Monostotic fibrous dysplasia of a lumbar vertebral body with secondary aneurysmal bone cyst formation: a case report

We report the case of a 25-year-old Caucasian woman with symptomatic monostotic fibrous dysplasia of the fourth lumbar vertebral body. The patient suffered from a five-week history of progressive low back pain, radiating continuously to the left leg. Her medical history and physical and neurological examination did not demonstrate any significant abnormalities. Radiographs, computed tomography and magnetic resonance imaging revealed an osteolytic expansive lesion with a cystic component of the fourth lumbar vertebral body. Percutaneous transpedicular biopsy showed histological characteristics of fibrous dysplasia superimposed by the formation of aneurysmal bone cyst components. The patient was treated by subtotal vertebrectomy of the L4 vertebral body with anterior reconstruction and her postoperative course was uncomplicated. To our knowledge, this is the first reported case of a monostotic fibrous dysplasia with superimposed secondary aneurysmal bone cysts of a lumbar vertebral body

Body mass index is associated with microvascular endothelial dysfunction in patients with treated metabolic risk factors and suspected coronary artery disease

Background--Obesity is key feature of the metabolic syndrome and is associated with high cardiovascular morbidity and mortality. Obesity is associated with macrovascular endothelial dysfunction, a determinant of outcome in patients with coronary artery disease. Here, we compared the influence of obesity on microvascular endothelial function to that of established cardiovascular risk factors such as diabetes mellitus, hypertension, hypercholesterolemia, and smoking in patients with suspected coronary artery disease. Methods and Results--Endothelial function was assessed during postocclusive reactive hyperemia of the brachial artery and downstream microvascular beds in 108 patients who were scheduled for coronary angiography. In all patients, microvascular vasodilation was assessed using peripheral arterial tonometry; laser Doppler flowmetry and digital thermal monitoring were performed. Body mass index was significantly associated with decreased endothelium-dependent vasodilatation measured with peripheral arterial tonometry (r=0.23, P=0.02), laser Doppler flowmetry (r=0.30, P < 0.01), and digital thermal monitoring (r=0.30, P < 0.01). In contrast, hypertension, hypercholesterolemia, and smoking had no influence on microvascular vasodilatation. Especially in diabetic patients, endothelial function was not significantly reduced (control versus diabetes mellitus, mean±SEM or median [interquartile range], peripheral arterial tonometry: 1.90±0.20 versus 1.67±0.20, P=0.19, laser Doppler flowmetry: 728% [interquartile range, 427-1110] v

Decay Constants and Semileptonic Decays of Heavy Mesons in Relativistic Quark Model

We investigate the $B$ and $D$ mesons in the relativistic quark model by applying the variational method with the Gaussian wave function. We calculate the Fermi momentum parameter $p_{_F}$, and obtain $p_{_F} = 0.50 \sim 0.54$ GeV, which is almost independent of the input parameters, $\alpha_s$, $m_b$, $m_c$ and $m_{sp}$. We then calculate the ratio $f_B$/$f_D$, and obtain the result which is larger, by the factor of about 1.3, than $\sqrt{M_D / M_B}$ given by the naive nonrelativistic analogy. This result is in a good agreement with the recent Lattice calculations. We also calculate the ratio $(M_{B^*}-M_{B})$/$(M_{D^*}-M_{D})$. In these calculations the wave function at origin $\psi (0)$ is essential. We also determine $p_{_F}$ by comparing the theoretical prediction of the ACCMM model with the lepton energy spectrum of $B \rightarrow e \nu X$ from the recent ARGUS analysis, and find that $p_{_F}=0.27~\pm~^{0.22}_{0.27}$ GeV, when we use $m_c=1.5$ GeV. However, this experimentally determined value of $p_{_F}$ is strongly dependent on the value of input parameter $m_c$.Comment: 15 pages (Latex) (uses epsfig.sty, 1 figure appended as a uuencoded compressed ps-file

Short-term exercise-induced protection of cardiovascular function and health: why and how fast does the heart benefit from exercise?

