Exploiting nonreciprocity in BOTDA systems.

In this Letter, we present and demonstrate a novel technique for distributed measurements in Brillouin optical time-domain analysis based on the use of the nonlinear phase-shift induced by stimulated Brillouin scattering. Employing a Sagnac interferometer (SI), the position-resolved Brillouin phase-shift spectrum (BPS) along the fiber can be obtained, benefiting from the sensitivity to nonreciprocal phase-shifts of the SI scheme. This proposal simplifies the existing methods to retrieve the BPS distribution along an optical fiber since phase modulation, filtering, and high-bandwidth detectors are not required. The fundamentals of the technique are described theoretically and validated through numerical simulations and experimental measurements.

[IL-6 and TNF-α gene expression in the rectal mucosal of patients with chronic idiopathic ulcerative colitis and controls]. / Expresion del gen de IL-6 y TNF-α en la mucosa rectal de pacientes con colitis ulcerosa crónica idiopática y controles.

BACKGROUND: It has been reported that pro-inflammatory cytokines levels like IL-6 and TNF-α can determine the degree of inflammation of ulcerative colitis (UC). AIMS: To measure the gene expression of IL-6 and TNF-á in patients with UC and controls and to correlate with histological activity. PATIENTS AND METHODS: We studied 36 patients with UC, 13 healthy controls and 11 with inflammation. After total ribonucleic acid (RNA) extraction, complementary deoxyribonucleic acid (DNA) was synthesized by polymerase chain reaction (PCR) and relative expression was determined through real-time PCR for IL-6 and TNF-á. Statistical analysis was performed using the Kruskal-Wallis test and Spearman correlation. RESULTS: The expression of IL-6 increases in patients with active UC compared to controls (p = 0.004) as well as UC patients in remission (p = 0.014). There was no significant difference between patients with active UC and controls with inflammation. (p = 0.446). Gene expression of TNF-α was higher in biopsies from patients with UC activity compred with control subjects (p = 0.004), as well as those in remission (p = 0.001). The expression of IL-6 correlated significantly (p = 0.02) with histological activity. CONCLUSIONS: The gene expression of IL-6 and TNF-α is increased in active UC. Interleukin 6 is better marker of bowel inflammation because its expression correlates with histological activity.

Early-onset type 2 diabetes: metabolic and genetic characterization in the mexican population.

The objective of this study was to investigate possible defects in the insulin sensitivity and/or the acute insulin response in a group of Mexican patients displaying early-onset type 2 diabetes and to evaluate the contribution of mutations in three of the genes linked to maturity-onset diabetes of the young. We studied 40 Mexican patients with an age of diagnosis between 20 and 40 yr in which the insulin sensitivity as well as the insulin secretory response were measured using the minimal model approach. A partial screening for possible mutations in 3 of the 5 genes linked to maturity-onset diabetes of the young was carried out by PCR-single strand conformation polymorphism analysis. A low insulin secretory capacity (AIRg = 68.5 +/- 5 muU/mL.min) and a near-normal insulin sensitivity (3.43 +/- 0.2 min/muU.mL x 10(4)) were found in these patients. Among this group we found two individuals carrying missense mutations in exon 4 of the hepatocyte nuclear factor-1alpha (HNF-4alpha) gene (Asp(126)-->His/Tyr and Arg(154)-->Gln, respectively) and one carrying a nonsense mutation in exon 7 of the HNF-1alpha gene (Gln(486)-->stop codon); 7.5% had positive titers for glutamic acid decarboxylase antibodies. Thirty-five percent of cases had insulin resistance; these subjects had the lipid abnormalities seen in the metabolic syndrome. A defect in insulin secretion is the hallmark in Mexican diabetic patients diagnosed between 20 and 40 yr of age. Mutations in either the HNF-1alpha or the HNF-4alpha genes are present among the individuals who develop early-onset diabetes in our population. These particular sequence changes have not been previously reported and therefore represent putative new mutations. Even in the absence of endogenous hyperinsulinemia, insulin resistance is associated with an adverse lipid profile.