A randomized, triple-blind, placebo-controlled, parallel study to evaluate the efficacy of a freshwater marine collagen on skin wrinkles and elasticity.

BACKGROUND: Collagen is the primary component in human skin. With age, there is loss of skin elasticity and collagen, resulting in wrinkle formation and reduction in skin appearance. AIMS: The objective of this randomized, triple-blind, placebo-controlled study was to evaluate the safety and efficacy of a hydrolyzed marine collagen (Vinh Wellness Collagen, VWC) on aspects of skin health and quality in women between 45 and 60 years of age. PATIENTS/METHODS: Assessments of skin wrinkles, elasticity, and self-reported appearance were conducted using the VISIA skin analysis system, Cutometer® , and Skin Quality Visual Analogue Scale. Outcomes were assessed at weeks 0 (baseline), 6, and 12. RESULTS: After 12 weeks, participants supplemented with VWC had a significant 35% reduction in wrinkle score (P = .035) from baseline. Participants in the VWC group showed a 24% greater reduction in wrinkles on the right side of the face than those on placebo. A planned subgroup analysis based on age showed women 45-54 years had a significant 20% and 10% improvement in cheek skin elasticity from baseline to week 6 (P = .016) and 12 (P = .022), respectively. At week 12, participants in the VWC group reported greater percentage improvements in overall skin score (9%) and wrinkle (15%), elasticity (23%), hydration (14%), radiance (22%), and firmness (25%) scores vs placebo. CONCLUSION: Supplementation with VWC was found to be safe and well-tolerated. The results of this study support the use of fish-derived hydrolyzed collagen for the improvement of skin health in an aging population.

Effect of a Euglena gracilis Fermentate on Immune Function in Healthy, Active Adults: A Randomized, Double-Blind, Placebo-Controlled Trial.

Euglena gracilis produce high amounts of algal ß-1,3-glucan, which evoke an immune response when consumed. This study investigated the effect of supplementation with a proprietary Euglena gracilis fermentate (BG), containing greater than 50% ß-1,3-glucan, on immune function as measured by self-reported changes in upper respiratory tract infection (URTI) symptoms. Thirty-four healthy, endurance-trained participants were randomized and received either 367 mg of BG or placebo (PLA) for 90 days. Symptoms were assessed by the 24-item Wisconsin Upper Respiratory Symptom Survey and safety via clinical chemistry, hematology, vitals, and adverse event reporting. Participants supplemented with BG over 90 days reported fewer sick days (BG: 1.46 ± 1.01; PLA: 4.79 ± 1.47 days; p = 0.041), fewer URTI symptoms (BG: 12.62 ± 5.92; PLA: 42.29 ± 13.17; p = 0.029), fewer symptom days (BG: 5.46 ± 1.89; PLA: 15.43 ± 4.59 days; p = 0.019), fewer episodes (BG: 2.62 ± 0.67; PLA: 4.79 ± 0.67; p = 0.032), and lower global severity measured as area under curve for URTI symptoms (BG: 17.50 ± 8.41; PLA: 89.79 ± 38.92; p = 0.0499) per person compared to placebo. Sick days, symptoms, and global severity were significantly (p < 0.05) fewer over 30 days in the BG group compared to PLA. All safety outcomes were within clinically normal ranges. The study provides evidence that supplementation with a proprietary Euglena gracilis fermentate containing greater than 50% ß-1,3-glucan may reduce and prevent URTI symptoms, providing immune support and protecting overall health.

Traumatic Brain Injury by a Closed Head Injury Device Induces Cerebral Blood Flow Changes and Microhemorrhages.