Abstract: Regular exercise training has potent and powerful protective effects against the development of cardiovascular disease. These cardioprotective effects of regular exercise training are partly explained through the effects of exercise on traditional cardiovascular risk factors and improvement in cardiac and vascular health, which take several weeks to months to develop. This review focuses on the observation that single bouts of exercise may also possess an underrecognized, clinically useful form of immediate cardioprotection. Studies, performed in both animals and humans, demonstrate that single or short-term exercise-induced protection (SEP) attenuates the magnitude of cardiac and/or vascular damage in response to prolonged ischaemia and reperfusion injury. This review highlights preclinical evidence supporting the hypothesis that SEP activates multiple pathways to confer immediate protection against ischaemic events, reduce the severity of potentially lethal ischaemic myocardial injury, and therefore act as a physiological first line of defence against injury. Given the fact that the extent of SEP could be modulated by exercise-related and subject-related factors, it is important to recognize and consider these factors to optimize future clinical implications of SEP. This review also summarizes potential effector signalling pathways (i.e. communication between exercising muscles to vascular/cardiac tissue) and intracellular pathways (i.e. reducing tissue damage) that ultimately confer protection against cardiac and vascular injury. Finally, we discuss potential future directions for designing adequate human and animal studies that will support developing effective SEP strategies for the (multi-)diseased and aged individual

Isoscalar resonances with J^{PC}=1^{--} in e^+e^-annihilation

The analysis of the vector isoscalar excitations in the energy range between 1 and 2 GeV of the $e^+e^-$ annihilation is presented for the final states $\pi^+\pi^-\pi^0$, $\omega\pi^+\pi^-$, $K^+K^-$, $K^0_SK^\pm\pi^\mp$ and $K^{\ast0}K^-\pi^++ c.c$. The effects of both the resonance mixing and the successive opening of multiparticle channels, with the energy dependent partial widths, are taken into account. The work extends our previous analysis hep-ph/9609216 of the vector isovector excitations and is aimed to compare the existing data with the predictions of the $q\bar q$ model. It is shown that this hypothesis does not contradict the data.Comment: 16 pages, revtex, 6 ps figures. Clarifying remarks, a table, and references are added. Accepted in Phys. Rev.

The decay constants of pseudoscalar mesons in a relativistic quark model

The decay constants of pseudoscalar mesons are calculated in a relativistic quark model which assumes that mesons are made of a valence quark antiquark pair and of an effective vacuum like component. The results are given in terms of quark masses and of some free parameters entering the expression of the internal wave functions of the mesons. By using the pion and kaon decay constants $F_{\pi^+}=130.7~MeV,~F_{K^+}=159.8~MeV$ to fix the parameters of the model one gets $60~MeV\leq F_{D^+}\leq 185~MeV,~95~MeV\leq F_{D_s}\leq230~MeV,~80~MeV\leq F_{B^+}\leq205~MeV$ for the light quark masses $m_u=5.1~MeV,~m_d=9.3~MeV,~m_s=175~MeV$ and the heavy quark masses in the range: $1.~GeV\leq m_c\leq1.6~GeV,~4.1~GeV\leq m_b\leq4.5~GeV$. In the case of light neutral mesons one obtains with the same set of parameters $F_{\pi^0}\approx 138~MeV,~F_\eta\approx~130~MeV,F_{\eta'} \approx~78~MeV$. The values are in agreement with the experimental data and other theoretical results.Comment: 11 pages, LaTe

A Brief Etymology of the Collateral Circulation

It is well known that the protective capacity of the collateral circulation falls short in many individuals with ischemic disease of the heart, brain and lower extremities. In the past fifteen years, opportunities created by molecular and genetic tools, together with disappointing outcomes in many “angiogenic” trials, has led to a significant increase in the number of studies that focus on: 1) understanding the basic biology of the collateral circulation; 2) identifying the mechanisms that limit the collateral circulation’s capacity in many individuals; 3) devising methods to measure collateral extent, which has been found to vary widely among individuals; and 4) developing treatments to increase collateral blood flow in obstructive disease. Unfortunately, accompanying this increase in reports has been a proliferation of vague terms used to describe the disposition and behavior of this unique circulation, as well as the increasing miss-use of well-ensconced ones by new (and old) students of the collateral circulation. With this in mind, we provide a brief glossary of readily understandable terms to denote the formation, adaptive growth, and mal-adaptive rarefaction of the collateral circulation. We also propose terminology for several newly discovered processes that occur in the collateral circulation. Finally, we include terms used to describe vessels that are sometimes confused with collaterals, as well as terms describing processes active in the general arterial-venous circulation when ischemic conditions engage the collateral circulation. We hope this brief review will help unify the terminology used in collateral research

