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African swine fever virus genotype II was detected in wild boar in Spain in 2025 after >30 years of absence. Whole-genome sequencing and molecular follow-up of 8 representative cases identified a stable 9.8-kb deletion affecting the multigene family in the left variable region, defining an ASFV genotype II variant.
Tachycardia to 240 beats/min in anaesthetized dogs increases coronary blood flow while flow in the left ventricular wall remains homogeneous. An arteriovenous fistula causes subendocardial ischaemia at 120 beats/min but pacing to 180 to 210 beats/min increases subendocardial blood flow by increasing diastolic coronary driving pressure per minute.
The variability of left ventricular ejection fraction, normalized mean ejection rate and regional wall motion was evaluated from first pass quantitative radionuclide angiocardiograms obtained with a computerized multicrystal scintillation camera. Three radionuclide studies separated by an average of 4.3 days were obtained in each of 20 patients. Ejection fraction and ejection rate obtained on the first, second and third studies did not differ significantly. The mean (+/- standard deviation) variability of sequential ejection fraction measurement was 4.4 +/- 3.6 percent, and of sequential ejection rate was 0.56 +/- 0.47 sec(-1). Variations in measurements were not related to fluctuations in heart rate or blood pressure. Variability in ejection rate was significantly greater in patients with normal function than in those with abnormal function. Regional wall motion analysis was constant in 19 of 20 patients. Thus, sequential quantitative radionuclide angiocardiography allows reproducible serial assessment of left ventricular performance that can be performed with a low level of intrinsic variability.
The effect of beta-blockade by acebutolol on global and regional myocardial perfusion (133Xenon wash-out) was studied in 10 patients with coronary artery disease. Another group of 10 similar patients was used to study the effect of acebutolol on left ventricular cavity size (metal markers--spot film camera). Global perfusion responses roughly paralleled the changes in rate-pressure variable which decreased in 8 patients and increased in 2 who had spontaneous angina pectoris. Regional perfusion decreased more in areas distal to less than 75% stenoses than in those distal to less than 75% stenoses (29 vs 12%; p = 0.10 less than 0.20). Left ventricular asynergy did not modify the response, nor did the presence or absence of collateral vessels. No evidence was found to support the thesis that beta-blockade may evoke a redistribution in perfusion which favours the potentially ischaemic areas of myocardium. Left ventricular cavity size remained unchanged after acebutolol, a cardioselective beta-blocking compound with some degree of agonist activity.
A new method is described for determining localized epicardial shortening in regions newly perfused after saphenous vein bypass grafting. Four to six radiopaque markers are sutured to the ventricular epicardium in pairs, 2 cm apart and 0 to 3 cm distal to the coronary anastomosis. Shortening fraction and time to onset of shortening are reported in 56 patients examined noninvasively with use of cinefluorography 1 week to 6 months after operation. The right coronary bypass region showed the greatest improvement in shortening fraction in 6 months (from 10.1 to 16.7 percent); the left anterior descending region showed the least (but still significant) improvement (from 8.6 to 11.5 percent). Paradoxical systolic expansion occurred predominantly in the region of the left anterior descending coronary bypass (95 percent of all such occurrences). Measurement error, observer variability and beat to beat variability were less important than the physiologic changes in the postoperative period. This technique is a direct method providing heretofore unavailable follow-up information on localized shortening in newly perfused myocardium after coronary bypass grafting.
1 The radioactive microsphere method was used to study the effects of ergotamine (5, 10 and 20 mug/kg, i.v.) on systemic and regional haemodynamic variables in chloralose-urethane anaesthetized cats. The influence of the drug was also studied on the number of 15 mum microspheres escaping entrapment in the head to emerge in the left external jugular vein.2 Ergotamine decreased the heart rate and cardiac output. Since arterial blood pressure remained unchanged, calculated total peripheral resistance increased.3 The regional distribution of cardiac output obtained with 15 mum microspheres agreed well with previous studies in cats where 25 mum spheres were used. The most pronounced difference was that in the present investigation more microspheres, apparently escaping through arteriovenous anastomoses (AVAs), were detected in the lungs than when larger spheres had been used.4 Coronary blood flow decreased, while uterine blood flow was increased by the drug. The microsphere content of the lungs, which receive the spheres not only via bronchial arteries but also via AVAs, was greatly reduced by all doses of ergotamine. Ergotamine did not influence tissue blood flow to other major organs such as the brain, kidneys, skin, liver, skeletal muscle or the gastrointestinal tract.5 In the 16 experiments, 0.46 +/- 0.05 (s.e. mean)% of the total microspheres injected (equivalent to 11.7 +/- 1.4% of microspheres detected in the left-side of the head) appeared within 2 min of microsphere injection into the left external jugular vein. The highest dose of ergotamine significantly reduced the shunting of the microspheres in the head.6 Since 15 mum microspheres are only likely to reach the lungs by passing into the venous circulation through large glomus-type AVAs, we conclude that ergotamine reduces the fraction of microspheres appearing in the lungs by causing strong vasoconstriction in the AVAs in the head.7 In conformity with the closure of head AVAs is the finding that ergotamine reduced the jugular venous Po(2) and O(2) saturation thereby increasing the A-V O(2) saturation difference.8 It is quite possible that decreased A-V shunting may be the prominent mechanism of the antimigraine action of the drug, since sudden opening of AVA's has been implicated in the pathophysiology of migraine-syndrome.
