[Screening for hemolytic streptococcus group B in pregnancy and prevention of infection in neonates]. / Skríning hemolytického streptokoka skupiny B v tehotnosti a prevencia infekcie novorodencov.

OBJECTIVE: The aim of this study was to evaluate the influence of Group B streptococcus (GBS) screening and intrapartum antibiotic prophylaxis to the incidence of GBS disease in newborns. DESIGN: Prospective non-randomised study. SETTING: IInd Clinic of Obstetric and Gynaecology LFUK and FNsP Ruzinov, Bratislava, Slovakia. METHODS: We enrolled 3023 newborns (754 in the study group, 2269 in the control group), which were born between 1.9.2000 and 31.3.2003. In both groups we compared following variables: total number of infectious diseases in newborns, number and forms of GBS neonatal disease, number of perinatal death due to GBS disease. RESULTS: There was no GBS disease in the study group of 754 newborns. Mothers of these newborns had one screening culture in 35-36th week of gestation. One swab was taken from vagina and anus. GBS carriers (161-21.4%) were administered i.v. intrapartum antibiotic prophylaxis with Penicillin G i.v., or, when allergy to penicillin was in history, with Clindamycin i.v. In the control group of 2269 newborns, whose mothers had no prevention, the incidence of GBS neonatal disease reached 7.5/1000 newborns (17 cases). The incidence of invasive GBS neonatal disease was 2.6/1000 newborns. CONCLUSION: The authors have noticed a significant decrease in incidence of GBS neonatal disease after implication of GBS screening and intrapartum antibiotic prophylaxis.

Coxsackie viral infection and orofacial cleft.

The incidence of orofacial cleft (OC) in newborns was compared with the occurrence of virus-neutralizing antibodies to coxsackie viruses in the serum of newborns and their mothers. No significant difference was found when comparing the seropositivity rates between the group of patients and the control group of healthy newborns. If the patients were divided according to the place of residence however, marked differences occurred between the regions. The lowest incidence of both--coxsackie infection and OC was determined in the region of Bratislava and the highest in the region of Zilina. The explanation of these findings recquires a more detailed analysis of genetic background, social and hygienic status, style of life and other factors, known to influence the development of OC as multi-etiological developmental disorder. (Tab. 2, Fig. 4, Ref. 12.).

Mechanisms of iron-induced oxidative modifications of creatine kinase in rat brain in vitro. possible involvement of HNE.

The model of oxidative stress induced by Fe/ascorbate in rat brain in vitro was used to compare the antioxidant capacity of known antioxidants. Creatine kinase (CK) was selected as a marker of protein injury in such studies. Of the antioxidant enzymes (catalase, superoxide dismutase), oxygen radical scavengers (mannitol, glutathione), and the chelator (EDTA) tested in this work and this system, only catalase and glutathione prevented the injury induced by oxidative stress, indicating that H2O2 and the glutathione peroxidase reaction were involved in the preventive effect. Additionally, the preventive effect of glutathione may be caused also by the fact that glutathione easily reacts with 4-hydroxynonenal (HNE), generated in rat brain homogenate, thus protecting CK from inactivation by this aldehyde. To find out whether and if at which concentrations CK may be oxidatively modified by HNE, pure CK was incubated in the presence of 10 and 64 micromol/l HNE for 30 min at 37 degrees C. The activity of CK incubated with HNE decreased significantly. Simultaneously, the protein carbonyls, determined by electrophoresis and immunoblotting increased at 10 micromol/l HNE or disappeared probably due to crosslinking of CK at 64 micromol/l HNE. The concentration of HNE in rat brain homogenates after oxidative stress was determined by HPLC and was in the range of 10-16 nmol/mg prot., corresponding to a concentration of 10-16 micromol/l HNE. This indicates that CK of rat brain homogenates oxidized by Fe/ascorbate may be impaired not only directly by oxygen radicals but also secondarily by HNE.

Gap junctional channels regulate acid secretion in the mammalian gastric gland.

Gap junction channels are regarded as a primary pathway for intercellular message transfer, including calcium wave propagation. Our study identified two gap junctional proteins, connexin26 and connexin32, in rat gastric glands by RT-PCR, Western blot analysis, and immunofluorescence. We demonstrated a potential physiological role of the gap junctional channels in the acid secretory process using the calcium indicator fluo-3, and microinjection of Lucifer Yellow. Application of gastrin (10-7 m) to the basolateral membrane resulted in the induction of uniphasic calcium signals in adjacent parietal cells. In addition, single parietal cell microinjections in intact glands with the cell-impermeant dye Lucifer Yellow resulted in a transfer of dye from the injected cell to the adjacent parietal cell following gastrin stimulation, demonstrating gastrin-induced cell-to-cell communication. Both calcium wave propagation and Lucifer Yellow transfer were blocked by the gap junction inhibitor 18alpha-glycyrrhetinic acid. Our studies demonstrate that functional gap junction channels in gastric glands provide an effective means for rapid cell-to-cell communication and allow for the rapid onset of acid secretion.

[Relation between toxoplasmosis and orofacial clefts in children]. / Nase sledovanie vzt'ahu toxoplazmózy k orofaciálnym rázstepom detí.

The authors performed a serological observation of toxoplasmosis by using the methods of IFT, CFT and ELISA in 118 mothers and their children with orofacial clefts. The results were compared with those gained in the control group of healthy mothers and their children. Titre means of toxoplasma antibodies in inflicted mothers and their children were higher than in the control group. The results were evaluated statistically. The authors assume that a certain proportion of orofacial clefts may be induced by toxoplasmosis. (Tab. 6, Ref. 13.).