IMproving Preclinical Assessment of Cardioprotective Therapies (IMPACT) criteria : guidelines of the EU-CARDIOPROTECTION COST Action

Full list of the EU-CARDIOPROTECTION COST Action CA16225 Working group members is provided at the end of the article in Acknowledgements section. Funding Information: This article is based on the work from COST Action EU-CARDIOPROTECTION CA16225 supported by COST (European Cooperation in Science and Technology). DJH is supported by the Duke-National University Singapore Medical School, Singapore Ministry of Health’s National Medical Research Council under its Clinician Scientist-Senior Investigator scheme (NMRC/CSA-SI/0011/2017) and Collaborative Centre Grant scheme (NMRC/CGAug16C006). SL is supported by grants from the South African Department of Science and Technology and the South African National Research Foundation. SMD is supported by grants from the British Heart Foundation (PG/19/51/34493 and PG/16/85/32471). GH is supported by the German Research Foundation (SFB 1116 B8). MRM is supported by the Spanish Institute of Health Carlos III (FIS PI19/01196 and CIBER-CV). RS is supported by Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [Project number 268555672—SFB 1213, Project B05]. PF is supported by the National Research, Development and Innovation Office of Hungary (Research Excellence Program—TKP, National Heart Program NVKP 16-1-2016-0017) and by the Higher Education Institutional Excellence Program of the Ministry of Human Capacities in Hungary, within the framework of the Therapeutic Development thematic program of the Semmelweis University. Funding Information: The IMPACT criteria were presented for approval to the Management Committee of the EU-CARDIOPROTECTION COST Action CA16225: Pavle Adamovski, Ioanna Andreadou, Saime Batirel, Monika Bartekov?, Luc Bertrand, Christophe Beauloye, David Biedermann, Vilmante Borutaite, Hans Erik Botker, Stefan Chlopicki, Maija Dambrova, Sean Davidson, Yvan Devaux, Fabio Di Lisa, Dragan Djuric, David Erlinge, Ines Falcao-Pires, P?ter Ferdinandy, Eleftheria Galatou, Alfonso Garcia-Sosa, Henrique Girao, Zoltan Giricz, Mariann Gyongyosi, Derek J Hausenloy, Donagh Healy, Gerd Heusch, Vladimir Jakovljevic, Jelena Jovanic, George Kararigas, Risto Kerkal, Frantisek Kolar, Brenda Kwak, Przemys?aw Leszek, Edgars Liepinsh , Jacob Lonborg, Sarah Longnus, Jasna Marinovic, Danina Mirela Muntean, Lana Nezic, Michel Ovize, Pasquale Pagliaro, Clarissa Pedrosa Da Costa Gomes, John Pernow, Andreas Persidis, S?ren Erik Pischke, Bruno Podesser, Ines Poto?njak, Fabrice Prunier, Tanya Ravingerova, Marisol Ruiz-Meana, Alina Serban, Katrine Slagsvold, Rainer Schulz, Niels van Royen, Belma Turan, Marko Vendelin, Stewart Walsh, Nace Zidar, Coert Zuurbier, Derek Yellon. Publisher Copyright: © 2021, The Author(s).Acute myocardial infarction (AMI) and the heart failure (HF) which may follow are among the leading causes of death and disability worldwide. As such, new therapeutic interventions are still needed to protect the heart against acute ischemia/reperfusion injury to reduce myocardial infarct size and prevent the onset of HF in patients presenting with AMI. However, the clinical translation of cardioprotective interventions that have proven to be beneficial in preclinical animal studies, has been challenging. One likely major reason for this failure to translate cardioprotection into patient benefit is the lack of rigorous and systematic in vivo preclinical assessment of the efficacy of promising cardioprotective interventions prior to their clinical evaluation. To address this, we propose an in vivo set of step-by-step criteria for IMproving Preclinical Assessment of Cardioprotective Therapies (‘IMPACT’), for investigators to consider adopting before embarking on clinical studies, the aim of which is to improve the likelihood of translating novel cardioprotective interventions into the clinical setting for patient benefit.publishersversionPeer reviewe