Efficiency of polylactide/polyglycolide copolymers bone replacements in bone defects healing measured by densitometry

Healing of bone defects is the most frequent cause of failure in surgical treatments of an odontogenic ostitic processes. The aim of this study was to determine successfulness in healing of bone defects after implantation of alloplastic co-polymer-polyglycol bone implant. A group of 45 cases with periradicular ostitic processes were examined. The densitometric measurements were taken from radiovisiographic dental x-ray images. Patients were observed throughout a period of one year. The results obtained were analyzed and presented graphically. Thirty-eight patients (84%) were treated successfully, and seven patients (16%) showed unsuccessful healing of the bone defects. The results obtained indicate that polyglycol copolymer bone implants can be successfully used in a treatment of odontogenically caused bone defects. Their fundamental advantage is a slow biodegradation, which ensures a more suitable area for the apposition of a new bone in the defect, simple application in clinical work and the possibility of a mutual combination of all three available forms.     

Histopathological analysis of UV-B irradiated retina by Cavia Coba'ya and with protection of transmission light lambda 550-600 nm

In 14 experimental Cavia Coba'ya eyes were irradiated with UV-B light, lambda 312 nm, 25 J/cm2 in 15 minute exposure. Including the transmission of light through optical media: cornea, lens, humor aqueous and vitreous body, and pupil surface of 7 mm2, we can calculate that in these conditions retina can be really irradiated with 10 J/cm2. The half number of Cavia Coba'ya was simultaneously irradiated with visible light, lambda of 550-600 nm (1000 Lx). Control group was 5 Cavia Coba'ya. Two months after irradiation, eyes were enucleated and fixed in 4% formaldehyde. Histopathological findings showed alterations of all retinal layers: loss of ganglion cells, axons, reduction of photoreceptors, vacuolar degeneration and hyperplasia of retinal pigment epithelium. In the second group of irradiance, the eyes with visible light lambda 550-600 nm, all retinal alterations were in 50% decreased.     

A behavioural study of the effect of pentadecapeptide BPC 157 in Parkinson's disease models in mice and gastric lesions induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydrophyridine.

The effect of a stomach pentadecapeptide, BPC 157, on Parkinson's disease in mice was investigated, along with its salutary activity on stomach lesions induced by parkinsongenic agents. Parkinsongenic agents, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30.0 mg x kg(-1)b.w. i.p. once daily for 6d, and after 4d once 50.0 mg x kg(-1)b.w. i.p.) or reserpine (5.0 mg x kg(-1)b.w. i.p.) were applied i.p. BPC 157 (1.50 microg or 15.0 ng x kg(-1)b.w. i.p.) was applied 15 min before or alternatively 15 min after each MPTP administration. In reserpine studies, BPC 157 (10.0 microg or 10.0 ng x kg(-1)b.w. i.p.) was given either 15 min before reserpine or in the already established complete catalepsy 24 h thereafter. BPC 157 strongly improved the MPTP-impaired somatosensory orientation and reduced the MPTP-induced hyperactivity, and most importantly, MPTP-motor abnormalities (tremor, akinesia, catalepsy -otherwise very prominent in saline control), leading to almost complete abolition of otherwise regularly lethal course of MPTP treatment in controls. Likewise, in reserpine experiments, BPC 157 strongly prevented the development of otherwise very prominent catalepsy and when applied 24 h thereafter reversed the established catalepsy. In addition, a reduction of reserpine-hypothermy (BPC 157 pre-treatment) and reversal of further prominent temperature fall (BPC 157 post-treatment) have been consistently observed. Taking together these data, as the two most suitable animal models were consistently used and since the high effectiveness was demonstrated in pre- and post-treatment, microg and ng regimens, BPC 157 as an organoprotector should be further therapeutically investigated. Additionally, given in either regimen, pentadecapeptide BPC 157 strongly attenuated the stomach lesions in mice that otherwise consistently appeared in mice treated with the parkinsogenic neurotoxin MPTP.     

Therapy effect of antiulcer agents on new chronic cysteamine colon lesion in rat

After demonstration that cysteamine induced duodenal lesions in gastrectomized rats, while a number of antiulcer drugs mitigated these lesions, it was shown that one single intrarectal (i.r.) cysteamine application produced severe colon lesions in acute studies in rats. Thus, the further focus was on the protracted effect of cysteamine challenge (400 mg/kg b.w. i.r.) and therapy influence in chronic experiments in female rats. Regularly, cysteamine colon lesions were markedly mitigated by ranitidine (10), omeprazole (10), atropine (10), methylprednisolone (1), sulphasalazine (50; mg/kg), pentadecapeptide BPC 157 (PL-10, PLD-116; 10 microg or 10 ng/kg). Specifically, after 1 or 3 months following initial challenge (cysteamine 400 mg/kg i.r.) in female rat, the therapy [BPC 157 (PL-10, PLD-116 (10.0 microg or 10.0 ng/kg; i.g., i.p., i.r.), ranitidine, omeprazole, atropine, methylprednisolone, sulphasalazine (i.p.)] reversed the protracted cysteamine colon injury: the 1 week-regimen (once daily application) started after 1 month post-cysteamine, as well as the 2 weeks-regimen (once daily application), which started after 3 months. The effect on recidive lesion was also tested. These cysteamine lesions may reappear after stopping therapy (after stopping therapy for 3 weeks at the end of 2-weeks regimen started in 3 months-cysteamine female rats) in sulphasalazine group, while this reappearance is markedly antagonized in pentadecapeptide BPC 157 (PL-10, PLD-116)-rats (cysteamine-colon lesion still substantially low).