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Scientific Data Jun 2024Accurate differentiation between angina with no obstructive coronary arteries (ANOCA) and mental stress-induced myocardial ischemia (MSIMI) is crucial for tailored...
Accurate differentiation between angina with no obstructive coronary arteries (ANOCA) and mental stress-induced myocardial ischemia (MSIMI) is crucial for tailored treatment strategies, yet public data scarcity hampers understanding. Given the higher incidence of both conditions in women, this study prospectively enrolled 80 female ANOCA and 39 age-matched female controls, subjecting them to three types of mental stress tasks. ECGs were continuously monitored across Rest, Stress, and Recover stages of the mental stress tasks, with PET/CT imaging during the Stress stage to evaluate myocardial perfusion. With PET/CT serving as the gold standard for MSIMI diagnosis, 35 of the 80 ANOCA patients were diagnosed as MSIMI. Using ECG variables from different stages of mental stress tasks, we developed five machine learning models to diagnose MSIMI. The results showed that ECG data from different stages provide valuable information for MSIMI classification. Additionally, the dataset encompassed demographic details, physiological, and blood sample test results of the patients. We anticipate this new dataset will significantly push further progress in ANOCA and MSIMI research.
Topics: Humans; Female; Myocardial Ischemia; Stress, Psychological; Electrocardiography; Machine Learning; Positron Emission Tomography Computed Tomography; Middle Aged; Angina Pectoris; Prospective Studies
PubMed: 38937514
DOI: 10.1038/s41597-024-03462-2 -
Journal of the Association For Research... Jun 2024Tone-pip-evoked otoacoustic emissions (PEOAEs) are transient-evoked otoacoustic emissions (OAEs) that are hypothesized to originate from reflection of energy near the...
PURPOSE
Tone-pip-evoked otoacoustic emissions (PEOAEs) are transient-evoked otoacoustic emissions (OAEs) that are hypothesized to originate from reflection of energy near the best-frequency (BF) cochlear place of the stimulus frequency. However, individual PEOAEs have energy with a wide range of delays. We sought to determine whether some PEOAE energy is consistent with having been generated far from BF.
METHODS
PEOAEs from 35 and 47 dB SPL tone pips were obtained by removing pip-stimulus energy by subtracting the ear-canal sound pressure from scaled-down 59 dB SPL tone pips (which evoke relatively small OAEs). PEOAE delays were measured at each peak in the PEOAE absolute-value waveforms. While measuring PEOAEs and auditory-nerve compound action potentials (CAPs), amplification was blocked sequentially from apex to base by cochlear salicylate perfusion. The perfusion time when a CAP was reduced identified when the perfusion reached the tone-pip BF place. The perfusion times when each PEOAE peak was reduced identified where along the cochlea it received cochlear amplification. PEOAEs and CAPs were measured simultaneously using one pip frequency in each ear (1.4 to 4 kHz across 16 ears).
RESULTS
Most PEOAE peaks received amplification primarily between the BF place and 1-2 octaves basal of the BF place. PEOAE peaks with short delays received amplification basal of BF place. PEOAE peaks with longer delays sometimes received amplification apical of BF place, consistent with previous stimulus-frequency-OAE results.
CONCLUSION
PEOAEs provide information about cochlear amplification primarily within ~ 1.5 octave of the tone-pip BF place, not about regions > 3 octaves basal of BF.
PubMed: 38937327
DOI: 10.1007/s10162-024-00955-0 -
Journal of Cardiothoracic and Vascular... May 2024To describe perfusionist perspectives regarding waste anesthetic gas (WAG) management during cardiopulmonary bypass (CPB) and compare results to existing American...
OBJECTIVES
To describe perfusionist perspectives regarding waste anesthetic gas (WAG) management during cardiopulmonary bypass (CPB) and compare results to existing American Society of Extracorporeal Technology (AmSECT) guidelines and the 2016 National Institute of Occupational Safety and Health Survey of healthcare workers and anesthesia care providers.
DESIGN
We developed a questionnaire with 26 questions covering institutional demographics, use of anesthetic gases, scavenging systems, and air monitoring practices.
SETTING
Web-based survey.
PARTICIPANTS
Self-identified board-eligible perfusionist members of AmSECT, the American Academy of Cardiovascular Perfusion, and the Maryland and Wisconsin State Perfusion Societies in 2022.
