Unusual early peaks of airborne ragweed (Ambrosia L.) pollen in the Pannonian Biogeographical Region.

Early peaks of airborne ragweed (Ambrosia L.) pollen concentrations were observed at several monitoring stations in Hungary in June 2017 and 2018, one month before the usual start of the pollen season at the end of July. Backward trajectories were calculated to simulate potential sources of pollen collected at different locations in the Pannonian Biogeographical Region. In a collaboration between aerobiological and phenological networks, a nationwide campaign was conducted to collect field data of ragweed blooming. During field surveys, ragweed plants having extremely early blooming were found most abundantly in a rural site near Vaja (North-East Hungary) and other locations in Hungary. Field observations matched with source areas identified by trajectory analyses; i.e., early-flowering ragweed plants were found at some of these locations. Although similar peaks of airborne pollen concentrations were not detected in other years (e.g., 2016, 2019-2021), alarming results suggest the possibility of expanding seasons of ragweed allergy.

Para-atrial non-acute mediastinal hematoma after left atrial maze procedure mimicking tumor in a patient with treated melanoma.

INTRODUCTION: The Cox Maze III procedure is considered the gold standard open surgical procedure for management of atrial fibrillation. This article outlines a unique case of a para-atrial mediastinal hematoma following a bilateral thoracoscopic left atrial Maze procedure mimicking malignancy. REPORT: A 60-year-old male, with past history of melanoma, underwent bilateral thoracoscopic left atrial mini maze procedure with radiofrequency energy and exclusion of the left atrial appendage. Seven months later, a chest computed tomography (CT) scan was performed to evaluate for pulmonary embolism. The CT scan unexpectedly showed an ill-defined, heterogeneous para-atrial mass immediately superior to the left atrium concerning for tumor and mediastinal adenopathy. The mass was moderately hypermetabolic on subsequent 2-[fluorine-18]fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) scan. A follow-up PET/CT three months later demonstrated near-complete resolution of the para-atrial mass with minimal residual hematoma. CONCLUSION: Non-acute mediastinal hematoma following a maze procedure can potentially be confused with a tumor mass and/or lymphadenopathy on CT and FDG PET/CT. With knowledge of the potential for false-positive FDG uptake in a hematoma, the lesion was monitored, and unnecessary biopsy was avoided.

Diagnostic value of ocular melanoma immunoscintigraphy.

PURPOSE: To estimate the diagnostic value of ocular immunoscintigraphy (ISG) in the differentiation of melanoma from other ocular tumors or lesions. PATIENTS AND METHODS: ISG was performed in 27 patients. Twenty-four patients were suspected of having ocular melanoma and 3 patients had previous eye enucleation for melanoma and were without recurrent disease. Monoclonal antibody (MoAb) 225.28S was administered intravenously and the patient's head was imaged with gamma camera after 5 minutes and after 5 hours collecting 500.00 counts per image. RESULTS: The diagnosis of malignant melanoma was established by clinical examination in 12 patients (10 of them were subjected to enucleation and histopathological confirmation). ISG was positive in 10 out of 12 patients (sensitivity 83%). Two patients with operated melanoma had negative scintigraphic result. Fifteen patients with non melanoma lesions had negative findings except one patient with haemangioma who had positive ISG. The specificity of ISG was 93%. CONCLUSION: ISG is a sensitive and specific diagnostic method for ocular melanoma. The reliability of the results depends on proper acquisition of data and interpretation of images, including comparison of both eyes and early and late images with contrast enhancement.

Cellular energetics in the preconditioned state: protective role for phosphotransfer reactions captured by 18O-assisted 31P NMR.

Cell survival is critically dependent on the preservation of cellular bioenergetics. However, the metabolic mechanisms that confer resistance to injury are poorly understood. Phosphotransfer reactions integrate ATP-consuming with ATP-producing processes and could thereby contribute to the generation of a protective phenotype. Here, we used ischemic preconditioning to induce a stress-tolerant state and (18)O-assisted (31)P nuclear magnetic resonance spectroscopy to capture intracellular phosphotransfer dynamics. Preconditioning of isolated perfused hearts triggered a redistribution in phosphotransfer flux with significant increase in creatine kinase and glycolytic rates. High energy phosphoryl fluxes through creatine kinase, adenylate kinase, and glycolysis in preconditioned hearts correlated tightly with post-ischemic functional recovery. This was associated with enhanced metabolite exchange between subcellular compartments, manifested by augmented transfer of inorganic phosphate from cellular ATPases to mitochondrial ATP synthase. Preconditioning-induced energetic remodeling protected cellular ATP synthesis and ATP consumption, improving contractile performance following ischemia-reperfusion insult. Thus, the plasticity of phosphotransfer networks contributes to the effective functioning of the cellular energetic system, providing a mechanism for increased tolerance toward injury.

[Dynamic scintigraphy of the kidney using 99m-Tc-DTPA before and after extracorporeal shock wave lithotripsy]. / Dinamska scintigrafija bubrega pomocu 99m-Tc-DTPA pre i posle ESWL.

