The goal of this study was to investigate the Magnum OPUS supplement in terms of its ability to enhance athletic performance and possess a tolerable safety profile.  Two groups (placebo and experimental) performed a series of exercises (pushups, dips, squats, lunges) with each repetition being recorded and compared to the baseline.  Upon completion of four sessions by all twenty participants, the results were scored and significant differences were noted (t(18)= -5.41, p < 0.001, 95% CI [-24.25, -10.68]).  In addition, participants recorded all adverse effects experienced with the use of the supplement.  It was concluded that the participants taking OPUS had a significant increase in athletic performance when compared against the placebo group.  OPUS was shown to be a reasonably safe supplement that may help athletes with their training and other athletic activities.

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This small pilot study used a double blind, between-subject, experimental design for the goal of investigating Magnum ROCKET SCIENCE and assess its claim to enhance memory, athletic performance, endurance, and energy.  The placebo and the experimental groups performed four separate measures for each of the dependent variables.  Memory was measured using a short-term memory test.  Athletic performance was measured using repetitive exercise.  Endurance was measured through exercise eliciting 70% of VO2 max.  Energy was measured through a subjective questionnaire.  All the results were recorded and compared to baseline assessments.  Once the ten participants (N = 5 per group) completed two full sessions, the results were scored and significant differences were noted: Memory t (7.26) = p < 0.05, Athletic Performance t (6.04) = p < 0.05, Endurance t (6.43) = p < 0.05, and Energy t (4.78) = p < 0.05.  There was zero adverse effects experienced with the use of the supplement.  It was concluded that the participants taking ROCKET SCIENCE had a significant increase in memory, athletic performance, endurance, and energy when compared to the placebo group.  ROCKET SCIENCE was shown to be reasonably safe with no side effects reported and may help athletes reach their individual training goals related to the product’s claims while performing similar exercises.

BACKGROUND: Orthopedic surgical patients have reported significantly lower numeric pain scores using a Wi-Fi oral patient-controlled analgesia (PCA) device compared to patients receiving oral as-needed (PRN) medication by manual administration. More than 90% of nurses using the oral PCA device have agreed that the device saved them time. The manual administration of PRN pain medication is frequently delayed and consumes a significant amount of nursing time. Delays in PRN pain medication delivery have been classed as missed nursing care, called an error of omission. PURPOSE: The purpose of this timing study was to examine if the use of the oral PCA device would reduce the nursing time to accomplish the delivery of PRN oral pain medication compared to the manual administration by nursing staff. METHODS: Each total task for the manual and device administration of a single PRN delivery of an oral pain medication was divided into subtasks. Personal data assistant (PDA) devices were programmed to enable the collection of timing data for each subtask for both methods. RESULTS: The manual administration time was 12.7 minutes per single dose beginning with the patient medication request and ending with pain reassessment. The oral PCA device steps to program the device, deliver one of eight doses of medication, and discharge the patient from the device required 2.06 minutes of nursing time. Reloading an additional eight-dose tray required 40 seconds of nursing time per dose of medication administered. CONCLUSION: The oral PCA saved 84% of the nursing time to administer each dose of PRN medication manually. These data provide evidence that the oral PCA device would reduce the nursing time to deliver a single dose of PRN oral pain medication.

The dorsal motor nucleus of the vagus (DMV) is a functionally heterogeneous vagal motor region which controls a variety of digestive and metabolic functions but also innervates the heart, where its role in controlling heart rate is less clear. We therefore chemogenetically activated DMV neurons in awake behaving mice while monitoring heart rate. To selectively activate DMV neurons, we injected an adeno-associated virus (AAV) which expresses the excitatory chemogenetic receptor, hM3Dq (8 injections, 40nl each), only after recombination by both Cre and Flp recombinases, into the DMV of Chat-Cre::Phox2b-Flp mice. Several months later, we injected the hM3Dq ligand clozapine N-oxide (CNO; 1mg/kg) via intraperitoneal injection (n=2 females, 3 males; mean age ± S.D., 32 ± 2 weeks) to activate hM3Dq+ DMV neurons while measuring heart rate via a non-invasive ECG system (ECGenie). We measured heart rate 20 minutes prior to CNO and 0, 20, 40 minutes and 1, 2, 6, 8, 24 hours later. CNO administration significantly but reversibly decreased heart rate (mean ± standard deviation, S.D.: 20min before CNO, 705 ± 15 bpm; 40min after CNO, 536 ± 86 bpm, p=0.0271; 24hr after CNO, 727 ± 25 bpm, p=0.7347; one-way ANOVA, all timepoints, F1.660, 6.638=10.31; Dunnet's post-hoc test, p=0.0107). In order to identify the specific neurons responsible, we repeated these studies in Calb2-Cre::Chat-Flp mice (n=2 females, 3 males; mean age ± S.D., 29 ± 2 weeks) to target Calb2+ DMV neurons, a recently identified DMV molecular subtype. However, in striking contrast to what we observed when activating DMV neurons generally, administering CNO to activate Calb2+ DMV neurons specifically did not significantly affect heart rate (mean ± S.D.: 20min before CNO, 691 ± 69 bpm; 40min after CNO, 718 ± 31 bpm, p=0.6787; 24hr after CNO, 710 ± 54 bpm, p=0.4701; one-way ANOVA, all timepoints, F2.911, 11.65=0.6277; Dunnet’s, p=0.6069). A higher dose of CNO (3.5mg/kg) also had no effect on heart rate in Calb2-Cre::Chat-Flp mice (data not shown). Together, our studies indicate that DMV neurons are capable of suppressing heart rate and that the underlying neurons likely do not express Calb2. Uncovering the DMV’s role in heart rate will expand our understanding of how this clinically relevant metric, associated with a host of cardiovascular disorders, is controlled. Ingrassia Family Echols Scholars Research Grant and Schwager Summer Research Scholarship to L.S.K.; ADA Pathway to Stop Diabetes Award 1-18-INI-14 and NIH grant HL153916 to J.N.C. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.