33 research outputs found

    PROJEKT "IZBOR VIŠE" KAO RESOCIJALIZACIJSKI RAD S ADOLESCENTIMA U RIZIKU OD OVISNOSTI

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    Ovaj rad prikazuje ideju, razvoj i realizaciju resocijalizacijskog rada građanske udruge „Kameleon i mreža“ za resocijalizaciju adolescenata u riziku ovisnosti od THC-a kroz projekt „Izbor više“ u Slavonskom Brodu. Projekt je ostvaren dragovoljnim radom cijenjenih osoba prisutnih u njihovom profesionalnom javnom radu u gradu u području astronomije, informatike, art-dizajna, video-arta i sporta, radionicama s vršnjačkom grupnom edukacijom potpomognutom od psihijatra u motivacijskom i organizacijskom pristupu. Postavka malih grupnih radionica jednom tjedno u trajanju od 90 min tijekom šest tjedana mobilizirala je u razdoblju od 2005. do 2009. godine 90 adolescenata. U radu prikazujemo rezultate testova subjektivnih samoprocjena koji su visoko pozitivni i prikazuju vrlo dobru prihvaćenost takvog načina rada s adolescentima

    Pentadecapeptide BPC 157 therapy in rats with cysteamine induced-terminal ileitis

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    We introduce pentadecapeptide BPC 157 therapy in rats with cysteamine induced-terminal ileitis 1h/1month/2months. We counteracted gross hyperemia, edema, erosion, bleeding, microscopically significant loss of villous architecture, loss and shortening of villae and severe lymphocytic infiltrate. Pentadecapeptide counteracts various lesions in the whole GI-tract and free radical formation, and tested in ulcerative colitis trials and now in multiple sclerosis. Cysteamine was known to induce gastric-acid hypersecretion as a prototype of duodenal lesion. Cysteamine induced duodenal lesions after gastrectomy, and applied as an enema, ulcerative colitis in rats Cysteamine was applied in female Albino Wistar rats into the terminal ileum, 5 cm segment up to ileocecal valve, which was kept gently compressed for 1 min, and then released. Medication(BPC, or saline (controls)) was applied as an abdominal bath immediately after the end of the cysteamine application procedure, and then if rats were not sacrificed at 1 h, continuously, perorally in drinking water till the end of 1 or 2 months The hyperemia, edema, erosion and bleeding scores were summarized. Microscopically, cysteamine induced terminal ileitis presents with: submucosal congestion, significant loss of villous architecture, loss and shortening of villae and lamina propria infiltrated with mild to severe lymphocytic infiltrate, much like intraepithelial lymphocyte infiltration and some epithelial elevation from lamina propria. Better preservation of mucosal architecture appears in pentadecapeptide treated rats. There is only mild villous edema with capillary congestion and mild lymphocytic infiltrate. No epithelial elevation from lamina propria For further therapy, beneficial effect of the BPC counteracts cysteamine- terminal ileitis

    BPC 157 pentadecapepide attenuates acute renal ischemia injury, prevents ensuing hemodynamic disturbances, peaked and inverted p waves, and gastrointestinal lesions

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    We focused on the effects of BPC 157 on acute unilateral renal ischemia in rats, subsequent severe portal (PV) and inferior vena cava (IVC) hypertension and thrombosis, abdominal aorta (AA) hypotension, peaked or inverted P waves and gastrointestinal lesions. Medication (/kg) (BPC 157 (10 μg)(treated group) or saline (5 ml)(control group)) was applied as an abdominal bath immediately after the right renal artery was ligated. 10min, 1h, and 24h after ligation electrocardiography, USB microcamera recording, intravascular cannulation, and thrombi extraction was performed. Control rats exhibited PV and IVC hypertension, aortic hypotension (mmHg) (10min: 32±2 PV, 24±4 IVC, 75±2 AA; 1h: 43±4 PV, 46±3 IVC, 73±4 AA; 24h: 30±2 PV, 34±1 IVC, 86±3 AA) and thrombosis (thrombus weight, mg) (10min: 1.3±0.3 IVC, 3.5±0.4 PV; 1h: 15.1±0.5 IVC, 5.4±0.2 PV; 24h: 16.3±1.5 IVC, 6.1±0.9 PV). Treated group showed improved pressure values (10min: 4±1 PV, 8±1 IVC, 84±3 AA; 1h: 18±2 PV, 6±1 IVC, 92±3 AA; 24h: 5±1 PV, 10±1 IVC, 97±2 AA) and milder thrombosis (10min: no thrombi; 1h: 7.7±0.3 IVC, 2.3±0.2 PV; 24h: 11.6±0.5 IVC, 3.2±0.2 PV). Control rats exhibited peaked (10 min, 1h) or inverted (24h) P waves, gastric and intestinal lesions (24h) and complete renal infarction (24h), whereas the treated rats exhibited no P wave abnormalities, significantly mitigated gastrointestinal lesions (24h) and only partial renal infarction (24h). BPC 157 therapy reduces the severity of renal ischemia injury, counteracts hemodynamic disturbances, P wave abnormalities and gastrointestinal lesions that follow

