[Glicemic control in prepubertal and pubertal patients with diabetes type 1 - a one year ambulatory follow-up] / Controle glicêmico de pré-púberes e púberes com diabetes mellitus tipo 1 durante um ano de acompanhamento ambulatorial.

OBJECTIVE: To evaluate glycemic control in type 1 diabetes mellitus patients followed in 1998. PATIENTS AND METHODS: We studied 38 patients [22 males; age = 10.4 -/+ 4.1 years; 12 (31.6%) prepubertal, 26 (68.4%) pubertal], with diabetes duration of 3.7-/+3.4 years and age of diagnosis of 7.2 -/+ 4.7 years. HbA1c was determined using high-performance liquid chromatography (L-9100 Merck Hitachi, reference value =2.6 to 6.2%). RESULTS: HbA1c was 8.04 -/+ 2.4%, without association with gender and puberty. In the 27 patients with at least two HbA1c determinations, the level of glycemic control changed in 8 (29.6%) and remained the same in 19 (70.4%). From these, glycemic control was poor in 3 (11.1%) and good in 16 (59.3%). Among the patients with good glycemic control, HbA1c was always within reference values in 4 (25%); 7 (43.75%) had at least one HbA1c measurement within these limits; and in 5 (31.25%), all HbA1c measurements were above the upper limit of the reference range. There was no association between the last glycemic control evaluation and the number of HbA1c determinations. The intraindividual coefficient of variation of HbA1c in the group that had at least three HbA1c determinations (n = 19) was 11.2 -/+ 5.6% (P = 0.0000). CONCLUSION: In our study, although most patients presented satisfactory glycemic control during the follow-up period, only 4 patients (14.8%) maintained normal values of HbA1c. The variability of HbA1c must be evaluated when considering the interrelation between glycemic control and evolution to microvascular complications in diabetis.

Longevity genes in the nematode Caenorhabditis elegans also mediate increased resistance to stress and prevent disease.

More than 40 single-gene mutants in Caenorhabditis elegans have been demonstrated to lead to increased lifespan (a rigorous, operational test for being a gerontogene) of 20% or more; these are referred to collectively as 'Age' mutants. Age mutants must change key functions that are rate-limiting determinants of longevity; moreover, important genes can be identified independently of prior hypotheses as to actual mode of gene action in extending longevity and/or 'slowing' of ageing. These Age mutants define as many as nine (possibly) distinct pathways and/or modes of action, as defined by primary phenotype. Each of three well-studied mutants (age-1, clk-1, and spe-26) alters age-specific mortality rates in a fashion unique to itself. In age-1 mutants, the decreases in mortality rates are quite dramatic, with an almost tenfold drop in mortality throughout most of life. All Age mutants (so far without exception) increase the ability of the worm to respond to several (but not all) stresses, including heat, UV, and reactive oxidants. We have used directed strategies as well as random mutagenesis to identify novel genes that increase the worm's ability to resist stress. Two genes (daf-16 and old-1) are epistatic to the long-life phenotype of most mutants and also yield over-expression strains that are stress-resistant and long-lived. We have also used a variety of approaches to determine what transcriptional alterations are associated with increased longevity (and with ageing itself), including whole-genome expression studies using microarrays and GFP reporter constructs. We suggest that the role of the Age genes in both longevity and stress resistance indicates that a major evolutionary determinant of longevity is the ability to respond to stress. In mammals, both dietary restriction and hormesis are phenomena in which the endogenous level of resistance to stress has been upregulated; both of these interventions extend longevity, suggesting possible evolutionary conservation.

Sindrome nefrotica secundaria a sifilis congenita precoce. / Nephrotic syndrome secondary to precocious congenital syphilis

Os autores apresentam um caso clinico de paciente portador de sifilis congenita precoce que cursou com sindrome nefrotica. Estabelecem o perfil clinico e laboratorial do paciente, enfatizando a evolucao para a cura da sindrome nefrotica. Aborda-se a revisao literaria da associacao de sindrome nefrotica e sifilis congenita precoce