Enzymatic markers of salivary cell injury in saliva of type 1 diabetic children

To find evidence of salivary gland involvement in human type I diabetes, we explored the changes in aminotransferase and lactate dehydrogenase activities, as indices of cellular injury, in the whole saliva of diabetic children. Although no significant difference in these enzymatic activities was observed between control and diabetic children as a whole, a negative correlation was found between enzymatic activities and duration of the disease, the highest values being detected in the diabetic subgroup diagnosed for less than 4 years. This suggests that some cell damage could be present in salivary glands of recently diagnosed diabetic children, likely as a result of immune-mediated alterations. In conclusion, these results may support the hypothesis that, as in rodents, the salivary glands could be an additional target of the immunological attack mainly directed against pancreatic beta-cells and resulting in type 1 diabetes.     

Periodontal clinical and microbiological data in desquamative gingivitis patients

Objectives

A series of patients affected by desquamative gingivitis (DG) was investigated in order to evaluate relation patterns among clinical parameters relevant to plaque-induced periodontitis, periodontal microbiological data and the presence of DG lesions.

Patients and methods

Eight oral lichen planus (OLP) and four mucous membrane pemphigoid (MMP) patients were examined. Periodontal measurements (performed at six sites per tooth on all teeth) included probing depth (PD), gingival recession (REC), clinical attachment loss (CAL) and full-mouth plaque (FMPS) and bleeding (FMBS) scores; the presence and the exact location (site by site) of DG lesions were carefully recorded. Sub-gingival plaque samples were collected and examined by means of real-time PCR for the quantitative determination of the six most important marker organisms of periodontitis. Statistically significant differences and correlation of studied variables between DG-positive and DG-negative sites were investigated in MMP and OLP cases using Mann–Whitney test (p?<?0.05) and the Spearman rank correlation coefficient, respectively.

Results

OLP gingival lesions do not significantly affect CAL, although the presence of such lesions may reduce REC and increase PD and FMPS. MMP gingival lesions significantly worsened CAL and increased REC and FMPS. In both OLP and MMP cases, no significant difference was found between DG-positive and DG-negative sites as regards the relative percentage of the investigated species on the total bacterial load. Correlations between the presence of DG lesions and clinical parameters (CAL, PD, REC) were not significant (p?<?0.05). Significant correlations were found for the presence of gingival OLP lesions and Aggregatibacter actinomycetemcomitans (AA) and for the absence of gingival MMP lesions and AA.

Conclusions

These findings are not definitive, but highlight the need for further investigations of periodontal clinical and microbiological aspects of disorders causing DG in order to clarify their potential interference with plaque-related periodontitis.     

How cyclodextrin incorporation affects the properties of protein-loaded PLGA-based microspheres: the case of insulin/hydroxypropyl-beta-cyclodextrin system.

The aim of this work was to study the influence of cyclodextrin (CD) incorporation on the properties of protein-loaded poly(lactide-co-glycolide) (PLGA) microspheres, with particular regards to protein release kinetics. To this purpose, insulin-loaded microspheres were prepared by spray-drying emulsion or solution formulations, with or without hydroxypropyl-beta-cyclodextrin (HPbetaCD), and fully characterized for encapsulation efficiency and release kinetics of both insulin and cyclodextrin. Homogeneous populations of spherical microparticles entrapping both insulin and HPbetaCD were obtained. In order to get an insight into insulin/HPbetaCD interactions occurring inside microspheres, Fourier transform infrared (FTIR) analysis in the Amide I region was performed. FTIR spectra of dried microspheres containing HPbetaCD showed a change in insulin secondary structure, attributed to the presence of insulin/HPbetaCD complexes within microspheres. Insulin release was affected by the presence of HPbetaCD depending on the initial formulation conditions. In the case of microspheres prepared from emulsion, cyclodextrin reduced only insulin burst, whereas in the case of microspheres obtained from solution, the overall insulin release rate was slowed down. Combining the release kinetics of HPbetaCD with the FTIR results on hydrated microspheres, it was concluded that the formation of insulin/HPbetaCD complexes inside microspheres is critical to decrease protein diffusivity in the polymer matrix and achieve an effective modulation of protein release rate.     

Fetal RHD genotyping by analysis of maternal plasma in a mixed population

Background: Maternal plasma analysis for the determination of the fetal RHD status is an exciting tool for the management of RhD‐negative pregnant women, specially sensitized women. We assessed the accuracy of fetal RHD genotyping by analysis of maternal plasma in a multi‐ethnic population. Methods: We analyzed plasma samples from 88 RhD‐negative pregnant women between 11 and 39 weeks of gestation, median age of 28 years old to determine the fetal RHD genotype. This population was from Southeastern Brazil with high mixed ethnic background. Fourteen patients (16%) had anti‐D alloantibody. We used Taqman primers and probes to detect by real‐time PCR, exons 4, 5, and 10 of RHD. As internal controls we used primers/probes sets to SRY and CCR5. Peripheral or umbilical cord bloods from respective nenonates were collected during delivery and hemagglutination was performed. Results: Fifty‐eight samples (66%) were genotyped as RHD+, 27 samples (31%) showed complete absence of RHD and 3 samples (3 %) presented a D variant (RHDψ). All the results agreed with the neonatal typing, including the three fetuses with the RHDψ, phenotyped as RhD‐negative. Thus, the accuracy of the fetal RHD genotyping in this mixed population was 100%. The earliest pregnancy in which fetal RHD was detected was 11 weeks. Conclusion: Our findings indicate that the accuracy of RHD gene using three regions (exons 4, 5, and 10) can be sufficient for clinical application in a multi‐ethnic population. This knowledge helped us on the development of a feasible protocol for fetal RHD genotyping on DNA from maternal plasma for our population. J. Clin. Lab. Anal. 25:100–104, 2011. © 2011 Wiley‐Liss, Inc.     

An atypical myeloproliferative disorder with t(8;13) (p11;q12): a third case

Summary. A 43-year-old male presented with a myeloproliferative disorder with prominent lymphadenopathy. Examination of the bone marrow showed almost complete replacement by a population of cells with an acquired chromosomal translocation t(8;13) (p11;q12). There are two other case reports describing a similar clinical syndrome with t(8;13) (p11;12) as the sole chromosomal aberration in bone marrow cells, suggesting a role for this translocation in the pathogenesis of this myeloproliferative disorder.