Cardiovascular responses were noninvasively monitored as the legs of 16 supine human subjects were passively elevated to increase return of blood to the heart. Forearm vasodilation occurred promptly as previously observed by Roddie and Shepard (7). Arterial pressure and heart rate were unchanged. Ventricular performance, monitored by systolic-time-interval analysis, was enhanced after a delay of approximately 6 s, an effect which lasted throughout the 40-s leg-elevation period. All affected variables returned to control levels after the legs were lowered. This delayed response could result reflexly from stimulation of receptors in the left atrial region causing an increase in sympathetically mediated contractility or directly from the Frank-Starling mechanism in response to increased left ventricular filling.
BACKGROUND: Patients with posttraumatic stress disorder (PTSD) exhibit smaller regional brain volumes in commonly reported regions including the amygdala and hippocampus, regions associated with fear and memory processing. In the current study, we have conducted a voxel-based morphometry (VBM) meta-analysis using whole-brain statistical maps with neuroimaging data from the ENIGMA-PGC PTSD working group. METHODS: T1-weighted structural neuroimaging scans from 36 cohorts (PTSD n = 1309; controls n = 2198) were processed using a standardized VBM pipeline (ENIGMA-VBM tool). We meta-analyzed the resulting statistical maps for voxel-wise differences in gray matter (GM) and white matter (WM) volumes between PTSD patients and controls, performed subgroup analyses considering the trauma exposure of the controls, and examined associations between regional brain volumes and clinical variables including PTSD (CAPS-4/5, PCL-5) and depression severity (BDI-II, PHQ-9). RESULTS: PTSD patients exhibited smaller GM volumes across the frontal and temporal lobes, and cerebellum, with the most significant effect in the left cerebellum (Hedges' g = 0.22, pcorrected = .001), and smaller cerebellar WM volume (peak Hedges' g = 0.14, pcorrected = .008). We observed similar regional differences when comparing patients to trauma-exposed controls, suggesting these structural abnormalities may be specific to PTSD. Regression analyses revealed PTSD severity was negatively associated with GM volumes within the cerebellum (p corrected  = .003), while depression severity was negatively associated with GM volumes within the cerebellum and superior frontal gyrus in patients (p corrected  = .001). CONCLUSIONS: PTSD patients exhibited widespread, regional differences in brain volumes where greater regional deficits appeared to reflect more severe symptoms. Our findings add to the growing literature implicating the cerebellum in PTSD psychopathology.
The reliability of myocardial perfusion scintigrams with thallium-201 (201Tl) for detecting areas of hypoperfusion was assessed in 16 closed-chest dogs. Variable areas of ischemia were produced either by occluding or stenosing the left anterior descending coronary artery. Cardiac scintigrams taken in four projections were compared with regional myocardial perfusion maps. Segmental concentrations and segmental perfusions were quantitated by counting the emissions from 201Tl and the microspheres in each of 96 segments of the left ventricle. In addition, studies with a phantom were performed. The results indicate: 1) The emissions from 201Tl and from microspheres correlated well in ischemic segments (r = 0.93 +/- SE 0.02). 2) Seven of twelve ischemic hearts had definitely abnormal scintigrams and in each of these the hypoperfused zone was greater than 4.9 grams and perfusion was decreased by more than 45%. 3) In the phantom, abnormal scintigrams could be detected in the presence of lesser deficits than in the dogs. The limitation of the thallium perfusion scintigrams will be the inconsistent detection of small perfusion deficits.