    BPC 157 pentadecapepide attenuates acute renal ischemia injury, prevents ensuing hemodynamic disturbances, peaked and inverted p waves, and gastrointestinal lesions

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    We focused on the effects of BPC 157 on acute unilateral renal ischemia in rats, subsequent severe portal (PV) and inferior vena cava (IVC) hypertension and thrombosis, abdominal aorta (AA) hypotension, peaked or inverted P waves and gastrointestinal lesions. Medication (/kg) (BPC 157 (10 μg)(treated group) or saline (5 ml)(control group)) was applied as an abdominal bath immediately after the right renal artery was ligated. 10min, 1h, and 24h after ligation electrocardiography, USB microcamera recording, intravascular cannulation, and thrombi extraction was performed. Control rats exhibited PV and IVC hypertension, aortic hypotension (mmHg) (10min: 32±2 PV, 24±4 IVC, 75±2 AA; 1h: 43±4 PV, 46±3 IVC, 73±4 AA; 24h: 30±2 PV, 34±1 IVC, 86±3 AA) and thrombosis (thrombus weight, mg) (10min: 1.3±0.3 IVC, 3.5±0.4 PV; 1h: 15.1±0.5 IVC, 5.4±0.2 PV; 24h: 16.3±1.5 IVC, 6.1±0.9 PV). Treated group showed improved pressure values (10min: 4±1 PV, 8±1 IVC, 84±3 AA; 1h: 18±2 PV, 6±1 IVC, 92±3 AA; 24h: 5±1 PV, 10±1 IVC, 97±2 AA) and milder thrombosis (10min: no thrombi; 1h: 7.7±0.3 IVC, 2.3±0.2 PV; 24h: 11.6±0.5 IVC, 3.2±0.2 PV). Control rats exhibited peaked (10 min, 1h) or inverted (24h) P waves, gastric and intestinal lesions (24h) and complete renal infarction (24h), whereas the treated rats exhibited no P wave abnormalities, significantly mitigated gastrointestinal lesions (24h) and only partial renal infarction (24h). BPC 157 therapy reduces the severity of renal ischemia injury, counteracts hemodynamic disturbances, P wave abnormalities and gastrointestinal lesions that follow

    Spinal instability in rats counteracted by pentadecapeptide BPC 157

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    To induce spinal instability, we focused on bilateral facetectomy in rats and possible therapeutic benefit with the stable gastric pentadecapeptide BPC 157 given in the drinking water. Male Albino Wistar rats (12 weeks aged, 350-400 g b.w.), 4 rats per group, were used in the experiment. In this study, the bilateral paravertebral muscles attached to the L3–L4 segment were peeled from the lumbar spine to expose the posterior bony elements. The rats then underwent complete resection of bilateral L3–L4 facet joints without neural tissue injuries. After that, muscle and skin incsion were closed and animals returned to cages in pairs. The medication was administrated through drinking water (BPC 157 10 ng/kg, 0.16 ng/mL, 12 ml/rat/day), while controls received drinking water only. Next eight weeks we recorded and measured paw parameters (the lenght between left and right front and back paws) in control, treated and healthy rats. Radiological analysis was also performed. The paw parametars have shown that the front paws in the control group were approximately 35% and the back paws were 13% wider than in helathy rats. Contrarily, the front paws in medicated rats were only 9% and the back paws were only 4% wider than in healthy ones. Radiological assesment of rats spines acquired at 1 week or 8 weeks was conducted and BPC 157 drinking animals had higher bone density overall. BPC 157 improves damage caused by spine instability and it can be potentially used as a treatment for chronic back pain