INTERVENTIONS
None.
MEASUREMENTS AND MAIN RESULTS
Of the 4,303 providers sent the survey, 365 (8.5%) participated. Although 92% of the respondents (335/364) routinely administered inhaled anesthetics via the oxygenator, only 73.2% (259/354) routinely scavenged WAG during CPB cases. Only 6.6% of the respondents (22/336) conducted environmental monitoring for WAG levels. Cited reasons for not scavenging waste gases included a lack of applicable protocols and waste gas scavenging systems, excessive cost, and no need for scavenging.
CONCLUSIONS
Our findings identify a gap between AmSECT guidelines and current perfusionist behavior and suggest potential strategies for reducing WAG leakage during CPB. Effective management should incorporate hazard awareness training, availability of standard procedures to minimize exposure, scavenging systems, regular equipment inspection, and prompt attention to spills and leaks. In high-risk environments, environmental surveillance for waste gas levels would also contribute to waste gas safety. A comprehensive approach to managing waste anesthetic gases will reduce WAG leakage, help improve health care worker safety, and prevent potential adverse effects of exposure.
PubMed: 38937176
DOI: 10.1053/j.jvca.2024.05.005 -
Archives of Biochemistry and Biophysics Jun 2024It has been previously demonstrated that the maintenance of ischemic acidic pH or the delay of intracellular pH recovery at the onset of reperfusion decreases...
BACKGROUND
It has been previously demonstrated that the maintenance of ischemic acidic pH or the delay of intracellular pH recovery at the onset of reperfusion decreases ischemic-induced cardiomyocyte death.
OBJECTIVE
To examine the role played by nitric oxide synthase (NOS)/NO-dependent pathways in the effects of acidic reperfusion in a regional ischemia model METHODS: Isolated rat hearts perfused by Langendorff technique were submitted to 40 min of left coronary artery occlusion followed by 60 min of reperfusion (IC). A group of hearts received an acid solution (pH=6.4) during the first 2 min of reperfusion (AR) in absence or in presence of L-NAME (NOS inhibitor). Infarct size (IS) and myocardial function were determined. In cardiac homogenates, the expression of P-Akt, P-endothelial and inducible isoforms of NOS (P-eNOS and iNOS) and the level of 3-nitrotyrosine were measured. In isolated cardiomyocytes, the intracellular NO production was assessed by confocal microscopy, under control and acidic conditions. Mitochondrial swelling after Ca addition and mitochondrial membrane potential (Δψ) were also determined under control and acidosis RESULTS: AR decreased IS, improved postischemic myocardial function recovery, increased P-Akt and P-eNOS, and decreased iNOS and 3-nitrotyrosine. NO production increased while mitochondrial swelling and Δψ decreased in acidic conditions. L-NAME prevented the beneficial effects of AR CONCLUSIONS: Our data strongly supports that a brief acidic reperfusion protects the myocardium against the ischemia-reperfusion injury through eNOS/NO-dependent pathways.
PubMed: 38936683
DOI: 10.1016/j.abb.2024.110059 -
PloS One 2024Myocardial ischemia-reperfusion injury (MIRI) refers to the secondary damage to myocardial tissue that occurs when blood perfusion is rapidly restored following...
Myocardial ischemia-reperfusion injury (MIRI) refers to the secondary damage to myocardial tissue that occurs when blood perfusion is rapidly restored following myocardial ischemia. This process often exacerbates the injury to myocardial fiber structure and function. The activation mechanism of angiogenesis is closely related to MIRI and plays a significant role in the occurrence and progression of ischemic injury. In this study, we utilized sequencing data from the GEO database and employed WGCNA, Mfuzz cluster analysis, and protein interaction network to identify Stat3, Rela, and Ubb as hub genes involved in MIRI-angiogenesis. Additionally, the GO and KEGG analysis of differentially expressed genes highlighted their broad participation in inflammatory responses and associated signaling pathways. Moreover, the analysis of sequencing data and hub genes revealed a notable increase in the infiltration ratio of monocytes and activated mast cells. By establishing key cell ROC curves, using independent datasets, and validating the expression of hub genes, we demonstrated their high diagnostic value. Moreover, by scrutinizing single-cell sequencing data alongside trajectory analysis, it has come to light that Stat3 and Rela exhibit predominant expression within Dendritic cells. In contrast, Ubb demonstrates expression across multiple cell types, with all three genes being expressed at distinct stages of cellular development. Lastly, leveraging the CMap database, we predicted potential small molecule compounds for the identified hub genes and validated their binding activity through molecular docking. Ultimately, our research provides valuable evidence and references for the early diagnosis and treatment of MIRI from the perspective of angiogenesis.
