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Why are you taking BPC for a concussion?
You don't think any source is reliable for BPC?
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"The further extension could be the effect of BPC 157 after an induced traumatic brain injury (TBI) in mice by a falling weight. BPC 157 regimens (10 micrograms/kg, 10 ng/kg intraperito‐ neally) demonstrated a marked attenuation of damage with an improved early outcome and a minimal postponed mortality throughout a 24h post-injury period. Ultimately, the traumatic lesions (subarachnoidal and intraventricularhaemorrhage, brain laceration, haemorrhagic laceration) were less intense and consecutive brain edema had considerably improved. Given prophylactically (30 min before TBI) the improved conscious/unconscious/death ratio in TBI- mice was after force impulses of 0. 068 Ns, 0. 093 Ns, 0. 113 Ns, 0. 130 Ns, 0. 145 Ns, and 0. 159 Ns. Counteraction (with a reduction of unconsciousness, lower mortality) with both microg- and ng-regimens included the force impulses of 0. 068-0. 145 Ns. A higher regimen presented effectiveness also against the maximal force impulse (0. 159 Ns). Furthermore, BPC 157 application immediately prior to injury was beneficial in mice subjected to force impulses of 0. 093 Ns-TBI. For a more severe force impulse (0. 130 Ns, 0. 145 Ns, or 0159 Ns), the time- relation to improve the conscious/unconscious/death ratio was: 5 min (0. 130 Ns-TBI), 20 min (0. 145 Ns-TBI) or 30 min (0. 159 Ns-TBI) (Tudor et al., 2010)
3. Results
In conclusion, these results should be viewed with numerous compounds and neuroprotective strategies more extensively discussed, evaluated and reviewed elsewhere (Maas et al., 2005; Marklund et al., 2006). However, brain trauma results in brain damage and dysfunction from both primary injury (due to biomechanical effects) and subsequent secondary damage due to activation of pathophysiologic cascades (Muir, 2006), and this study with BPC 157 (Tudor et al., 2010) evidenced the preserved consciousness and reduced mortality immediately after trauma in pentadecapeptide BPC 157-mice and subsequently, markedly reduced mortality, lowered brain edema, lowered the number and size of haemorrhagic traumatic lacerations, and lowered the intensity of subarachnoidal bleeding with significantly less intraventricular‐ haemorrhage.
The additional extension could be the evidence that pentadecapeptide BPC 157 particularly attenuated neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) damage, including mortality (Sikiric et al., 1999)(of note, neuroprotection by immunophillin ligands lack the effect on MPTP-toxicity (Gold, 2000), significantly affected the dopamine system (Jelovac et al., 1998, 1999; Sikiric et al., 1999)(a system also implicated in the traumatic brain injury course) (Yan et al., 2001)and prevented/reversed catalepsy or stereotypy due to central dopamine system failure induced by various procedures (Jelovac et al., 1998, 1999; Sikiric et al., 1999). Accordingly, regional serotonin synthesis in the rat brain, assessed by α-methyl-L- tryptophan autoradiographic measurements showed that, BPC 157 given peripherally may readily cross the blood–brain barrier, affect region-specific brain 5-HT synthesis in rats leading to significantly increased synthesis in the substantianigra (compacta and reticulata) structure and counteract serotonin syndrome (BobanBlagaic et al., 2005; Tohyama et al., 2004). Very recently, BPC 157 counteracts cuprizone-brain damage and motoric disability (Klicek et al., 2013). An additional emphasize may be that BPC 157 largely interferes with different NSAIDs-...."

http://cdn.intechopen.com/pdfs-wm/47147.pdf
- - - Updated - - -
"The further extension could be the effect of BPC 157 after an induced traumatic brain injury (TBI) in mice by a falling weight. BPC 157 regimens (10 micrograms/kg, 10 ng/kg intraperito‐ neally) demonstrated a marked attenuation of damage with an improved early outcome and a minimal postponed mortality throughout a 24h post-injury period. Ultimately, the traumatic lesions (subarachnoidal and intraventricularhaemorrhage, brain laceration, haemorrhagic laceration) were less intense and consecutive brain edema had considerably improved. Given prophylactically (30 min before TBI) the improved conscious/unconscious/death ratio in TBI- mice was after force impulses of 0. 068 Ns, 0. 093 Ns, 0. 113 Ns, 0. 130 Ns, 0. 145 Ns, and 0. 159 Ns. Counteraction (with a reduction of unconsciousness, lower mortality) with both microg- and ng-regimens included the force impulses of 0. 068-0. 145 Ns. A higher regimen presented effectiveness also against the maximal force impulse (0. 159 Ns). Furthermore, BPC 157 application immediately prior to injury was beneficial in mice subjected to force impulses of 0. 093 Ns-TBI. For a more severe force impulse (0. 130 Ns, 0. 145 Ns, or 0159 Ns), the time- relation to improve the conscious/unconscious/death ratio was: 5 min (0. 130 Ns-TBI), 20 min (0. 145 Ns-TBI) or 30 min (0. 159 Ns-TBI) (Tudor et al., 2010)
3. Results
In conclusion, these results should be viewed with numerous compounds and neuroprotective strategies more extensively discussed, evaluated and reviewed elsewhere (Maas et al., 2005; Marklund et al., 2006). However, brain trauma results in brain damage and dysfunction from both primary injury (due to biomechanical effects) and subsequent secondary damage due to activation of pathophysiologic cascades (Muir, 2006), and this study with BPC 157 (Tudor et al., 2010) evidenced the preserved consciousness and reduced mortality immediately after trauma in pentadecapeptide BPC 157-mice and subsequently, markedly reduced mortality, lowered brain edema, lowered the number and size of haemorrhagic traumatic lacerations, and lowered the intensity of subarachnoidal bleeding with significantly less intraventricular‐ haemorrhage.
The additional extension could be the evidence that pentadecapeptide BPC 157 particularly attenuated neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) damage, including mortality (Sikiric et al., 1999)(of note, neuroprotection by immunophillin ligands lack the effect on MPTP-toxicity (Gold, 2000), significantly affected the dopamine system (Jelovac et al., 1998, 1999; Sikiric et al., 1999)(a system also implicated in the traumatic brain injury course) (Yan et al., 2001)and prevented/reversed catalepsy or stereotypy due to central dopamine system failure induced by various procedures (Jelovac et al., 1998, 1999; Sikiric et al., 1999). Accordingly, regional serotonin synthesis in the rat brain, assessed by α-methyl-L- tryptophan autoradiographic measurements showed that, BPC 157 given peripherally may readily cross the blood–brain barrier, affect region-specific brain 5-HT synthesis in rats leading to significantly increased synthesis in the substantianigra (compacta and reticulata) structure and counteract serotonin syndrome (BobanBlagaic et al., 2005; Tohyama et al., 2004). Very recently, BPC 157 counteracts cuprizone-brain damage and motoric disability (Klicek et al., 2013). An additional emphasize may be that BPC 157 largely interferes with different NSAIDs-...."

http://cdn.intechopen.com/pdfs-wm/47147.pdf