    Pentadecapeptide BPC 157 Counteracts the Adverse Effects of Lithium Overdose in Rats

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    INTRODUCTION We sought to determine whether stable gastric pentadecapeptide BPC 157 mitigates lithium intoxication in rats. METHODS: Lithium was applied at 500 mg/kg/day, intraperitoneally, once daily throughout 3 subsequent days. Medication used (in mg/kg) for the treatment group includes BPC 157 (0.01; 0.00001), L-NAME (5.0), L-arginine (100.0), applied alone and/or together, while control group rats received an equivolume of saline solution (5 mL/kg). At 20 minutes after drug application, we assessed muscular weakness (score 1-5) during the following 8 minutes. Then, for the next 5 minutes, we recorded an ECG. At 3 hours after that, the brain, the heart, the quadriceps muscle and the diaphragm muscle were used for histopathological analysis. RESULTS Consistently, lithium produced severe intoxication syndrome (muscular weakness and prostration, reduced quadriceps muscle fibers and diaphragm, myocardial infarction, and edema of various brain areas, most prominently in the cerebral cortex). The effects worsening with subsequent applications. L-NAME and L-arginine, given separately, both induced severe aggravation. This aggravation disappeared when L-NAME and L-arginine were given together. Contrarily, when given alone or together with NO-agents, BPC 157 reduced muscular weakness and prostration and muscle damage and mitigated lithium induced myocardial damage. BPC 157 reduced nerve damage and brain edema. CONCLUSION BPC 157 could be used as therapy for lithium intoxication

    Splenectomy induced portal and caval hypertension, aortic hypotension, venous thrombosis, peaked p waves, and tachycardia. therapy with pentadecapeptide BPC 157

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    We introduce BPC 157 therapy for a cluster of complications taking place after splenectomy in rats, including portal vein (PV), inferior vena cava (IVC), superior mesenteric vein (SMV) and lienal vein (LV) thrombosis, severe venous hypertension (PV, IVC), abdominal aorta (AA) hypotension, peaked P waves and tachycardia. Medication (/kg) (BPC 157 (10 μg)(treated group) or saline (5 ml)(control group)) was applied as an abdominal bath immediately after splenectomy. 10min, 3h, and 24h after splenectomy rats were assessed via electrocardiography, USB microcamera, intravascular cannulation, and thrombi extraction. Splenectomized rats exhibited PV and IVC hypertension, aortic hypotension (mmHg) (10min: 65±4 PV, 46±4 IVC, 71±3 AA; 3h: 42±4 PV, 61±4 IVC, 70±3 AA; 24h: 38±4 PV, 47±4 IVC, 68±3 AA) and thrombosis (thrombus weight, mg) (10min: 9.5±0.5 IVC, 6.6±0.9 PV, 4.8±0.9 SMV, 1.3±0.6 LV; 3h: 10.1±0.5 IVC, 5.3±0.8 PV, 19.2±0.9 SMV, 1.0±0.6 LV; 24h: 33.8±2.5 IVC, 27.5±2.9 PV, 8.8±0.9 SMV, 3.8±0.6 LV). BPC 157 normalised blood pressure (10min: 29±4 PV, 20±4 IVC, 87±3 AA; 3h: 20±4 PV, 17±4 IVC, 81±3 AA; 24h: 12±4 PV, 20±4 IVC, 82±3 AA) and reduced thrombosis (10min: 2.9±0.5 IVC, 2.6±0.9 PV, 3.2±0.3 SMV, 0.5±0.2 LV; 3h: 6.3±0.5 IVC, 2.3±0.5 PV, 5.9±0.9 SMV, 0.6±0.2 LV, 24h: 12.2±2.5 IVC, 1.9±0.5 PV, 4.8±0.9 SMV, 2.0±0.6 LV). Control group presented with peaked P waves, tachycardia and PV/SMV congestion, whereas the treated group showed none of the aforementioned phenomena. BPC 157 therapy counteracts hemodynamic disturbances, peaked P waves, and tachycardia as post-splenectomy complications

