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2,025 results for “R&D”
Data set from Brunetta E, Shiffer D, Mandelli P, Achenza S, Folci M, Zumbo A, Minonzio M, Cairo B, Jacob G, Boccassini L, Puttini PS, Porta A, Furlan R. Autonomic Abnormalities in Patients With Primary Sjogren's Syndrome - Preliminary Results. Front Physiol. 2019 Aug 27;10:1104. doi: 10.3389/fphys.2019.01104. PMID: 31551801; PMCID: PMC6736624.
<p>Data set from Brunetta E, Shiffer D, Mandelli P, Achenza S, Folci M, Zumbo A, Minonzio M, Cairo B, Jacob G, Boccassini L, Puttini PS, Porta A, Furlan R. Autonomic Abnormalities in Patients With Primary Sjogren's Syndrome - Preliminary Results. Front Physiol. 2019 Aug 27;10:1104. doi: 10.3389/fphys.2019.01104. PMID: 31551801; PMCID: PMC6736624.</p> <p> </p> <p>This is the abstract:</p> <p>Primary Sjögren's syndrome (pSS) is an autoimmune disease affecting exocrine glands and extra-glandular organs. There are conflicting reports on the presence of autonomic dysfunction in pSS and no data are available on the functional status of sympathetic outflow to the vessels and baroreceptor [baroreflex sensitivity (BRS)] control mechanisms. We investigated the cardiac (cBRS) and sympathetic (sBRS) baroreceptor modulation in both time and frequency domains and the cardiovascular autonomic profile in pSS patients compared to healthy controls. Autonomic symptoms were quantified by the Composite Autonomic Symptom Scale (COMPASS31) three-item questionnaire. The EULAR Sjogren's syndrome patient reported index (ESSPRI) questionnaire evaluated the magnitude of pSS clinical symptoms, i.e., fatigue, pain, and sicca symptoms. Electrocardiogram, beat-by-beat arterial pressure (AP) and respiratory activity were continuously recorded in 17 pSS patients and 16 healthy controls, while supine and during 75° head-up tilt. In seven patients and seven controls, muscle sympathetic nerve activity (MSNA) was measured. Spectrum analysis of RR variability provided markers of cardiac vagal modulation (HF<sub>RR</sub> nu) and sympatho-vagal balance [low frequency (LF)/high frequency (HF)]. The power of LF (0.1 Hz) oscillations of systolic arterial pressure (SAP) variability (LF<sub>SAP</sub>) evaluated the vasomotor response to sympathetic stimulation. Compared to controls, pSS patients scored higher in total COMPASS31 (<em>p</em> < 0.0001) and all ESSPRI subdomains (fatigue, <em>p</em> = 0.005; pain, <em>p</em> = 0.0057; dryness, <em>p</em> < 0.0001). Abnormal scialometry (<1.5 ml/15 min) and Schirmer tests (<5 mm/5 min) were found in pSS patients and salivary flow rate was negatively associated with ESSPRI dryness (<em>p</em> = 0.0014). While supine, pSS patients had lower SEQ<sub>cBRS</sub> index of cardiac baroreceptor sensitivity, higher HF<sub>RRnu</sub> (<em>p</em> = 0.021), lower LF/HF (<em>p</em> = 0.007), and greater MSNA (<em>p</em> = 0.038) than controls. No differences were observed in LF<sub>SAP</sub> between groups. During orthostatic challenge, although LF<sub>SAP</sub> increased similarly in both groups, MSNA was greater in pSS patients (<em>p</em> = 0.003). At rest pSS patients showed lower cBR control and greater parasympathetic modulation. Furthermore, greater sympathetic nerve activity was observed in pSS patients while supine and in response to gravitational challenge. We hypothesized that such enhanced sympathetic vasoconstrictor activity might reflect an attempt to maintain blood pressure in a setting of likely reduced vascular responsiveness.</p> <p> </p>
Data set from Barbic F, Heusser K, Minonzio M, Shiffer D, Cairo B, Tank J, Jordan J, Diedrich A, Gauger P, Zamuner RA, Porta A, Furlan R. Effects of Prolonged Head-Down Bed Rest on Cardiac and Vascular Baroreceptor Modulation and Orthostatic Tolerance in Healthy Individuals. Front Physiol. 2019 Aug 23;10:1061. doi: 10.3389/fphys.2019.01061. PMID: 31507438; PMCID: PMC6716544.