Utilizing semiselective 133Xenon injections and gamma camera recording, global and regional left ventricular myocardial perfusion were recorded under the influence of beta-blockade by metoprolol in 9 patients with angiographically proven coronary artery disease. Metoprolol reduced the rate--pressure variable in every patient, the mean reduction amounting to 24% (P less than 0.01). With one exception, the global left ventricular myocardial flow followed the change in the rate-pressure variable. No significant differences were detected in the flow responses of areas distal to only moderate coronary obstructions (less than 75%) and areas distal to significant (less than 75%) obstructions. The same was true when areas of asynergic contractions were compared with areas of normal contractions, or when areas supplied by collaterals were compared with areas devoid of collateral vessels. It is concluded that the reduction in myocardial flow after metoprolol is due to the reduction of the myocardial oxygen consumption, and no redistribution of flow occurs.
The ability of left ventricular angiography to detect regional ischemic dysfunction was assessed in 10 closed-chest dogs during the course of acute balloon occlusion of the anterior descending coronary artery. During the 2-minute period of occlusion, serial cineangiography revealed a sequence of wall motion abnormalities over the anteroapical region almost identical to that observed using directly implanted gauges. This sequence consisted of progressive reduction in regional systolic shortening with eventual replacement by systolic expansion. These changes preceded both electrocardiographic ST-segment and hemodynamic alterations, and were readily observed by gross subjective inspection of the cineangiograms, but with an intraobserver variability of 22%. Frame-by-frame motional analysis of the ventricular perimeter relative to its centroid of mass allowed more precise characterization of regional dysfunction. These data are consistent with previous studies demonstrating that regional wall motion abnormalities are both sensitive and specific markers of acute ischemia, and support the use of computerized left ventricular angiography for the quantitative assessment of clinical ischemic dysfunction.
Blocking and activation of constant focal EEG abnormalities by opening and closing the eyes were assessed by visual analysis in 173 EEG recordings of 173 patients. Correlations between single variable were weak in general and did not gain statistical significance in any case. The blocking response had similar extent on both hemispheres. There was no sign of direct dependence from extra- or intracerebral localisation of the causal process. However, the biplot method of computing the results discovered several constellations of variables responsible for blocking and activation. Two of them are reported here. 1) Both responses were more prominent at frontal than at occipital areas. 2) A prodominant slowing localized in mainly frontal regions on the left hemisphere and caused by a process extending from extracerebral or cortical to subcortical showed the greatest tendency to be blocked by opening the eyes while the cause of the focus had no influence.
Oxygen saturation of small arteries and veins (20-500 micron) was determined microspectrophotometrically in the hearts of 12 pentobarbital-anesthetized open-chest dogs. Hearts were removed, quick frozen in liquid propane, and O2 saturation was determined in blood vessels on a regional basis between and within ventricular walls. No significant differences existed in arterial O2 saturation between right, left, and septal walls or regionally within any wall by depth or in base-to-apex comparisons. Although there was variation in arterial saturation, it was independent of vessel size. Arteries were followed by serial section into the left ventricular wall for distances up to 7.5 mm without significant saturation change. The average venous saturations of the right, septal, and left ventricular walls were not significantly different. No regional differences in venous saturation were found within any ventricular wall in comparisons between base and apex. In the left ventricle, subepicardial venous saturation (29.8%) was significantly higher than subendocardial saturation (16.4%). In veins traced from the surface, saturation decreased with depth. Greater variability of saturation was found in small compared to large veins. The greater O2 extraction in the subendocardium may indicate a higher O2 consumption than in the subepicardium.
Post-COVID-19 sequelae have become an emerging global health issue, but the mechanisms for the sustained susceptibility of convalescents to the sequelae remain poorly understood. Here we report the use of a restricted open-search approach to explore the molecular imprints of SARS-CoV-2 infection left on the proteome of 412 COVID-19 patients and convalescences. A total of 827 non-standard amino acid variations, chemically modified residues as well as post-translational modifications, termed non-coded amino acids (ncAAs), are found spreading over 29,814 sites in patient's serum proteins. Markedly, widespread ncAAs are induced and sustainedly imprinted on the serum proteome predominately perturbing the immunoglobulin-mediated immune response, complement activation and coagulation regulation even 12 months after recovery. Sustained amino acid variations and chemical modifications are found in the complementary‑determining regions (CDRs) of the variable region of immunoglobulin contributing to the interactions between the emerging antibody and antigens; durable chemical amino acid modifications found in the hyper ncAA-modified regions of the constant region of immunoglobulin important for the interaction with the complement and regulatory receptors. In the complement system, inducible ncAAs are memorized in the components essential for the complement activation, amplification cascades and membrane attack processes. Thus, the workflow described in this study can be used to identify the molecular imprints of viral infection at the proteomic scale, particularly the specific antibodies and the immune targets left in COVID-19 patients and convalescents.