    Splenectomy induced portal and caval hypertension, aortic hypotension, venous thrombosis, peaked p waves, and tachycardia. therapy with pentadecapeptide BPC 157

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    We introduce BPC 157 therapy for a cluster of complications taking place after splenectomy in rats, including portal vein (PV), inferior vena cava (IVC), superior mesenteric vein (SMV) and lienal vein (LV) thrombosis, severe venous hypertension (PV, IVC), abdominal aorta (AA) hypotension, peaked P waves and tachycardia. Medication (/kg) (BPC 157 (10 μg)(treated group) or saline (5 ml)(control group)) was applied as an abdominal bath immediately after splenectomy. 10min, 3h, and 24h after splenectomy rats were assessed via electrocardiography, USB microcamera, intravascular cannulation, and thrombi extraction. Splenectomized rats exhibited PV and IVC hypertension, aortic hypotension (mmHg) (10min: 65±4 PV, 46±4 IVC, 71±3 AA; 3h: 42±4 PV, 61±4 IVC, 70±3 AA; 24h: 38±4 PV, 47±4 IVC, 68±3 AA) and thrombosis (thrombus weight, mg) (10min: 9.5±0.5 IVC, 6.6±0.9 PV, 4.8±0.9 SMV, 1.3±0.6 LV; 3h: 10.1±0.5 IVC, 5.3±0.8 PV, 19.2±0.9 SMV, 1.0±0.6 LV; 24h: 33.8±2.5 IVC, 27.5±2.9 PV, 8.8±0.9 SMV, 3.8±0.6 LV). BPC 157 normalised blood pressure (10min: 29±4 PV, 20±4 IVC, 87±3 AA; 3h: 20±4 PV, 17±4 IVC, 81±3 AA; 24h: 12±4 PV, 20±4 IVC, 82±3 AA) and reduced thrombosis (10min: 2.9±0.5 IVC, 2.6±0.9 PV, 3.2±0.3 SMV, 0.5±0.2 LV; 3h: 6.3±0.5 IVC, 2.3±0.5 PV, 5.9±0.9 SMV, 0.6±0.2 LV, 24h: 12.2±2.5 IVC, 1.9±0.5 PV, 4.8±0.9 SMV, 2.0±0.6 LV). Control group presented with peaked P waves, tachycardia and PV/SMV congestion, whereas the treated group showed none of the aforementioned phenomena. BPC 157 therapy counteracts hemodynamic disturbances, peaked P waves, and tachycardia as post-splenectomy complications

    BPC 157 given during reperfusion counteracts portal hypertension, caval hypertension, and aortal hypotension in rats with prior portal triad obstruction

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    Reperfusion provokes major disturbances after the Pringle maneuver. We demonstrated the usefulness of the stable gastric pentadecapeptide BPC 157 as therapy for the hemodynamic disturbances after the Pringle maneuver, a temporary portal triad obstruction (PTO) (hepatic artery, portal vein, common bile duct occlusion for 30 min), with BPC 157 given during reperfusion, in the post-PTO period. In deeply anesthetized and laparatomized rats that had a PTO, the recording lasted 5 minutes with a cannula connected to a pressure transducer, inserted into the portal vein, inferior caval vein and abdominal aorta at the level of its bifurcation at 24 h of reperfusion time. BPC 157 or saline was applied as an abdominal bath in rats that had a PTO, in the post-PTO-period, at 1 min or at 24 h reperfusion time. When BPC 157 was given in circumstances of portal and caval hypertension, and arterial hypotension, disturbances were completely eliminated. This presents a potential therapeutic advantage. Thereby, whithout therapy, the pressure of both the portal and the caval system remains elevated after removal of the portal clamp. Thus, the effectiveness of the therapy, when given at distinctive points during reperfusion, appears as conclusive evidence of its efficacy. BPC 157 therapy mitigates the whole syndrome, involving the course of an even more complex model that should include rats clamped by the hepatic artery, portal vein, and bile duct vs. rats that used to have a clamped portal triad and later underwent reperfusion
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