The results of dynamic scintigraphy of the kidneys using 99mTc-DTPA that is glomerular radiopharmaceutic in patients before and after ESWL (extracorporeal shock wave lithotripsy) are presented. Investigation was performed in 22 patients--in 8 patients immediately before ESWL, 7 days and 3 months later, and in 14 patients before and 7 days after ESWL. The time alteration of the achievement of the maximal values of radiorenographic curve obtained by dynamic scintigraphy (Tmax), as the alteration of separate clearance (SCI) counted as an integral below the other phase of renographic curve. No significant differences were observed in the values of separate clearance before and after ESWL, while Tmax was significantly reduced 3 months after ESWL (p < 0.05). Our results indicated the improvement of glomerular filtration of the kidneys 3 months after ESWL (faster passing of DTPA through the treated kidney).

Adenylate kinase phosphotransfer communicates cellular energetic signals to ATP-sensitive potassium channels.

Transduction of energetic signals into membrane electrical events governs vital cellular functions, ranging from hormone secretion and cytoprotection to appetite control and hair growth. Central to the regulation of such diverse cellular processes are the metabolism sensing ATP-sensitive K+ (K(ATP)) channels. However, the mechanism that communicates metabolic signals and integrates cellular energetics with K(ATP) channel-dependent membrane excitability remains elusive. Here, we identify that the response of K(ATP) channels to metabolic challenge is regulated by adenylate kinase phosphotransfer. Adenylate kinase associates with the K(ATP) channel complex, anchoring cellular phosphotransfer networks and facilitating delivery of mitochondrial signals to the membrane environment. Deletion of the adenylate kinase gene compromised nucleotide exchange at the channel site and impeded communication between mitochondria and K(ATP) channels, rendering cellular metabolic sensing defective. Assigning a signal processing role to adenylate kinase identifies a phosphorelay mechanism essential for efficient coupling of cellular energetics with K(ATP) channels and associated functions.

Compromised energetics in the adenylate kinase AK1 gene knockout heart under metabolic stress.

Rapid exchange of high energy carrying molecules between intracellular compartments is essential in sustaining cellular energetic homeostasis. Adenylate kinase (AK)-catalyzed transfer of adenine nucleotide beta- and gamma-phosphoryls has been implicated in intracellular energy communication and nucleotide metabolism. To demonstrate the significance of this reaction in cardiac energetics, phosphotransfer dynamics were determined by [(18)O]phosphoryl oxygen analysis using( 31)P NMR and mass spectrometry. In hearts with a null mutation of the AK1 gene, which encodes the major AK isoform, total AK activity and beta-phosphoryl transfer was reduced by 94% and 36%, respectively. This was associated with up-regulation of phosphoryl flux through remaining minor AK isoforms and the glycolytic phosphotransfer enzyme, 3-phosphoglycerate kinase. In the absence of metabolic stress, deletion of AK1 did not translate into gross abnormalities in nucleotide levels, gamma-ATP turnover rate or creatine kinase-catalyzed phosphotransfer. However, under hypoxia AK1-deficient hearts, compared with the wild type, had a blunted AK-catalyzed phosphotransfer response, lowered intracellular ATP levels, increased P(i)/ATP ratio, and suppressed generation of adenosine. Thus, although lack of AK1 phosphotransfer can be compensated in the absence of metabolic challenge, under hypoxia AK1-knockout hearts display compromised energetics and impaired cardioprotective signaling. This study, therefore, provides first direct evidence that AK1 is essential in maintaining myocardial energetic homeostasis, in particular under metabolic stress.

Reduced activity of enzymes coupling ATP-generating with ATP-consuming processes in the failing myocardium.

Coupling of ATP-generating with ATP-consuming processes is an essential component in the cardiac bioenergetics responsible for optimal myocardial function. Although a number of enzymatic systems have been implicated in securing proper intracellular energy communication, their integrative response in a failing myocardium has not been determined so far. Therefore, we measured catalytic activities of enzymes responsible for the communication between ATP-generating and ATP-consuming processes in ventricular samples obtained from normal dogs and dogs with tachycardia-induced heart failure. In the failing myocardium, phosphotransfer activities of creatine kinase, adenylate kinase, 3-phosphoglycerate kinase and pyruvate kinase, which collectively deliver ATP and remove ADP from myofibrillar ATPases, were depressed by 30, 21, 44 and 20%, respectively, when compared to normal controls. The activity of hexokinase, an enzyme which directs phosphoryls into the glycolytic phosphotransfer pathway, was unchanged. Also, the activity of glyceraldehyde-3-phosphate dehydrogenase, which may shuttle inorganic phosphate between ATPases and ATP-synthases, was not affected by heart failure. However, the CO2-hydration activity of carbonic anhydrase, which together with creatine kinase, is presumed responsible for removal of protons from ATPases, was diminished by 21%. As these enzymatic systems are collectively required for adequate delivery of high-energy phosphoryl to, and removal of end-products from, cellular ATPases, the cumulative deficit in their flux capacities may provide a bioenergetic basis for impaired contraction-relaxation in the failing heart.