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Biomedical subjects

P Latorre

Publications and source records attributed to P Latorre.

At least 19 recordsLinked to original sources
PubMed2005

[Rational treatment of nasal polyposis].

Despite the therapeutical advances of the last decade, nasal polyposis represents still a problem for rhinology, practitioners. A number of hypotheses have been formulated about its etiopathogenesis, but no one is confirmed, so that nowadays therapy continues to be only symptomatic and does not cure definitively the underlying pathology. Recurrences are frequent and discourage both the practitioner and the patient. Purpose of this paper is to illustrate Authors' therapeutical rationale aimed to reestablish nasal flow, reduce rhinorrhea, improve olfaction, decrease rhinosinusinusal infection rate and maintain as long as possible such a symptomatic improvement. These targets are best achieved by a combination of medical and surgical treatments in order to optimize the results and reduce the side-effects of both the therapeutical options. Moreover the treatment should be tailored on each patient and follow up should be careful and performed at regular interval. Authors reviewed the clinical records of patients who underwent surgery for nasal polyposis between 2002 and 2004 at Ospedale di Circolo e Fondazione Macchi, University of Insubria, Varese, Italy, with a minimum follow-up of 12 months. All patients underwent the complete set of diagnostic work-up. The choice between surgical or medical options was based on both the kind of the polyposis and the staging of the pathology. The therapy was as more "personalized" as possible, but a homogeneity of treatment was maintained. The results show that a correct "staging" of the patient allows an appropriate therapy and reduces recurrence rate. In conclusion, authors report their experience and propose a scheme of diagnostic work-up in order to define grading/staging of the pathology and establish a "tailored" therapeutic protocol aimed to control a pathology which is rarely definitively treated.

Adolescent↗
PubMed2001

Alzheimer's disease and the cystatin C gene polymorphism: an association study.

Cystatin C is an amyloidogenic protein that colocalizes with beta-amyloid (Abeta) within arteriolar walls in Alzheimer disease (AD) brains. Recently, a coding polymorphism in the cystatin C gene (CST3) has been claimed to confer risk for the development of late-onset AD. In the present work we have tested the frequencies of CST3-A and CST3-G alleles and used chi-square and logistic regression analyses to assess the association among the CST3 polymorphism, apolipoprotein E4 (APOE4), and AD in a series of 159 AD patients and 155 controls. The CST3-A allele was seen to be an accumulation risk factor for early-onset AD. Furthermore, a synergistic association among the CST3-A allele, APOE4 and AD was found in AD patients whose ages were between 60 and 74 years.

Aged↗
PubMed2000

Inhibition of cap-dependent gene expression induced by protein 2A of hepatitis A virus.

The viral protein 2A of hepatitis A virus (HAV) lacks the conserved 18 aa sequence found in other picornavirus proteases; hence, it is unclear whether the induction of CPE by culture-adapted HAV strains is due to 2A-mediated activity. Moreover, the cleavage sites and actual borders of HAV 2A are not known. Accordingly, a nested series of cDNA sequences encoding the segment of the HAV polyprotein (aa 760-1087) were linked to the 5'-UTR of poliovirus type 2 (Lansing strain) and inserted downstream of the gene encoding human growth hormone (GH). Following transfection of COS-1 cells, levels of GH (translation of which was entirely cap dependent) were determined in culture supernatants. Expression of HAV peptides extending from aa 764, 776 or 791 to 981 strongly inhibited cap-dependent translation of GH, whereas cap-independent expression of a reporter gene (CAT) directed by the poliovirus RNA 5'-UTR was unaffected. The inhibitory effect was absent in constructs expressing either the short peptide encompassing aa 760-836 or proteins initiated downstream of the putative cleavage site 836-837, suggesting that the boundaries of a functional HAV 2A may extend from the Gln/Ser junction 791-792 to residue 981, while peptides initiated at the Gln/Ala pair 836-837 may result from alternative cleavage. Point mutations that substituted members of the triad Ser(916), His(927) and Asp(931) abolished the inhibitory effect on cap-dependent translation, suggesting that the HAV-induced CPE may be mediated by 2A protein.

