TACTICS OF THE TREATMENT OF TEETH TRANSPOSITION (CASE REPORTS).

Transposition of teeth - mutual exchange of the teeth position in the dental arch, it's a rare anomaly of the dentoalveolar apparatus. Most often in the transposition process the upper canines are involved in combination with the first premolars. Anomaly is mainly caused by an incorrect location of the teeth germs.

Antibiotic functionalised polymers reduce bacterial biofilm and bioburden in a simulated infection of the cornea.

Microbial keratitis can arise from penetrating injuries to the cornea. Corneal trauma promotes bacterial attachment and biofilm growth, which decrease the effectiveness of antimicrobials against microbial keratitis. Improved therapeutic efficacy can be achieved by reducing microbial burden prior to antimicrobial therapy.

ALGORITHM FOR TREATMENT OF PATIENTS WITH MESIAL OCCLUSION USING PROPRIETARY ORTHODONTIC DEVICE.

Unlabelled: Early elimination of dentoalveolar apparatus orthodontic disorders is the dominant concept in the treatment technique.

Aim: to present a sagittal anomalies treatment algorithm, of Class III particularly, in the transitional bite period by the proposed design of individual orthodontic devices with a movable ramp. The treatment algorithm consisted of several blocks: the motivation, the etiological factors establishment, the plan and treatment tactics creation basing on careful diagnosis, the stages of the active period of treatment and the patient management in the retention period.

Extracellular DNA impedes the transport of vancomycin in Staphylococcus epidermidis biofilms preexposed to subinhibitory concentrations of vancomycin.

Staphylococcus epidermidis biofilm formation is responsible for the persistence of orthopedic implant infections. Previous studies have shown that exposure of S. epidermidis biofilms to sub-MICs of antibiotics induced an increased level of biofilm persistence.

Lanthanum suppresses arachidonic acid-induced cell death and mitochondrial depolarization in PC12 cells.

Within the framework of studying the mechanisms of acute toxicity of arachidonic acid and the role of ambient cations, we have investigated the effects of extracellular La(3+) on arachidonic acid-induced death (lactate dehydrogenase release) and mitochondrial depolarization (rhodamine 123 fluorescence) in PC12 cells. Micromolar La(3+) profoundly suppressed arachidonic acid toxicity and this effect was dependent on the presence of other cations. Whereas in the cation-free solution 10-20 microM La(3+) protected most cells from death caused by a 2 hour-long exposure to 20 microM arachidonic acid, the cytoprotective effect of 100 microM La(3+) was reduced to approximately 70% in the presence of a normal complement of monovalent cations and was hardly detectable with 5 mM Ca(2+) in the bath.