21 research outputs found
A Case of Meningococcal and HSV-2 Meningitis in a Patient Being Treated with Ustekinumab for Pityriasis Rubra Pilaris
Pityriasis rubra pilaris (PRP) is a rare chronic inflammatory papulosquamous dermatosis affecting both adults and children. Six subtypes of PRP have been described. Recently, the management of PRP with biologic immunosuppressive agents regularly used in psoriasis has been supported by several case reports and series. Ustekinumab is an anti-IL12/23 IgG1 kappa human monoclonal antibody. It has been approved for the treatment of Crohn’s disease, plaque psoriasis, psoriatic arthritis and ulcerative colitis. It has also been reported to be effective as an off-label treatment for PRP. Current data are equivocal regarding infectious disease risk with ustekinumab administration. We describe a case of meningococcal and HSV-2 infection of the central nervous system in a patient being treated with ustekinumab for PRP
Bilateral rectus femoris intramuscular haematoma following simultaneous quadriceps strain in an athlete: a case report
<p>Abstract</p> <p>Introduction</p> <p>Bilateral rectus femoris haematoma following a simultaneous strain of the quadriceps muscles is a very rare condition.</p> <p>Case presentation</p> <p>We report the case of a 21-year-old Greek Caucasian female rowing athlete who was injured on both thighs. She complained of pain and inability to walk. Physical examination revealed tenderness over the thighs and restriction of knee movement. The result of a roentgenogram was normal, and there was no evidence of fracture or patella displacement. Magnetic resonance imaging revealed haematoma formation in both the rectus femoris muscles. The diameters of the left and right haematomas within the muscles were 6 cm and 5 cm, respectively. Therapeutic approaches included compression bandages, ice application, rest, elevation, and administration of muscle relaxant drugs. Active stretching and isometric exercises were performed after three days. The patient was able to walk using crutches two days after the initiation of treatment. On the seventh day, she had regained her full ability to walk without crutches. Non-steroidal anti-inflammatory drugs were administered on the fifth day and continued for one week. Six weeks later, she had pain-free function and the result of magnetic resonance imaging was normal. She was able to resume her training programme and two weeks later, she returned to her previous sport activities and competitions.</p> <p>Conclusion</p> <p>There are references in the literature regarding the occurrence of unilateral quadriceps haematomas following strain and bilateral quadriceps tendon rupture in athletes. Simultaneous bilateral rectus femoris haematomas after a muscle strain is a rare condition. It must be diagnosed early. The three phases of treatment are rest, knee mobilization, and restoration of quadriceps function.</p
Comparison of primary health care services between urban and rural settings after the introduction of the first urban health centre in Vyronas, Greece
Extremely high-risk patients with acute coronary syndrome: how “extreme” should be the lipid-lowering therapy if the LDL-C target
Divalent Metal Vinylphosphonate Layered Materials: Compositional Variability, Structural Peculiarities, Dehydration Behavior, and Photoluminescent Properties
A family of M-VP (M = Ni, Co, Cd, Mn, Zn, Fe, Cu, Pb; VP = vinylphosphonate) and M-PVP (M = Co, Cd; PVP = phenylvinylphosphonate) materials have been synthesized by hydrothermal methods and characterized by FTIR, elemental analysis, and thermogravimetric analysis (TGA). Their structures were determined either by single crystal X-ray crystallography or from laboratory X-ray powder diffraction data. The crystal structure of some M-VP and M-PVP materials is two-dimensional (2D) layered, with the organic groups (vinyl or phenylvinyl) protruding into the interlamellar space. However, the Pb-VP and Cu-VP materials show dramatically different structural features. The porous, three-dimensional (3D) structure of Pb-VP contains the Pb center in a pentagonal pyramid. A Cu-VP variant of the common 2D layered structure shows a very peculiar structure. The structure of the material is 2D with the layers based upon three crystallographically distinct Cu atoms; an octahedrally coordinated Cu2+ atom, a square planar Cu2+ atom and a Cu+ atom. The latter has an unusual co-ordination environment as it is 3-coordinated to two oxygen atoms with the third bond across the double bond of the vinyl group. Metal-coordinated water loss was studied by TGA and thermodiffractometry. The rehydration of the anhydrous phases to give the initial phase takes place rapidly for Cd-PVP but it takes several days for Co-PVP. The M-VP materials exhibit variable dehydration-rehydration behavior, with most of them losing crystallinity during the process.Proyecto nacional MAT2010-15175 (MICINN, España
Molecular changes indicative of cartilage degeneration and osteoarthritis development in patients with anterior cruciate ligament injury
Physical Improvement and Biological Maturity of Young Athletes (11-12 Years) with Systematic Training