5' Untranslated Regions↗
PubMed1999

Sendai virus C proteins counteract the interferon-mediated induction of an antiviral state.

We have studied the relationship between the Sendai virus (SeV) C proteins (a nested set of four proteins initiated at different start codons) and the interferon (IFN)-mediated antiviral response in IFN-competent cells in culture. SeV strains containing wild-type or various mutant C proteins were examined for their ability (i) to induce an antiviral state (i.e., to prevent the growth of vesicular stomatitis virus [VSV] following a period of SeV infection), (ii) to induce the elevation of Stat1 protein levels, and (iii) to prevent IFN added concomitant with the SeV infection from inducing an antiviral state. We find that expression of the wild-type C gene and, specifically, the AUG114-initiated C protein prevents the establishment of an antiviral state: i.e., cells infected with wild-type SeV exhibited little or no increase in Stat1 levels and were permissive for VSV replication, even in the presence of exogenous IFN. In contrast, in cells infected with SeV lacking the AUG114-initiated C protein or containing a single amino acid substitution in the C protein, the level of Stat1 increased and VSV replication was inhibited. The prevention of the cellular IFN-mediated antiviral response appears to be a key determinant of SeV pathogenicity.

Animals↗
PubMed1999

Dentatorubropallidoluysian atrophy in a spanish family: a clinical, radiological, pathological, and genetic study.

UNLABELLED: The object was to describe the clinical, radiological, pathological, and genetic findings in a Spanish family with dentatorubropallidoluysian atrophy (DRPLA). This is an inherited neurodegenerative disease, well recognised in Japan, but with few cases reported from Europe and America and no cases published from Spain. The clinical misdiagnosis of Huntington's disease is not infrequent. Pedigree analysis and clinical data of a family were collected. A genetic study was performed in two patients. Pathological information was obtained from the necropsy of one patient. RESULTS: Pedigree analysis showed an autosomal dominant pattern of inheritance. Age at onset varied from 5 to 55 years. Ataxia and chorea were present in most of the members. Some of these had a long course disease with late dementia. Four patients had seizures and early mental impairment. In one patient, cranial MRI showed cortical, brain stem and cerebellar atrophy, and white matter changes. In another patient, necropsy showed atrophy of the globus pallidus and lipofuscin deposits in dentate and pallidal neuronal cells. Genetic study showed an abnormal CAG triplet expansion in the B37 gene on chromosome 12. As in other cases previously reported, Spanish cases of DRPLA show intrafamilial phenotypic heterogeneity. Clinical and MRI data could differentiate DRPLA from Huntington's disease but definitive diagnosis requires molecular studies. Pathological studies are still necessary to correlate DRPLA brain involvement with the clinical and molecular findings.

Adolescent↗
PubMed1998

The various Sendai virus C proteins are not functionally equivalent and exert both positive and negative effects on viral RNA accumulation during the course of infection.

Recombinant Sendai viruses were prepared which cannot express their Cprime, C, or Cprime plus C proteins due to mutation of their respective start codons ([Cprime-minus], [C-minus] and [double mutant], respectively). The [Cprime-minus] and [C-minus] stocks were similar to that of wild-type (wt) virus in virus titer and plaque formation, whereas the double-mutant stock had a much-reduced PFU or 50% egg infective dose/particle ratio and produced very small plaques. Relative to the wt virus infection, the [Cprime-minus] and [C-minus] infections of BHK cells resulted in significantly greater accumulation of viral RNAs, consistent with the known inhibitory effects of the Cprime and C proteins. The double-mutant infection, in contrast, was delayed in its accumulation of viral RNAs; however, once accumulation started, overaccumulation quickly occurred, as in the single-mutant infections. Our results suggest that the Cprime and C proteins both provide a common positive function early in infection, so that only the double mutant undergoes delayed RNA accumulation and exhibits the highly debilitated phenotype. Later in infection, the same proteins appear to act as inhibitors of RNA accumulation. In infections of mice, [Cprime-minus] was found to be as virulent as wt virus whereas [C-minus] was highly attenuated. These results suggest that the Cprime and C proteins cannot be functionally equivalent, since C can replace Cprime for virulence in mice whereas Cprime cannot replace C.