<p>Data set from Barbic F, Heusser K, Minonzio M, Shiffer D, Cairo B, Tank J, Jordan J, Diedrich A, Gauger P, Zamuner RA, Porta A, Furlan R. Effects of Prolonged Head-Down Bed Rest on Cardiac and Vascular Baroreceptor Modulation and Orthostatic Tolerance in Healthy Individuals. Front Physiol. 2019 Aug 23;10:1061. doi: 10.3389/fphys.2019.01061. PMID: 31507438; PMCID: PMC6716544.</p> <p> </p> <p>This is the abstract:</p> <p>Orthostatic intolerance commonly occurs after prolonged bed rest, thus increasing the risk of syncope and falls. Baroreflex-mediated adjustments of heart rate and sympathetic vasomotor activity (muscle sympathetic nerve activity - MSNA) are crucial for orthostatic tolerance. We hypothesized that prolonged bed rest deconditioning alters overall baroreceptor functioning, thereby reducing orthostatic tolerance in healthy volunteers. As part of the European Space Agency Medium-term Bed Rest protocol, 10 volunteers were studied before and after 21 days of -6° head down bed rest (HDBR). In both conditions, subjects underwent ECG, beat-by-beat blood pressure, respiratory activity, and MSNA recordings while supine (REST) and during a 15-min 80° head-up tilt (TILT) followed by a 3-min -10 mmHg stepwise increase of lower body negative pressure to pre-syncope. Cardiac baroreflex sensitivity (cBRS) was obtained in the time (sequence method) and frequency domain (spectrum and cross-spectrum analyses of RR interval and systolic arterial pressure - SAP, variability). Baroreceptor modulation of sympathetic discharge activity to the vessels (sBRS) was estimated by the slope of the regression line between the percentage of MSNA burst occurrence and diastolic arterial pressure. Orthostatic tolerance significantly decreased after HDBR (12 ± 0.6 min) compared to before (21 ± 0.6 min). While supine, heart rate, SAP, and cBRS were unchanged before and after HDBR, sBRS gain was slightly depressed after than before HDBR (sBRS: -6.0 ± 1.1 versus -2.9 ± 1.5 burst% × mmHg<sup>-1</sup>, respectively). During TILT, HR was higher after than before HDBR (116 ± 4 b/min versus 100 ± 4 b/min, respectively), SAP was unmodified in both conditions, and cBRS indexes were lower after HDBR (<em>α</em> index: 3.4 ± 0.7 ms/mmHg; BRS<sub>SEQ</sub> 4.0 ± 1.0) than before (<em>α</em> index: 6.4 ± 1.0 ms/mmHg; BRS<sub>SEQ</sub> 6.8 ± 1.2). sBRS gain was significantly more depressed after HDBR than before (sBRS: -2.3 ± 0.7 versus -4.4 ± 0.4 burst% × mmHg<sup>-1</sup>, respectively). Our findings suggest that baroreflex-mediated adjustments in heart rate and MSNA are impaired after prolonged bed rest. The mechanism likely contributes to the decrease in orthostatic tolerance.</p> <p> </p>
QCA-2024-SCC-BI51213 R&D data
Project Code: QCA-2024-SCC-BI51213.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
Raw data for "Effects of sacubitril/valsartan on exercise capacity: a prognostic improvement that starts during uptitration. Eur J Clin Pharmacol. 2023;79:1173-1184." and "Looking into the Kinetics of NT-proBNP and sST2 Changes in Patients with Heart Failure Treated with Sacubitril/Valsartan: A Hint to Different Therapeutic Pathways;Drugs R D. 2023 Sep 13. doi: 10.1007/s40268-023-00438-2."