OBJECTIVES: Traumatic brain injury is a poly-pathology characterized by changes in the cerebral blood flow, inflammation, diffuse axonal, cellular, and vascular injuries. However, studies related to understanding the temporal changes in the cerebral blood flow following traumatic brain injury extending to sub-acute periods are limited. In addition, knowledge related to microhemorrhages, such as their detection, localization, and temporal progression, is important in the evaluation of traumatic brain injury. MATERIALS AND METHODS: Cerebral blood flow changes and microhemorrhages in male Sprague Dawley rats at 4 h, 24 h, 3 days, and 7 days were assessed following a closed head injury induced by the Marmarou impact acceleration device (2 m height, 450 g brass weight). Cerebral blood flow was measured by arterial spin labeling. Microhemorrhages were assessed by susceptibility-weighted imaging and Prussian blue histology. RESULTS: Traumatic brain injury rats showed reduced regional and global cerebral blood flow at 4 h and 7 days post-injury. Injured rats showed hemorrhagic lesions in the cortex, corpus callosum, hippocampus, and brainstem in susceptibility-weighted imaging. Injured rats also showed Prussian blue reaction products in both the white and gray matter regions up to 7 days after the injury. These lesions were observed in various areas of the cortex, corpus callosum, hippocampus, thalamus, and midbrain. CONCLUSIONS: These results suggest that changes in cerebral blood flow and hemorrhagic lesions can persist for sub-acute periods after the initial traumatic insult in an animal model. In addition, microhemorrhages otherwise not seen by susceptibility-weighted imaging are present in diverse regions of the brain. The combination of altered cerebral blood flow and microhemorrhages can potentially be a source of secondary injury changes following traumatic brain injury and may need to be taken into consideration in the long-term care of these cases.

Temporal assessment of traumatic axonal injury in the rat corpus callosum and optic chiasm.

Impaired axoplasmic transport (IAT) and neurofilament compaction (NFC), two common axonal pathology processes involved in traumatic axonal injury (TAI), have been well characterized. TAI is found clinically and in animal models in brainstem white matter (WM) tracts and in the corpus callosum (CC), optic chiasm (Och), and internal capsule. Previous published quantitative studies of the time course of TAI expression induced by the Marmarou impact acceleration model have been limited to the brainstem. Accordingly, this study assessed the extent of IAT and NFC in the CC and Och at 8h, 28 h, 3 days and 7 days after traumatic brain injury (TBI) induction by the Marmarou impact acceleration model. IAT peak density was observed at 8h in the CC and 28 h in the Och post-TBI. NFC peak density was observed at 28 h in both structures. The density of IAT and NFC decreased with increasing survival time in both structures. The NFC density time profile followed a similar trend in both the Och and CC, whereas the IAT density time profile was variable between the Och and CC. Furthermore, a strong linear relationship was observed between IAT and NFC in the CC but not in the Och. These findings highlight the heterogeneity of TAI as evidenced by variable IAT and NFC injury time profiles in each anatomical structure. This variability indicates the requirement of multiple markers for a comprehensive TAI evaluation and multiple targeted treatments for TAI polypathology within its therapeutic window time frame.

Impaired axoplasmic transport is the dominant injury induced by an impact acceleration injury device: an analysis of traumatic axonal injury in pyramidal tract and corpus callosum of rats.

Traumatic axonal injury (TAI) involves neurofilament compaction (NFC) and impaired axoplasmic transport (IAT) in distinct populations of axons. Previous quantification studies of TAI focused on limited areas of pyramidal tract (Py) but not its entire length. Quantification of TAI in corpus callosum (CC) and its comparison to that in Py is also lacking. This study assessed and compared the extent of TAI in the entire Py and CC of rats following TBI. TBI was induced by a modified Marmarou impact acceleration device in 31 adult male Sprague Dawley rats by dropping a 450 gram impactor from either 1.25 m or 2.25 m. Twenty-four hours after TBI, TAI was assessed by beta amyloid precursor protein (ß-APP-IAT) and RMO14 (NFC) immunocytochemistry. TAI density (ß-APP and RMO14 axonal swellings, retraction balls and axonal profiles) was counted from panoramic images of CC and Py. Significantly high TAI was observed in 2.25 m impacted rats. ß-APP immunoreactive axons were significantly higher in number than RMO14 immunoreactive axons in both the structures. TAI density in Py was significantly higher than in CC. Based on our parallel biomechanical studies, it is inferred that TAI in CC may be related to compressive strains and that in Py may be related to tensile strains. Overall, IAT appears to be the dominant injury type induced by this model and injury in Py predominates that in CC.