By means of an autoradiographic technique employing 14C-2-deoxyglucose, abnormalities of local brain glucose utilization were studied 90 minutes following occlusion of the left middle cerebral and common carotid arteries in a series of pentobarbital-anesthetized cats. Sham-insulted control animals exhibited a normal pattern of regional glucose utilization. In animals with vascular occlusion, a zone of greatly suppressed glucose utilization occupied the caudate nucleus of the ischemic hemisphere, with variable extension, and was surrounded by a narrow rim of increased local brain glucose utilization, suggesting the occurrence of enhanced anaerobic glycolysis in the latter zones. The cerebral cortex, which was less constantly affected, showed alternating regions of increased and decreased glucose utilization. Quantitation of local brain glucose utilization values from the contralateral nonischemic hemisphere revealed a mild suppression of cortical glucose utilization relative to the control animals. This may be the metabolic equivalent of diaschisis.
Choline acetyltransferase (CAT) catalyzes the biosynthesis of acetylcholine according to the chemical equation: Acetyl-CoA + Choline in equilibrium Acetylcholine + CoA. To demonstrate the neuronal relationship of this enzyme, CAT activity was measured in hearts to which the extrinsic innervation was completely interrupted by extirpation of the heart from a donor animal and transplantation in a heterotopic position into the recipient's abdominal cavity. After the animals were killed at 8 days, enzyme activity in the transplanted hearts was measured and compared with that of the recipient. Choline acetyltransferase activity decreased 98% in the right atrium of the transplanted denervated hearts, 94% in the SA node, 87% in the left atrium, 80% in the right ventricle, and about 50% in the interventricular septum and left ventricle. These data show that sectioning the extrinsic parasympathetic innervation to the heart results in variable decreases in CAT activity, a finding which confirms that CAT activity is related to the extrinsic cholinergic innervation. The extrinsic (preganglionic) component of the parasympathetic system is nonuniform and supplies predominantly the specialized regions of the heart with conduction tissue. The residual enzyme activity is related to intrinsic (postganglionic) parasympathetic neurons. The intrinsic component is uniformly distributed to both specialized and contractile regions of the heart.
Genetic variation within species shapes phenotypes, but identifying the specific genes and variants that cause phenotypic differences is costly and challenging. Here, we introduce CRI-SPA-Map, a genetic mapping strategy combining CRISPR-Cas9 genome engineering, selective ploidy ablation (SPA), and high-throughput phenotyping for precise genetic mapping with or without genotyping in the yeast Saccharomyces cerevisiae. In CRI-SPA-Map, a donor strain carrying SPA machinery is mated to a genetically different recipient strain harboring a genome-integrated selectable cassette. In the resulting diploid, CRISPR-Cas9 cuts the cassette for replacement with DNA from the homologous donor chromosome. Donor chromosomes are then removed using SPA to yield haploid recombinant strains. To establish CRI-SPA-Map, we mated a W303 SPA strain to 92 strains from the BY4742 yeast knockout collection that carry gene deletion cassettes on the left arm of chromosome XIV and created 1,451 recombinant isolates. Whole-genome sequencing verified that deletion cassette replacement introduced short donor DNA tracts of variable length, resulting in a finely recombined mapping population. Using only the known location of the gene deletions, which marks where donor DNA is introduced, we identified a 6.5 kb-region shaping yeast growth. Further dissection of this region pinpointed two causal variants in two genes, MKT1 and SAL1. Engineering these variants alone and in combination revealed gene-by-environment interactions at both genes, as well as epistatic interactions between them that were in turn dependent on the environment. CRI-SPA-Map is a cost-effective strategy for creating high-resolution recombinant panels of yeast strains for identifying the genetic basis of phenotypic variation.
The temporal evolution of myocardial ischemia was studied in open chest dogs at constant preload, afterload and heart rate. In one group of animals, a variable circumflex arterial stenosis was used to maintain constant distal circumflex arterial hypotension (40 to 50 mm Hg). During a 3 hour period of stenosis, flow in the subendocardial fourth of the ischemic ventricular wall decreased from 0.22 to 0.09 ml/g per min (P less than 0.02), whereas subepicardial flow was not significantly changed. Local vascular resistance, therefore, doubled in the most ischemic area of myocardium. In a second group of animals in which proximal coronary stenosis was held constant and pressure varied, an ischemia-mediated increase in local vascular resistance was also demonstrated. In addition, a reciprocal relation was observed between changes in flow in the left anterior descending coronary region and changes in collateral flow to the region of the circumflex artery. A coronary steal mechanism and an ischemia-mediated resistance increase may be two means by which ischemia is self-propagating.