<p><strong>Looking into the Kinetics of NT-proBNP and sST2 Changes in Patients with Heart Failure Treated with Sacubitril/Valsartan: A Hint to Different Therapeutic Pathways:</strong></p> <p><strong>Background and objective: </strong>N-terminal pro-B-type natriuretic peptide (NT-proBNP) and soluble interleukin 1 receptor-like 1 ST2 (sST2) are biomarkers used to grade heart failure with reduced ejection fraction (HFrEF) severity. Both are potential targets of HFrEF treatment, but the first is associated with the patient's hemodynamic status, while the second is more indicative of the inflammatory status and of myocardial fibrosis. The aim of this study was to assess the kinetics of these biomarkers after treatment with sacubitril/valsartan in HFrEF.</p> <p><strong>Methods: </strong>We analyzed blood samples of patients with HFrEF at baseline (before sacubitril/valsartan treatment), after 1, 2, and 3 months (respectively, after a month taking the 24/26 - 49/51 - 97/103 mg twice daily, or b.i.d., doses), and 6 months after the maximum-tolerated dose was reached (end study).</p> <p><strong>Results: </strong>We obtained samples from 72 patients with HFrEF (age 64.0 ± 10.5 years, 83% males). NT-proBNP and sST2 values progressively and significantly reduced to 37% and 16%, respectively, with a greater reduction for NT-proBNP (p < 0.001). Specifically, NT-proBNP reduced from 1144 [593-2586] pg/mL to 743 [358-1524] pg/mL and sST2 from 27.3 [20.5-35.0] ng/mL to 23.1 [15.9-30.7] ng/mL, p for trend < 0.001 in both cases. The reduction of the two biomarkers over time occurred with statistically significant different kinetics: deferred for sST2 and faster for NT-proBNP. No significant changes in renal function and potassium levels were recorded.</p> <p><strong>Conclusion: </strong>These findings suggest that, in patients with HF, sacubitril/valsartan effects on the cardiovascular system share a double pathway: a first, hemodynamic, faster pathway and a second, non-hemodynamic anti-fibrotic, delayed one. Both likely contribute to the sacubitril/valsartan benefits in HFrEF.</p> <p> </p> <p><strong>Effects of sacubitril/valsartan on exercise capacity: a prognostic improvement that starts during uptitration</strong></p> <p><strong>Purpose: </strong>Sacubitril/valsartan is a mainstay of the treatment of heart failure with reduced ejection fraction (HFrEF); however, its effects on exercise performance yielded conflicting results. Aim of our study was to evaluate the impact of sacubitril/valsartan on exercise parameters and echocardiographic and biomarker changes at different drug doses.</p> <p><strong>Methods: </strong>We prospectively enrolled consecutive HFrEF outpatients eligible to start sacubitril/valsartan. Patients underwent clinical assessment, cardiopulmonary exercise test (CPET), blood sampling, echocardiography, and completed the Kansas City Cardiomyopathy Questionnaire (KCCQ-12). Sacubitril/valsartan was introduced at 24/26 mg b.i.d. dose and progressively uptitrated in a standard monthly-based fashion to 97/103 mg b.i.d. or maximum tolerated dose. Study procedures were repeated at each titration visit and 6 months after reaching the maximum tolerated dose.</p> <p><strong>Results: </strong>Ninety-six patients completed the study, 73 (75%) reached maximum sacubitril/valsartan dose. We observed a significant improvement in functional capacity across all study steps: oxygen intake increased, at peak exercise (from 15.6 ± 4.5 to 16.5 ± 4.9 mL/min/kg; p trend = 0.001), while minute ventilation/carbon dioxide production relationship reduced in patients with an abnormal value at baseline. Sacubitril/valsartan induced positive left ventricle reverse remodeling (EF from 31 ± 5 to 37 ± 8%; p trend < 0.001), while NT-proBNP reduced from 1179 [610-2757] to 780 [372-1344] pg/ml (p trend < 0.0001). NYHA functional class and the subjective perception of limitation in daily life at KCCQ-12 significantly improved. The Metabolic Exercise Cardiac Kidney Index (MECKI) score progressively improved from 4.35 [2.42-7.71] to 2.35% [1.24-4.96], p = 0.003.</p> <p><strong>Conclusions: </strong>A holistic and progressive HF improvement was observed with sacubitril/valsartan in parallel with quality of life. Likewise, a prognostic enhancement was observed.</p>
Dataset & R code used to analyse the prevalence of the FME-D combination in Parids
<p>This R code and the associated dataset are the raw and organised data used to analyse the prevalence of the FME-D combination in Parids. We recorded 7 different species of Parids when mobbing and analysed whether (1) they produced two distinct classes on notes (FME and D notes) and (2) whether they combined it with the FME followed by the D notes. </p>
Data set from Spinelli D, Marconi S, Caruso R, Conti M, Benedetto F, De Beaufort HW, Auricchio F, Trimarchi S. 3D printing of aortic models as a teaching tool for improving understanding of aortic disease. J Cardiovasc Surg (Torino). 2019 Oct;60(5):582-588. doi: 10.23736/S0021-9509.19.10841-5. Epub 2019 Jun 26. PMID: 31256581.
