose considered as an elective treatment); group B (acarbose considered to be of uncertain benefit): group C (acarbose deemed not to be appropriate). Group B patients were randomized either to continue their standard treatment or to add acarbose to it. Patients with type II diabetes mellitus were recruited from 17 diabetes outpatient clinics from one Italian region (Lombardy). A total of 1027 patients were recruited (group A: 283; group C: 494; group B: 250, of whom 124 were randomly assigned to standard treatment + acarbose and 126 to standard treatment alone). Acarbose was administered for 1 year at a median dose of 100 mg 3 times daily. Drug efficacy was evaluated in terms of mean HbAlc, pre- and post-prandial glycaemic values. Additional endpoints were the proportion of patients with HbA1c levels below 8% at the end of the study period and the proportion of subjects who needed a modification in the standard treatment. The safety and tolerability profiles of the drug were also investigated. Data on HbA1c, fasting and post-prandial blood glucose levels were analysed over time using repeated-measures analysis [Generalized Estimating Equation (GEE) models]. RESULTS: The analysis of Group B showed that, after treatment for 1 year, the mean reduction in HbA1c levels in the acarbose group with respect to the control group was 0.30% (95% confidence limits -0.60 +0.02; P = 0.07), while the mean reduction in post-prandial glycaemia was 17 mg-dl(-1) (95% c.l. -33.5 -0.8; P = 0.04). No difference resulted for fasting blood glucose levels. When looking at the baseline HbA1c levels, it emerged that the mean benefit associated with the use of acarbose was 0.14% (95% c.l. -0.6 +0.28; P = 0.5) in patients with HbAlc levels below 8%, 0.28% (95% c.l. -0.6 +0.05; P = 0.09) in those with values between 8% and 9.9% and 0.65% (95% c.l. -1.36 +0.06; P = 0.07) in those with values > or =10%. Only patients treated with diet+/-oral anti-diabetic agents (OAA) benefited from acarbose treatment (mean benefit = 0.37%, 95% c.l. -0.65 -0.08), while no effect was shown for insulin-treated subjects. The proportion of patients with HbA1c below 8% increased from 31% to 44% in the acarbose group and from 40% to 45% in the control group (absolute difference between baseline and end-of-study values = 8.0% in favour of acarbose-treated patients; P = 0.058). Patients treated with acarbose were significantly more likely to undergo a dose reduction in concomitant diabetic treatments compared with the control group; they were also less likely to require an increase in the dose of standard treatment and to start insulin during the study period. One third of the patients could not assume the drug for the whole study period, mainly due to gastrointestinal side-effects. CONCLUSIONS: The design adopted in this study allowed an integrated evaluation of the overall effectiveness of acarbose in clinical practice. The benefits of the drug in an unselected population of non-insulin-dependent diabetes mellitus (NIDDM) patients are significant but of marginal clinical relevance. Only a better definition of the subgroups of patients who are more likely to benefit from long-term treatment, particularly through possible postponement of secondary OAA failure, will allow a reliable definition of the cost-effectiveness of this complementary component of anti-diabetic strategy.
The phenotype of Apert osteoblasts differs from that of normal osteoblasts in the accumulation of macromolecules in the extracellular matrix. Apert osteoblasts increase type I collagen, fibronectin and glycosaminoglycans secretion compared with normal osteoblasts. Because the extracellular matrix macromolecule accumulation is greatly modulated by transforming growth factor-beta(1), we examined the ability of normal and Apert osteoblasts to secrete transforming growth factor-beta(1) by CCL-64 assay and to produce transforming growth factor-beta(1 )by analysis of the mRNA expression of transforming growth factor-beta(1). Northern blot analysis revealed an increased amount of transforming growth factor-beta(1) mRNA expression in Apert osteoblasts compared with normal ones. Moreover, the level of the active transforming growth factor-beta(1) isoform was higher in Apert than in normal media. In pathologic cells, the increase in transforming growth factor-beta(1) gene expression was associated with a parallel increase in the factor secreted into the medium. The level of transforming growth factor-beta(1) was decreased by the addition of basic fibroblast growth factor. Transforming growth factor-beta(1) is controlled temporally and spatially during skeletal tissue development and produces complex stimulatory and inhibitory changes in osteoblast functions. We hypothesise that in vitro differences between normal and Apert osteoblasts may be correlated to different transforming growth factor-beta(1) cascade patterns, probably due to an altered balance between transforming growth factor-beta(1) and basic fibroblast growth factor.
