Use of gases to improve survival of Bifidobacterium bifidum by modifying redox potential in fermented milk.

The aim of this work was to study the effect of the oxidoreduction potential, modified using gas, on the growth and survival of a probiotic strain, Bifidobacterium bifidum, and 2 yogurt strains, Streptococcus thermophilus and Lactobacillus delbrueckii ssp. bulgaricus. Three fermented milks were manufactured with an initial oxidoreduction potential value adjusted to +440 mV (control milk), +350 mV (milk gassed with N(2)), and -300 mV [milk gassed with N(2) plus 4% (vol/vol) H(2) (N(2)-H(2))]. Acidification profiles, growth during milk fermentation and survival during storage at 4 °C for 28 d were determined. This study showed that fermented probiotic dairy products made from milk gassed with N(2) and, more particularly, those made from milk gassed with N(2)H(2) were characterized by a significant increase in B. bifidum survival during storage without affecting the fermentation kinetics and the survival of Strep. thermophilus and L. delbrueckii ssp. bulgaricus.

Placental fetal thrombotic vasculopathy in severe congenital anomalies prompting EXIT procedure.

OBJECTIVE: The ex-utero intrapartum treatment (EXIT) procedure is used to secure fetal airway, cannulate for extracorporeal membrane oxygenation (ECMO), or resect a tumor during partial delivery in a modified cesarean section. This is a retrospective study of placental pathology from EXIT procedures. METHODS: Placental reports and glass slides from 36 placentas delivered by EXIT procedure (study group SG) and 36 placentas from pregnancies without perinatal mortality and delivered by cesarean sections and matched for gestational age were blindly reviewed. Indications for EXIT procedures were: 11 cervical teratomas, 9 diaphragmatic hernias, 4 pulmonary airway malformations, 4 micrognathias, 3 vascular malformations, 3 CHAOS, and 2 aortic stenoses. 22 clinical and 43 gross and histological placental features were compared using the analysis of variance or Yates χ(2) with Holm-Bonferroni correction, where appropriate. RESULTS: The average gestational age in the SG and the CG was 34.9 weeks. Histological features of fetal thrombotic vasculopathy were more frequently seen in the SG. Of the placental features, statistically significant differences were found in, partial fibrosis of chorionic villi (9.7 ± 7.9 vs. 6.1 ± 5.3 villi per placental section) [p = 0.035], clusters of at least 3 avascular chorionic villi (33 v. 6%) [p = 0.042], and abnormal umbilical cord insertion (8% vs. 0% (p = 0.045), in the SG and the CG respectively. CONCLUSION: To the best of our knowledge, this is the first study to describe the placentas from EXIT procedures. The presence of increased frequency of fetal thrombotic vasculopathy on histology indicates an underlying chronic and on-going stasis in fetal circulation due to the presence of conditions which were indications for the EXIT procedures. The possibility of coagulopathy should be considered in management of the fetuses and neonates undergoing EXIT procedure. Detailed examination of the placenta is of utmost importance in order to recognize and treat potentially life-threatening complications.

13C labeling indicates that the epoxide-containing amino acid of HC-toxin is biosynthesized by head-to-tail condensation of acetate.

HC-toxin, cyclo(D-Pro-L-Ala-D-Ala-L-Aeo), where Aeo stands for 2-amino-9,10-epoxi-8-oxodecanoic acid, is a potent inhibitor of histone deacetylase. Previous molecular genetic studies indicated that HC-toxin biosynthesis requires a dedicated fatty acid synthase. The incorporation of [13C]acetate into HC-toxin was studied using NMR. The pattern of incorporation of 13C was consistent with the carbons of Aeo being derived from head-to-tail condensation of acetate.

Reciprocal up- and down-regulation of BDNF mRNA in tetanus toxin-induced epileptic focus and inhibitory surround in cerebral cortex.

Chronic focal epilepsy is associated with synaptic plasticity and growth of new connections. Brain-derived neurotrophic factor (BDNF) is associated with each of these processes in normal brain and shows acute up-regulation in models of generalized epilepsy. Here, using an experimental model of focal epilepsy, we show persistent up-regulation of BDNF mRNA, independent of that of other growth factors, in association with the development and persistence of chronic seizures. In situ hybridization histochemistry revealed that rats perfused within 2-3 days after seizure onset had widespread increases in BDNF mRNA levels in the neocortex. Rats perfused at later times, however, showed focal up-regulation of BDNF mRNA at the injection site and down-regulation in a surrounding cortical zone. Nerve growth factor and neurotrophin-3 mRNAs were not significantly altered. These reciprocal changes in BDNF gene expression in the epileptic focus and the cortical surround may contribute to plastic changes in epileptic neuronal circuits that accompany the transition from acute to chronic epilepsy. BDNF down-regulation in the surround is likely to be associated with the inhibitory surround that hampers seizure spread, but facilitates the persistence of a chronic epileptic focus.