<p>Data set from Spinelli D, Marconi S, Caruso R, Conti M, Benedetto F, De Beaufort HW, Auricchio F, Trimarchi S. 3D printing of aortic models as a teaching tool for improving understanding of aortic disease. J Cardiovasc Surg (Torino). 2019 Oct;60(5):582-588. doi: 10.23736/S0021-9509.19.10841-5. Epub 2019 Jun 26. PMID: 31256581.</p> <p> </p> <p>This is the abstract:</p> <p><strong>Background: </strong>A geometrical understanding of the individual patient's disease morphology is crucial in aortic surgery. The aim of our study was to validate a questionnaire addressing understanding of aortic disease and use this questionnaire to investigate the value of 3D printing as a teaching tool for surgical trainees.</p> <p><strong>Methods: </strong>Anonymized CT-angiography images of six different patients were selected as didactic cases of aortic disease and made into 3D models of transparent rigid resin with the Vat-photopolymerization technique. The 3D aortic models, which could be disassembled and reassembled, were displayed to 37 surgical trainees, immediately after a seminar on aortic disease. A questionnaire was developed to compare the trainees' understanding before (T0) and after (T1) demonstration of the 3D printed models.</p> <p><strong>Results: </strong>A panel of 15 experts participated in evaluating face and content validity of the questionnaire. The questionnaire validity was established and therefore the information investigated by the questionnaire could be synthetized using the mean of the items to indicate the understanding. The participants (mean age 28 years, range 26-34, male 59%) showed a significant improvement in understanding from T0 (median=7.25; IQR=1.50) to T1 (median=8.00; IQR=1.50; P=0.002).</p> <p><strong>Conclusions: </strong>Preliminary data suggest that the use of 3D-printed aortic models as a teaching tool was feasible and improved the understanding of aortic disease among surgical trainees.</p>
Data set from Barbic F, Minonzio M, Cairo B, Shiffer D, Dipasquale A, Cerina L, Vatteroni A, Urechie V, Verzeletti P, Badilini F, Vaglio M, Iatrino R, Porta A, Santambrogio M, Gatti R, Furlan R. Effects of different classroom temperatures on cardiac autonomic control and cognitive performances in undergraduate students. Physiol Meas. 2019 Jun 4;40(5):054005. doi: 10.1088/1361-6579/ab1816. PMID: 30970334.
