Ozone Therapy Enhances Osseous Healing in Rats With Diabetes With Calvarial Defects: A Morphometric and Immunohistochemical Study

Background: Bone healing is impaired in diabetes mellitus (DM) cases. The aim of this study is to investigate, both morphometrically and immunohistochemically, the effect of gaseous ozone on bone healing in diabetic rat calvarial defects treated with xenografts. Methods: DM was induced with 50 mg/kg intraperitoneal streptozotocin in 56 male Wistar rats. Study groups were as follows: 1) empty defect (control, n = 14); 2) xenograft (XG, n = 14); 3) empty defect treated with ozone therapy (control + ozone, n = 14); and 4) xenograft and ozone application (XG + ozone, n = 14). Critical‐size defects were created in all rats. Bovine‐derived xenograft was applied to XG groups. Gaseous ozone was applied on the operation day and daily for 2 weeks (140 ppm at 2 L/d, 2.24 mg). Rats were sacrificed at 4 or 8 weeks post‐surgery. Total bone area, newly formed bone, and residual graft material were measured histomorphometrically. Osteocalcin and bone morphogenic protein (BMP)‐2 expression was evaluated immunohistochemically. Results: Osteoclast numbers in the XG + ozone group were higher than the other groups at week 4 (P <0.05). XG + ozone group revealed more total bone area and new bone area than the XG group at weeks 4 (P <0.05) and 8 (P >0.05). Residual graft materials were decreased in the XG + ozone group and the same group revealed more BMP‐2 positivity compared with other groups. Osteocalcin positivity in XG groups was higher than in control groups. Conclusion: Within the limitations of this DM animal study, gaseous ozone application accelerates xenograft resorption and enhances bone regeneration, especially in the early stages of bone healing.     

Right ventricular infarction

The cases of 27 consecutive patients aged 40 to 78 years with ventricular septal rupture during acute myocardial infarction were reviewed. Myocardial infarction was inferior in 16 patients and anterior in 11. The time from myocardial infarction to rupture was less than 24 hours in 9 patients, 24 to 48 hours in 6 patients, 2 to 7 days in 11 patients, and 14 days in 1 patient. In 23 patients pressures (in mm Hg) were pulmonary arterial systolic 28 to 70 (mean 52), diastolic 9 to 34 (mean 23) and left ventricular end-diastolic 15 to 35 (mean 24). Cardiac index was 1.1 to 2.5 (mean 2.0) liters/min per m² and the ratio of pulmonary to systemic flow ($\text{Q}{}_{\mathrm{<mtext>p</mtext>}}\text{Q}{}_{\mathrm{<mtext>s</mtext>}}$) 1.5 to 4.8 (mean 3.4). The number of coronary vessels with more than 50 percent obstruction was one in 8 patients, two in 11 patients and three or more in 8 patients. Of the eight patients with single vessel disease three had right, one had left circumflex, and four had left anterior descending coronary artery disease.All seven patients treated without surgery died 1 to 13 days after ventricular septal rupture; all seven had inferior myocardial infarction, and none had previous transmural myocardial infarction. Of these seven patients, two were considered inoperable, one died during study, and four died abruptly while awaiting study. Eleven of 20 patients (55 percent) survived operation. The survival rate in seven patients operated on less than 2 days after ventricular septal rupture was 72 percent. Of 11 patients operated on 2 to 28 days after ventricular septal rupture 4 survived, whereas the 2 patients operated on later than 4 weeks after rupture survived. It is concluded that (1) early surgery in ventricular septal rupture has relatively low mortality; (2) delay of study and surgery is done at the expense of unacceptable and unpredictable mortality; and (3) ventricular septal rupture can occur with single vessel coronary artery disease.     

The association between mutations in the lysosomal protein glucocerebrosidase and parkinsonism

A body of work has emerged over the past decade demonstrating a relationship between mutations in glucocerebrosidase gene (GBA), the gene implicated in Gaucher disease (GD), and the development of parkinsonism. Several different lines of research support this relationship. First, patients with GD who are homozygous for mutations in GBA have a higher than expected propensity to develop Parkinson's disease (PD). Furthermore, carriers of GBA mutations, particularly family members of patients with GD, have displayed an increased rate of parkinsonism. Subsequently, investigators from centers around the world screened cohorts of patients with parkinsonism for GBA mutations and found that overall, subjects with PD, as well as other Lewy body disorders, have at least a fivefold increase in the number of carriers of GBA mutations as compared to age‐matched controls. In addition, neuropathologic studies of subjects with parkinsonism carrying GBA mutations demonstrate Lewy bodies, depletion of neurons of the substantia nigra, and involvement of hippocampal layers CA2–4. Although the basis for this association has yet to be elucidated, evidence continues to support the role of GBA as a PD risk factor across different centers, synucleinopathies, and ethnicities. Further studies of the association between GD and parkinsonism will stimulate new insights into the pathophysiology of the two disorders and will prove crucial for both genetic counseling of patients and family members and the design of relevant therapeutic strategies for specific patients with parkinsonism. © 2009 Movement Disorder Society     

Respiratory sinus arrhythmia during feeding: a measure of vagal regulation of metabolism, ingestion, and digestion in preterm infants

Respiratory sinus arrhythmia (RSA), a non-invasive indicator of vagal regulation of the heart, and heart period (HP) were monitored before, during, and after oral or gastric-tube bolus feedings in 32 preterm infants. Group 1 infants (n=15) were < or =30 weeks gestational age (GA) at birth (mean 28.3 weeks) and group 2 infants (n=17) were > or =31 weeks GA at birth (mean=33.2 weeks). Mean postmenstrual ages at the time of study were 33.5 +/- 2.3 (SD) weeks in group 1 and 33.9 +/- 1.6 (SD) weeks in group 2. RSA and HP decreased in both groups during feeding. However, postfeeding RSA and HP increased toward prefeed levels only for group 2 infants. In addition, RSA and HP changes during feeding were correlated only for group 2 infants. The results suggest that the preterm infant may experience a maturational lag in vagal function and in the influence of vagal activity on metabolic mechanisms (i.e. heart rate) related to ingestive needs. This maturational lag may contribute to continued feeding difficulties and may be a measurable marker of subtle neurodevelopmental problems.     

Respiratory failure and multiple fractures in vitamin D-dependent rickets

A 20-month-old boy presented with multiple fractures and respiratory failure. He was found to have vitamin D-dependent rickets. The rickets did not improve with phosphate, calcium and calciferol. The rickets healed, however, with large doses of 1-alpha-hydroxycholecalciferol. The presentation is unusual and the response to therapy suggests metabolic heterogeneity in vitamin D-dependent rickets.     

'Educated' dendritic cells act as messengers from memory to naive T helper cells.

Ingested antigens lead to the generation of effector T cells that secrete interleukin 4 (IL-4) rather than interferon-gamma (IFN-gamma) and are capable of influencing naive T cells in their immediate environment to do the same. Using chimeric mice generated by aggregation of two genotypically different embryos, we found that the conversion of a naive T cell occurs only if it can interact with the same antigen-presenting cell, although not necessarily the same antigen, as the effector T cell. Using a two-step culture system in vitro, we found that antigen-presenting dendritic cells can act as 'temporal bridges' to relay information from orally immunized memory CD4 T cells to naive CD4 T cells. The orally immunized T cells use IL-4 and IL-10 (but not CD40 ligand) to 'educate' dendritic cells, which in turn induce naive T cells to produce the same cytokines as those produced by the orally immunized memory T cells.