Animals↗
PubMed1998

Sendai virus Y proteins are initiated by a ribosomal shunt.

The Sendai virus P/C mRNA expresses eight primary translation products by using a combination of ribosomal choice and cotranscriptional mRNA editing. The longest open reading frame (ORF) of the mRNA starts at AUG104 (the second initiation site) and encodes the 568-amino-acid P protein, an essential subunit of the viral polymerase. The first (ACG81), third (ATG114), fourth (ATG183), and fifth (ATG201) initiation sites are used to express a C-terminal nested set of polypeptides (collectively named the C proteins) in the +1 ORF relative to P, namely, C', C, Y1, and Y2, respectively. Leaky scanning accounts for translational initiation at the first three start sites (a non-ATG followed by ATGs in progressively stronger contexts). Consistent with this, changing ACG81/C' to ATG (GCCATG81G) abrogates expression from the downstream ATG104/P and ATG114/C initiation codons. However, expression of the Y1 and Y2 proteins remains normal in this background. We now have evidence that initiation from ATG183/Y1 and ATG201/Y2 takes place via a ribosomal shunt or discontinuous scanning. Scanning complexes appear to assemble at the 5' cap and then scan ca. 50 nucleotides (nt) of the 5' untranslated region before being translocated to an acceptor site at or close to the Y initiation codons. No specific donor site sequences are required, and translation of the Y proteins continues even when their start codons are changed to ACG. Curiously, ATG codons (in good contexts) in the P ORF, placed either 16 nt upstream of Y1, 29 nt downstream of Y2, or between the Y1 and Y2 codons, are not expressed even in the ACGY1/ACGY2 background. This indicates that ATG183/Y1 and ATG201/Y2 are privileged start sites within the acceptor site. Our observations suggest that the shunt delivers the scanning complex directly to the Y start codons.

Base Sequence↗
PubMed1995

Central nervous system disease in Sjögren's syndrome.

Our prospective study consisted of a general and neurological evaluation in 48 patients (41 females, 7 males; mean age: 58.2 years) with primary Sjögren's syndrome (PSS). We performed serologic studies and cranial magnetic resonance imaging (MRI). Main extraglandular features were arthralgias and non-erosive arthritis (37.5%). Raynaud (21%) and pulmonary fibrosis (12.5%). Antinuclear antibodies were positive in 42.5% and anti-SS-A (Ro) in 20%. Migraine (52%), neuropsychiatric disease (29%) and a past history of focal acute neurological deficits (23%), were the central nervous system (CNS) manifestations more frequently observed. Cranial MRI examination detected hyperintense small subcortical lesions in 51.3% of patients and in 36.6% of age and sex matched controls (P < 0.001). CNS disease was not serious concerning vital prognosis, but produced significant morbidity in some patients. Late onset "migraine-like" episodes with prolonged sensoromotor deficits and coexisting neuropsychiatric disease emerged as a characteristic clinical spectrum in those patients diagnosed in a neurological setting. Cranial MRI was frequently abnormal, but findings were not specific. Neurologic manifestations reminiscent of multiple sclerosis were rarely seen.

Aged↗
PubMed1993

Acromegaly: an epidemiological study.