Topics: Myocardial Reperfusion Injury; Humans; STAT3 Transcription Factor; Biomarkers; Transcription Factor RelA; Protein Interaction Maps; Neovascularization, Pathologic; Gene Expression Profiling; Angiogenesis
PubMed: 38935597
DOI: 10.1371/journal.pone.0300790 -
EJNMMI Radiopharmacy and Chemistry Jun 20244-[F]fluorobenzyl-triphenylphosphonium ([F]FBnTP) is a lipophilic cation PET tracer. The cellular uptake of [F]FBnTP is correlated with oxidative phosphorylation by...
BACKGROUND
4-[F]fluorobenzyl-triphenylphosphonium ([F]FBnTP) is a lipophilic cation PET tracer. The cellular uptake of [F]FBnTP is correlated with oxidative phosphorylation by mitochondria, which has been associated with multiple critical diseases. To date, [F]FBnTP has been successfully applied for imaging myocardial perfusion, assessment of severity of coronary artery stenosis, delineation of the ischemic area after transient coronary occlusion, and detection/quantification of apoptosis in various animal models. Recent preclinical and clinical studies have also expanded the possibilities of using [F]FBnTP in oncological diagnosis and therapeutic monitoring. However, [F]FBnTP is typically prepared through a tediously lengthy four-step, three-pot reaction and required multiple synthesizer modules; Thus, such an approach remains a challenge for this promising radiopharmaceutical to be implemented for routine clinical studies. Herein, we report an optimized one-step, one-pot automated approach to produce [F]FBnTP through a single standard commercially-available radiosynthesizer that enables centralized production for clinical use.
RESULTS
The fully automated production of [F]FBnTP took less than 55 min with radiochemical yields ranging from 28.33 ± 13.92% (non-decay corrected), apparent molar activity of 69.23 ± 45.62 GBq/µmol, and radiochemical purities of 99.79 ± 0.41%. The formulated [F]FBnTP solution was determined to be sterile and colorless with a pH of 4.0-6.0. Our data has indicated no observable radiolysis after 8 h from the time of final product formulation and maximum assay of 7.88 GBq.
CONCLUSIONS
A simplified and cGMP-compliant radiosynthesis of [F]FBnTP has been established on the commercially available synthesizer in high activity concentration and radiochemical purity. While the preclinical and clinical studies using [F]FBnTP PET are currently underway, the automated approaches reported herein facilitate clinical adoption of this radiotracer and warrant centralized production of [F]FBnTP for imaging multiple patients.
PubMed: 38935218
DOI: 10.1186/s41181-024-00274-y -
Archives of Dermatological Research Jun 2024Current strategies for hypertrophic scar prevention and treatment are limited.
BACKGROUND
Current strategies for hypertrophic scar prevention and treatment are limited.
OBJECTIVE
To facilitate these efforts, a minimally invasive hypertrophic scar model was created in a rabbit ear for the first time based on previous methods used to induce ischemia.
METHODS
Six New Zealand white rabbits (12 ears total) were studied. First, ischemia was achieved by ligating the cranial artery, cranial vein and central artery, while preserving the caudal artery, caudal vein and central vein, respectively. The relative level of ischemia induced at time of surgery, both baseline and maximum perfusion, was assessed with a fluorescent light-assisted angiography and demonstrated lower rates of perfusion in the ischemic ears. Following vascular injury, a 2-cm full thickness linear wound was created on the ventral ear and closed with 4 - 0 Nylon sutures under high tension. For each rabbit, one ear received a combination of ischemia and wounding with suture tension (n = 6), while the other ear was non-ischemic with wounding and suture tension alone (n = 6).
RESULTS
Four weeks post-operatively, ischemic ears developed scar hypertrophy (histological scar thickness: 1.1 ± 0.2 mm versus 0.5 ± 0.1 mm, p < 0.05).