<p>Data set from Barbic F, Minonzio M, Cairo B, Shiffer D, Dipasquale A, Cerina L, Vatteroni A, Urechie V, Verzeletti P, Badilini F, Vaglio M, Iatrino R, Porta A, Santambrogio M, Gatti R, Furlan R. Effects of different classroom temperatures on cardiac autonomic control and cognitive performances in undergraduate students. Physiol Meas. 2019 Jun 4;40(5):054005. doi: 10.1088/1361-6579/ab1816. PMID: 30970334.</p> <p> </p> <p>This is the abstract:</p> <p><strong>Objective: </strong> Indoor microclimate may affect students' wellbeing, cardiac autonomic control and cognitive performance with potential impact on learning capabilities. To assess the effects of classroom temperature variations on the autonomic profile and students' cognitive capabilities.</p> <p><strong>Approach: </strong> Twenty students attending Humanitas University School, (14M, age 21 ± 3 years) underwent a single-lead ECG continuous recording by a portable device during a 2 h lecture when classroom temperature was set 'neutral' (20 °C-22 °C, Day 1) and when classroom temperature was set to 24 °C-26 °C (Day 2). ECGs were sent by telemetry to a server for off-line analysis. Spectral analysis of RR variability provided indices of cardiac sympathetic (LF<sub>nu</sub>), vagal (HF, HF<sub>nu</sub>) and cardiac sympatho-vagal modulation (LF/HF). Symbolic analysis of RR variability provided the percentage of sequences of three heart periods with no significant change in RR interval (0V%) and with two significant variations (2V%) reflecting cardiac sympathetic and vagal modulation, respectively. Students' cognitive performance (memory, verbal comprehension and reasoning) was assessed at the end of each lecture using the Cambridge Brain Sciences cognitive evaluation tool.</p> <p><strong>Main results: </strong> Classroom temperature and CO<sub>2</sub> were assessed every 5 min. Classroom temperatures were 22.4 °C ± 0.1 °C (Day 1) and 26.2 °C ± 0.1 °C (Day 2). Student's thermal comfort was lower during Day 2 compared to Day 1. HR, LF/HF and 0V% were greater during Day 2 (79.5 ± 12.1 bpm, 6.9 ± 7.1 and 32.8% ± 10.3%) than during Day 1 (72.6 ± 10.8 bpm, 3.4 ± 3.7, 21.4% ± 9.2%). Conversely, 2V% was lower during Day 2 (23.1% ± 8.1%) than during Day 1 (32.3% ± 11.4%). Short-term memory, verbal ability and the overall cognitive C-score scores were lower during Day 2 (10.3 ± 0.3; 8.1 ± 1.2 and 10.9 ± 2.0) compared to Day 1 (11.7 ± 2.1; 10.7 ± 1.7 and 12.6 ± 1.8).</p> <p><strong>Significance: </strong> During Day 2, a shift of the cardiac autonomic control towards a sympathetic predominance was observed compared to Day 1, in the presence of greater thermal discomfort. Furthermore, during Day 2 reduced cognitive performances were found.</p>
Data set from Dalla Vecchia LA, Barbic F, De Maria B, Cozzolino D, Gatti R, Dipaola F, Brunetta E, Zamuner AR, Porta A, Furlan R. Can strenuous exercise harm the heart? Insights from a study of cardiovascular neural regulation in amateur triathletes. PLoS One. 2019 May 7;14(5):e0216567. doi: 10.1371/journal.pone.0216567. PMID: 31063482; PMCID: PMC6504093.
<p>Data set from Dalla Vecchia LA, Barbic F, De Maria B, Cozzolino D, Gatti R, Dipaola F, Brunetta E, Zamuner AR, Porta A, Furlan R. Can strenuous exercise harm the heart? Insights from a study of cardiovascular neural regulation in amateur triathletes. PLoS One. 2019 May 7;14(5):e0216567. doi: 10.1371/journal.pone.0216567. PMID: 31063482; PMCID: PMC6504093</p> <p> </p> <p>This is the abstract:</p> <p>Regular exercise is recommended to improve the cardiovascular risk profile. However, there is growing evidence that extreme volumes and intensity of long-term exertion may increase the risk of acute cardiac events. The aim of this study is to investigate the after-effects of regular, strenuous physical training on the cardiovascular neural regulation in a group of amateur triathletes compared to age-matched sedentary controls. We enrolled 11 non-elite triathletes (4 women, age 24±4 years), who had refrained from exercise for 72 hours, and 11 age-matched healthy non-athletes (3 women, age 25±2 years). Comprehensive echocardiographic and cardiopulmonary exercise tests were performed at baseline. Electrocardiogram, non-invasive blood pressure, respiratory activity, and muscle sympathetic nerve activity (MSNA) were continuously recorded in a supine position (REST) and during an incremental 15° step-wise head-up tilt test up to 75° (TILT). Blood samples were collected for determination of stress mediators. Autoregressive spectral analysis provided the indices of the cardiac sympathetic (LFRR) and vagal (HFRR) activity, the vascular sympathetic control (LFSAP), and the cardiac sympatho-vagal modulation (LF/HF). Compared to controls, triathletes were characterized by greater LFRR, LF/HF ratio, LFSAP, MSNA, and lower HFRR at REST and during TILT, i.e. greater overall cardiovascular sympathetic modulation together with lower cardiac vagal activity. Cortisol and adrenocorticotropic hormone concentrations were also higher in triathletes. In conclusion, triathletes were characterized by signs of sustained cardiovascular sympathetic overactivity. This might represent a risk factor for future cardiovascular events, given the known association between chronic excessive sympathetic activity and increased cardiovascular risk.</p>
Data set fromMazzaccaro D, Miri R, Derbel B, Modafferi A, Nano G. Hypogastric artery coverage during endovascular aneurysm repair in octogenarian and younger patients. J Cardiovasc Med (Hagerstown). 2019 Aug;20(8):557-563. doi: 10.2459/JCM.0000000000000799. PMID: 30950984.