Although morbility and mortality in acromegaly are higher than in the general population, there have been very few previous epidemiological studies. This study tries to answer "why". Seventy-four patients affected by acromegaly in Vizcaya (Spain) between 1970 and 1989 were considered for an epidemiological study. The prevalence of known cases at the end of 1989 was 60 per million inhabitants. The average incidence of newly diagnosed cases was 3.1 per million people per year. Unexpectedly, acromegaly was more frequent in women (n = 48) than in men (n = 26), with a ratio of 1.8:1. Mean age at diagnosis was significantly higher in women (46.1 +/- 2.2 yr) than in men (39.5 +/- 2.2 yr) (p < 0.05) There was a positive correlation between age at diagnosis and the estimated duration of the disease (r = 0.56, p < 0.05) and a negative one between age and basal GH serum levels (r = -0.52 p < 0.002). The age at diagnosis was significantly higher in patients with invasive tumors (grade III and IV) than in those with enclosed tumors (grade I and II) (47.7 +/- 1.8 vs 40.1 +/- 3.3 p < 0.05). In general, mortality was higher than the expected for the control population (standardized mortality ratio, SMR = 3.2, 95% confidence interval. Cl = 1.55-5.93). However, mortality was higher in men (SMR = 7, 95% Cl = 2.81-14.4) but not in women (SMR = 1.4 95% Cl = 0.29-4.17).(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1984

Rifampicin in tuberculous meningitis: a retrospective assessment.

To shed some light on the potential value of rifampicin in the treatment of tuberculous meningitis (TBM) in adults, a retrospective analysis has been made of 143 medical records from 4 hospitals for the period 1967-80. Treatment of TBM with rifampicin and other antituberculous drugs in combination (Group B) was compared to other regimes which did not include rifampicin (Group A). There were 64 patients in Group B and 79 in Group A. The two groups of patients did not differ significantly in their prognostic characteristics. The total mortality was 14.7%: it was higher among patients not treated with rifampicin (24%; Group A) than amongst those given rifampicin (3.1%; Group B; chi 2 = 10.74; p less than 0.005). The difference was also statistically significant (chi 2 = 6.88; p less than 0.01) if patients who died during the first 48 h after the institution of treatment were excluded. No significant difference in mortality rate was found when patients treated with rifampicin plus isoniazid (INH) 8-10 mg/kg (1 death out of 41 patients) were compared to patients treated with INH 15 mg/kg (2 deaths out of 20 patients). Neurological sequelae recorded during a 6 month follow-up period were more severe among patients not treated with rifampicin.

Adolescent↗
PubMedDate not supplied

Oxidative damage to RBC membranes and pentose phosphate shunt activity in hemodialysis patients after suspension of erythropoietin treatment.

During follow-up of anemic hemodialysis patients (HDP) treated with recombinant human erythropoietin (rHuEpo), it was noticed that in five HDP, some time after suspension of rHuEpo, hemoglobin (Hb) levels remained at acceptable levels. A metabolic block of the pentose phosphate shunt (PPS) has been described in HDP, which leads to increased oxidative damage of red blood cell (RBC) membranes and increased susceptibility to hemolysis. The increased production of short-chain fatty aldehydes, including malonyldialdehyde (MDA), is an appropriate index of oxidative damage. This study aimed to verify whether the maintenance of acceptable levels of Hb was related to a change in RBC membrane oxidative damage and pentose phosphate shunt activity. In the five HDP in question who required rHuEpo (150 U/kg/week) for severe anemia (Hb = 7.48 +/- 0.95 g/dl), after a stable level of Hb > 10 g/dl was reached for at least 1 month, rHuEpo treatment was stopped. Hb levels remained adequate (Hb = 10.68 +/- 0.77 g/dl) after 14.6 +/- 7.64 months. The oxidative damage was evaluated by measuring RBC MDA (microgram/ml packed RBC) basal levels, and PPS activity by measuring MDA levels after incubation with ascorbate and cyanide (delta % RBC MDA production). Ten anemic HDP not treated with rHuEpo were used as controls (Hb = 8.12 +/- 1.32 g/dl). It was found that the maintenance of adequate levels of serum Hb after suspension of rHuEpo therapy is related to a decrease in RBC membrane oxidative damage (RBC MDA HDP = 2.40 +/- 0.41 vs. RBC MDA controls = 18.23 +/- 6.56; P < 0.005) in consequence of the normalization of pentose phosphate shunt activity.

Aged↗