CONCLUSION
Herein, we describe a novel, prototypical minimally invasive rabbit ear model of hypertrophic scar formation that can allow investigation of new drugs for scar prevention.
Topics: Animals; Rabbits; Cicatrix, Hypertrophic; Disease Models, Animal; Minimally Invasive Surgical Procedures; Ear; Ischemia; Humans; Wound Healing; Suture Techniques
PubMed: 38935157
DOI: 10.1007/s00403-024-03185-9 -
Journal of the American Heart... Jun 2024Experimental preeclampsia (ePE) has been shown to have worsened outcome from stroke. We investigated the effect of low-dose aspirin, known to prevent preeclampsia, on...
BACKGROUND
Experimental preeclampsia (ePE) has been shown to have worsened outcome from stroke. We investigated the effect of low-dose aspirin, known to prevent preeclampsia, on stroke hemodynamics and outcome, and the association between the vasoconstrictor and vasodilator cyclooxygenase products thromboxane A and prostacyclin.
METHODS AND RESULTS
Middle cerebral artery occlusion was performed for 3 hours with 1 hour of reperfusion in normal pregnant rats on day 20 of gestation and compared with ePE treated with vehicle or low-dose aspirin (1.5 mg/kg per day). Multisite laser Doppler was used to measure changes in cerebral blood flow to the core middle cerebral artery and collateral vascular territories. After 30 minutes occlusion, phenylephrine was infused to increase blood pressure and assess cerebral blood flow autoregulation. Infarct and edema were measured using 2,3,5-triphenyltetrazolium chloride staining. Plasma levels of thromboxane A, prostacyclin, and inflammatory markers in plasma and cyclooxygenase levels in cerebral arteries were measured. ePE had increased infarction compared with normal pregnant rats (<0.05) that was reduced by aspirin (<0.001). ePE also had intact cerebral blood flow autoregulation and reduced collateral perfusion during induced hypertension that was also prevented by aspirin. Aspirin increased prostacyclin in ePE (<0.05) without reducing thromboxane B, metabolite of thromboxane A, or 8-isoprostane-prostaglandin-2α, a marker of lipid peroxidation. There were no differences in cyclooxygenase levels in cerebral arteries between groups.
CONCLUSIONS
Low-dose aspirin in ePE reduced infarction that was associated with increased vasodilator prostacyclin and improved collateral perfusion during induced hypertension. The beneficial effect of aspirin on the brain and cerebral circulation is likely multifactorial and worth further study.
PubMed: 38934871
DOI: 10.1161/JAHA.124.035990 -
Polish Archives of Internal Medicine Jun 2024Medications are a common cause of acute kidney injury (AKI). There are various mechanisms that medications can induce AKI, and a better understanding of this...
Medications are a common cause of acute kidney injury (AKI). There are various mechanisms that medications can induce AKI, and a better understanding of this pathophysiology can aid in clinician recognition, treatment and prevention. Hemodynamic-mediated AKI is often associated with drugs that alter renal perfusion and its autoregulation. Acute tubular injury is the result of direct renal tubular cell toxicity. Acute interstitial nephritis is a T-cell mediated immune hypersensitivity reaction to drugs leading to tubule-interstitial inflammation and AKI. Crystalline nephropathy can be caused by medications themselves that crystalize or from the altered urinary chemistries caused by medications. Some medications can cause AKI through uncommon mechanisms such as glomerulonephritis and thrombotic microangiopathy. Notably, some medications may cause a phenomenon called "pseudo-AKI" where serum creatinine is elevated without a true reduction in kidney function. Commonly used medications in clinical practice are reviewed with the focus on mechanisms of injury, diagnosis, treatment, and prevention. Recognizing the common medications that are associated with AKI is an important first step in reducing the risk of AKI. For each medication, understanding general and specific risk factors for AKI allows for early identification and timely discontinuation of offending agents. These measures will help mitigate the risk of AKI and promote renal recovery.
PubMed: 38934852
DOI: 10.20452/pamw.16780 -
Panminerva Medica Jun 2024
Analysis of the short-term efficacy and impact on the quality of life of patients with bladder cancer after surgery treated with Shenhu soup empirical formula combined with bladder perfusion.
PubMed: 38934767
DOI: 10.23736/S0031-0808.24.05136-X