Virgínia Minghelli Schmitt

Bronquiolite aguda por rinovírus em lactentes jovens

OBJECTIVE: To determine the prevalence of rhinovirus infection in hospitalized young infants with acute bronchiolitis. METHODS: Hospitalized children with acute bronchiolitis admitted to the Hospital Sao Lucas/PUCRS between May and September 2002 were selected prospectively. Nasopharyngeal samples were assayed for respiratory syncytial virus, parainfluenza, influenza and adenovirus by immunofluorescence. For rhinovirus test a reverse transcription-polymerase chain reaction for picornavirus was used, followed by hybridization with rhinovirus specific probes. RESULTS: Forty-five patients were selected for the study. The median age of the subjects studied was 2 months. Positive samples for respiratory viruses were found in 35/45 (77.8%) subjects and 7/35 (20%) patients had dual infection. Respiratory syncytial virus was detected in 33/35 (94%) cases. Rhinovirus was detected in 6/35 patients (17%). CONCLUSIONS: Rhinovirus was the second most common agent detected in nasal secretions from young infants hospitalized with acute bronchiolitis.

Transition of cervical carcinoma in situ to invasive cancer: Role of p16INK4a expression in progression and in recurrence

To investigate the expression of p16(INK4a) in cervical carcinoma and its relation to the transition of carcinoma in situ to invasive carcinoma, and its role in recurrence of cervical lesions as well, a series of 90 patients with cervical carcinoma (49 with in situ lesion and 41 with invasive lesion) were selected from July 2001 and September 2002. Groups with in situ and invasive lesions were paired for a series of risk variables for cervical cancer and followed up for 60 months. The follow-up visits occurred every 6 months in the first three years and annually up to the fifth year. It was observed that 87.9% of the patients with invasive lesion showed overexpression of p16(INK4a), in comparison with 37.6% of those with in situ lesion (X(2): 13.68; 2 df; p=0.0002; OR: 12.08), demonstrating overexpression of p16(INK4a) as a risk of invasion of the basal layer by dysplastic cells. We also observed an association between overexpression of p16(INK4a) and staging of cancer (X(2): 18.38; 6 df; p=0.0003). A prospective analysis, when controlled for interaction with cervical lesion groups (by Cox regression), demonstrated a risk of recurrence of 4.83 times attributed to overexpression of p16(INK4a), albeit not statistically significant (p=0.14).

Evaluation of the brain and kidney renin‐angiotensin system and oxidative stress in neonatal handled rats

The aim of this study was to test the hypothesis that the renin-angiotensin system (RAS) components, as well as the oxidative stress system, would respond to early environmental changes. Thus, we have evaluated the effects of neonatal handling on both brain and kidney RAS and oxidative stress. Pups were divided into two groups: nonhandled and handled. The procedure consisted of handling them for 1 min/day in the first 10 days of life. On days 1, 5, and 10, animals were killed by decapitation. Blood samples were collected and the brain and kidneys were removed. Renin, AT(1), and AT(2) mRNA expression were evaluated through RT-PCR. Angiotensin II (ANG II) serum concentration was also measured. An increased ANG II concentration, brain and kidney AT(2) mRNA expression were demonstrated. The kidney mRNA AT(1) expression was decreased. There was also a kidney lipid peroxidation increase and a brain superoxide dismutase and catalase decrease. In conclusion, handling in the neonatal period induces the activation of the angiotensinergic system, as well as modulates its mRNA receptor expression. The oxidative stress balance system seems not to be involved.

Associação entre o polimorfismo no códon 72 da p53 e as lesões pré-malignas e malignas cervicais

OBJETIVOS: testar a hipotese de que o polimorfismo no codon 72 do gene TP53 e fator de risco para as lesoes pre-malignas e malignas cervicais associadas ou nao ao papilomavirus humano (HPV). METODOS: foram incluidas amostras de cervice uterina, para pesquisa de DNA de HPV e do polimorfismo no codon 72 da p53 com o uso da reacao em cadeia da polimerase (PCR), de 155 pacientes que se submeteram a biopsia cervical. Foram formados tres grupos de acordo com o diagnostico histologico: lesao escamosa intra-epitelial de baixo grau (LSIL), lesao escamosa intra-epitelial de alto grau (HSIL) e carcinoma cervical. Aquelas pacientes sem alteracoes displasicas, citologicas e histologicas, foram consideradas controles. Para testar a associacao entre o polimorfismo no codon 72 do gene TP53 e os grupos, foi utilizado o teste de c2. Considerou-se como significativo o intervalo de confianca no nivel de 95% (a=0,05). RESULTADOS: quarenta pacientes tiveram o diagnostico histologico de carcinoma cervical, 18 tinham HSIL, 24 tinham LSIL e 73 foram consideradas controles. O genotipo Arg/Arg p53 foi encontrado em 60,0% das pacientes com câncer, 50,0% dos casos com HSIL, 45,8% dos casos com LSIL e em 45,2% dos controles. Nao houve diferenca significativa entre as proporcoes de cada genotipo da p53 nos diferentes grupos independente da presenca do HPV (c2: 3,7; p=0,716). CONCLUSOES: nossos dados nao suportam a hipotese de que o polimorfismo no codon 72 do gene TP53 e importante no desenvolvimento de lesoes cervicais pre-malignas e malignas associadas ou nao ao HPV.

Human papillomavirus and oral squamous cell carcinoma in a south Brazilian population

a Curso de Odontologia, Universidade Luterana do Brasil—ULBRA, Av. Farroupilha, 8001, Pd 59, Bairro São José, CEP 92425‐900, Canoas/RS, Brazil b Instituto de Pesquisas Biomédicas, Pontifícia Universidade Católica do Rio Grande do Sul, PUCRS, Av. Ipiranga, 6690, Bairro Jardim Botânico, CEP 90610‐000, Porto Alegre/RS, Brazil c Faculdade de Farmácia, Pontifícia Universidade Católica do Rio Grande do Sul, PUCRS, Av. Ipiranga, 6681, Pd 12, Bairro Partenon , CEP 90619‐900, Porto Alegre/RS, Brazil d Faculdade de Odontologia, Universidade Federal do Rio Grande do Sul—UFRGS, Rua Ramiro Barcelos, 2492, Bairro Santana, CEP 90035‐903, Porto Alegre/RS, Brazil