BACKGROUND: The efficacy of reperfusion therapy after acute myocardial infarction is time dependent. The risk profile of every patient should be available as soon as possible. Our aim was to determine whether collection of simple clinical markers at hospital admission might allow reliable risk stratification for in-hospital mortality. METHODS: The subjects were 11,483 patients with acute myocardial infarction from the GISSI-2 cohort. The GISSI-1 and GISSI-3 populations were selected to validate the classification. To stratify patients, the tree-growing method called recursive partitioning and amalgamation (RECPAM) was used. This method is used to identify homogeneous and distinct subgroups with respect to outcome. RESULTS: The RECPAM algorithm provided 6 classes. RECPAM class I included Killip class 3 to class 4 patients (516 deaths/1000). RECPAM class II included Killip 2 patients older than 66 years and with anterior infarction or sites of infarction that could not be evaluated (314 deaths/1000). Killip 1 patients older than 75 years and with anterior or multiple sites or sites that could not be evaluated were included in RECPAM class III with Killip class 2 patients younger than 66 years and with systolic blood pressure less than 120 mm Hg or older than 66 years and with any other infarction site (207 deaths/1000). The other classes showed lower mortality rates (91, 32, and 12 deaths/1000 for RECPAM classes IV, V, and VI). In the GISSI 1 and GISSI 3 samples the 6 classes ranked in the same order in terms of mortality rate. With respect to low-risk strata, patients belonging to RECPAM class VI without serious clinical events in the first 4 days had a very low incidence of in-hospital death (0.9%) or morbidity. Cumulative 6-month mortality for the 6 RECPAM classes was 59.6%, 41.2%, 26.4%, 12.9%, 4. 8%, and 2.2%. CONCLUSIONS: Four simple clinical markers readily available at admission of patients with myocardial infarction allow a quick, reliable, and inexpensive prediction of risk for in-hospital and 6-month mortality. The RECPAM classification also helped identify a large subgroup of patients fit for early hospital discharge.
Bone development is controlled by the autocrine and/or paracrine effects of regulatory molecules. We previously showed that the phenotype of fibroblasts obtained from patients affected by Crouzon's syndrome, an autosomal dominant disease characterized by pathological skull bone development, differed from that of normal cells and was regulated by interleukin treatments. The changes in the relative concentrations of extracellular macromolecules (glycosaminoglycans-GAG, collagen and fibronectin) were associated with abnormal interleukin secretion that affected the microenvironment where the osteogenic processes take place. Mutations in human fibroblast growth factor receptors are now thought to be involved in Crouzon's syndrome. Since coactivation of interleukins and basic fibroblast growth factor (bFGF) is probably implicated in morphogenetic and osteogenic processes and heparan sulphate proteoglycans have a critical role in regulating bFGF activity, the phenotypes of normal and Crouzon osteoblasts were studied and the effects of bFGF on the expression of bFGF, procollagen alpha1 (I), and proteoglycan (PG) genes for biglycan, decorin, betaglycan and syndecan analyzed. Specific human cDNA probes were used to screen the relative levels of mRNA by Northern analysis. Spontaneous or bFGF-modulated release of interleukins was also assayed. The bFGF gene transcript was detected only in Crouzon osteoblasts. We showed for the first time that Crouzon osteoblasts, despite a mutation in the FGF receptor, still responded to exogenous bFGE In fact, the growth factor induced changes in the GAG profile and in the levels of mRNA coding for PG and procollagen alpha1 (I) and down-regulated heparan sulfate GAG chains. ELISA showed that bFGF-induced interleukin secretion differed in normal and Crouzon osteoblasts. The observed differences in PG core protein, procollagen alpha1 (I) and bFGF could be associated with the Crouzon bone phenotype and also should provide further understanding on the molecular basis of the diseased state of bone.
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