Background: Substantial fat loss may occur during continuous feeding of human milk (HM). A decrease of fat loss has been described following homogenization. Well-established methods of homogenization of HM for routine use in the neonatal intensive care unit (NICU) would be desirable.
Objective: We compared the loss of fat based on the use of 3 different methods for homogenizing thawed HM during continuous feeding.
Methods: Sixteen frozen donor HM samples were thawed, homogenized with ultrasound and separated into 3 aliquots ("baseline agitation," "hourly agitation," and "ultrasound"), and then frozen for 48 hours. Aliquots were thawed again and a baseline agitation was applied. Subsequently, aliquots baseline agitation and hourly agitation were drawn into a syringe, while ultrasound was applied to aliquot ultrasound before it was drawn into a syringe. The syringes were loaded into a pump (2 mL/h; 4 hours). At hourly intervals the hourly agitation infusion was stopped, the syringe was disconnected and gently shaken. During infusion, samples from the 3 groups were collected hourly for analysis of fat and caloric content.
Results: The 3 groups of homogenization showed similar fat content at the beginning of the infusion. For fat, mean (SD) hourly changes of -0.03 (0.01), -0.09 (0.01), and -0.09 (0.01) g/dL were observed for the hourly agitation, baseline agitation, and ultrasound groups, respectively. The decrease was smaller for the hourly agitation group (P < .001).
Conclusion: When thawed HM is continuously infused, a smaller fat loss is observed when syringes are agitated hourly versus when ultrasound or a baseline homogenization is used.
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http://dx.doi.org/10.1177/0890334414546044 | DOI Listing |
Alzheimers Dement
December 2024
Sapienza University of Rome, Rome, Rome, Italy.
Background: Biological sex influences Alzheimer's disease (AD) development, particularly concerning brain insulin resistance (bIR) and early energy metabolism defects. Biliverdin reductase-A (BVR-A) plays a crucial role in insulin signaling, and its downregulation leads to bIR. However, the sex-related differences in AD neuropathology and underlying mechanisms remain unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Background: MODEL-AD (Model Organism Development and Evaluation for Late-onset AD) is developing, characterizing, and distributing novel mouse models expressing humanized, clinically relevant genetic risk factors. Models expressing human-relevant risk genetic risk factors are expected to better phenocopy LOAD than widely used transgenic models.
Method: Here, two genetic risk factors APOE4 and Trem2*R47H, were incorporated into C57BL/6J (B6) mice along with humanized amyloid-beta to produce the LOAD2 model.
Alzheimers Dement
December 2024
University of Utah, Salt Lake City, UT, USA.
Background: Neurodegenerative disorders such as Alzheimer's Disease (AD) are increasingly associated with irregular lipid accumulation. Dysfunction in the catabolism of sphingolipids leads to many neurodegenerative disorders but has only recently garnered interest in AD. Excess ceramide deposition has been observed in Aβ-plaques, plasma, and cerebrospinal fluid in AD patients and AD mouse models.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Arizona, Tucson, AZ, USA.
Background: Research into Alzheimer's Disease (AD) pathomechanisms frequently utilizes animal models with dominant mutations; however, the vast majority (>95%) of AD cases are idiopathic. Animal models with AD risk factors represent an approach with potentially greater translational validity. The predominant genetic risk factor for AD is the Apolipoprotein E ε4 (APOE4) polymorphism, with APOE4 homozygosity conferring approximately 15-fold higher risk relative to the normative APOE3/3 genotype.
View Article and Find Full Text PDFAesthet Surg J
January 2025
Department of Dermatology, Erasmus Universiteit Rotterdam, Rotterdam, Netherlands.
Background: Midfacial aging involves skeletal changes, muscle weakening, and fat redistribution, resulting in volume loss, skin sagging, and deepened nasolabial folds. High-Intensity Facial Electrical Stimulation (HIFES) combined with Radiofrequency (RF) is a novel non-invasive method to address these changes by enhancing muscle mass and remodeling subcutaneous tissue.
Objectives: To assess the efficacy of HIFES and Synchronized RF in improving midfacial aesthetics, specifically muscle thickness, skin displacement, and facial volume.
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