<p>Data set fromMazzaccaro D, Miri R, Derbel B, Modafferi A, Nano G. Hypogastric artery coverage during endovascular aneurysm repair in octogenarian and younger patients. J Cardiovasc Med (Hagerstown). 2019 Aug;20(8):557-563. doi: 10.2459/JCM.0000000000000799. PMID: 30950984.</p> <p> </p> <p>This is the abstract:</p> <p><strong>Aim: </strong> To report our experience about hypogastric artery coverage during endovascular aneurysm repair (EVAR) for aortoiliac aneurysms in patients younger than 80 years (group A) compared with octogenarian patients (group B).</p> <p><strong>Methods: </strong> Data of consecutive EVAR with hypogastric artery coverage from 01/1998 to 12/2016 were retrospectively analyzed. Primary outcomes were the occurrence of ischemic colitis, type II endoleak and buttock claudication both at 30 days and in the long term. P values less than 0.05 were considered statistically significant.</p> <p><strong>Results: </strong> The hypogastric artery was covered in 107 patients. Twenty-three (21.5%) were octogenarian (group B). At 30 days, one type II endoleak occurred in group B, whereas 16 patients of group A experienced buttock claudication. There were no cases of ischemic colitis. During follow-up (median 63.5 months), no cases of ischemic colitis occurred. Six new type II endoleaks were recorded (five in group B and one in group A, P = 0.0001). Buttock claudication persisted in four patients of group A. No new cases of buttock claudication were observed.</p> <p><strong>Conclusion: </strong> Unilateral hypogastric artery coverage during EVAR for aortoiliac aneurysms can be performed with an acceptable rate of postoperative complication. Postoperative buttock claudication was more frequent in younger patients, whereas a type II endoleak occurred mostly in octogenarian patients during follow-up.</p>
QCA-2024-SCC-SU25530 R&D data
Project Code: QCA-2024-SCC-SU25530.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-KE23187 R&D data
Project Code: QCA-2024-SCC-KE23187.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-VH24614 R&D data
Project Code: QCA-2024-SCC-VH24614.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-RX21950 R&D data
Project Code: QCA-2024-SCC-RX21950.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-CD78114 R&D data
Project Code: QCA-2024-SCC-CD78114.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-JR44097 R&D data
Project Code: QCA-2024-SCC-JR44097.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-GQ29860 R&D data
Project Code: QCA-2024-SCC-GQ29860.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-QN78209 R&D data
Project Code: QCA-2024-SCC-QN78209.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-FJ03428 R&D data
Project Code: QCA-2024-SCC-FJ03428.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-FE55363 R&D data
Project Code: QCA-2024-SCC-FE55363.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
QCA-2024-SCC-GX86713 R&D data
Project Code: QCA-2024-SCC-GX86713.This project is classified as CONFIDENTIAL. All information, data, and results associated with this project are strictly restricted to authorized personnel only. Any dissemination, distribution, or copying of the project details is strictly prohibited without prior approval from the project lead and the university's Office of Research Compliance.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.