AIM: The aim of this study was to investigate the infl uence of systematic training in physical growth and biological maturity in prepubertal males and estimate how this affects the physical growth and skeletal maturity. MATERIALS AND METHODS: 177 primary school students of the fifth and sixth grade, from schools in Alexandroupolis, participated voluntarily in our study. Questionnaires were used in order to measure physical activity levels. The subjects were subdivided into two groups; control group (prepubertal, whose physical activity was the physical education of their school and which had never participated in systematic training, n = 95) and experimental group (prepubertal, whose weekly physical activity included physical education in their schools and additionally 3-4 training units organized training in various sports clubs in the city, n = 82). The following parameters were recorded: biological age measured by determination of skeletal age; bone density measured by ultrasound methods; anthropometric and morphological features such as height, body composition, selected diameters, circumferences and skinfolds; motor ability features. RESULTS: The experimental group exhibited older biological age (p = 0.033), higher bone density (p < 0.001), lower BMI and body fat (p < 0.001), better anthropometric features and higher performance throughout all motor ability tests (p < 0.05), compared to the control group. CONCLUSION: The present study demonstrates that systematic physical activity has a positive effect on both the physical and biological maturity of pre-pubertal children. This effect is mainly expressed in bone strengthening as a result of the increased bone density and in improvement of the kinetic skills of pupils who participated in organized extracurricular sport-activities
Molecular Insights in Atrial Fibrillation Pathogenesis and Therapeutics: A Narrative Review
The prevalence of atrial fibrillation (AF) is bound to increase globally in the following years, affecting the quality of life of millions of people, increasing mortality and morbidity, and beleaguering health care systems. Increasingly effective therapeutic options against AF are the constantly evolving electroanatomic substrate mapping systems of the left atrium (LA) and ablation catheter technologies. Yet, a prerequisite for better long-term success rates is the understanding of AF pathogenesis and maintenance. LA electrical and anatomical remodeling remains in the epicenter of current research for novel diagnostic and treatment modalities. On a molecular level, electrical remodeling lies on impaired calcium handling, enhanced inwardly rectifying potassium currents, and gap junction perturbations. In addition, a wide array of profibrotic stimuli activates fibroblast to an increased extracellular matrix turnover via various intermediaries. Concomitant dysregulation of the autonomic nervous system and the humoral function of increased epicardial adipose tissue (EAT) are established mediators in the pathophysiology of AF. Local atrial lymphomononuclear cells infiltrate and increased inflammasome activity accelerate and perpetuate arrhythmia substrate. Finally, impaired intracellular protein metabolism, excessive oxidative stress, and mitochondrial dysfunction deplete atrial cardiomyocyte ATP and promote arrhythmogenesis. These overlapping cellular and molecular alterations hinder us from distinguishing the cause from the effect in AF pathogenesis. Yet, a plethora of therapeutic modalities target these molecular perturbations and hold promise in combating the AF burden. Namely, atrial selective ion channel inhibitors, AF gene therapy, anti-fibrotic agents, AF drug repurposing, immunomodulators, and indirect cardiac neuromodulation are discussed here
Molecular Insights in Atrial Fibrillation Pathogenesis and Therapeutics: A Narrative Review
The prevalence of atrial fibrillation (AF) is bound to increase globally
in the following years, affecting the quality of life of millions of
people, increasing mortality and morbidity, and beleaguering health care
systems. Increasingly effective therapeutic options against AF are the
constantly evolving electroanatomic substrate mapping systems of the
left atrium (LA) and ablation catheter technologies. Yet, a prerequisite
for better long-term success rates is the understanding of AF
pathogenesis and maintenance. LA electrical and anatomical remodeling
remains in the epicenter of current research for novel diagnostic and
treatment modalities. On a molecular level, electrical remodeling lies
on impaired calcium handling, enhanced inwardly rectifying potassium
currents, and gap junction perturbations. In addition, a wide array of
profibrotic stimuli activates fibroblast to an increased extracellular
matrix turnover via various intermediaries. Concomitant dysregulation of
the autonomic nervous system and the humoral function of increased
epicardial adipose tissue (EAT) are established mediators in the
pathophysiology of AF. Local atrial lymphomononuclear cells infiltrate
and increased inflammasome activity accelerate and perpetuate arrhythmia
substrate. Finally, impaired intracellular protein metabolism, excessive
oxidative stress, and mitochondrial dysfunction deplete atrial
cardiomyocyte ATP and promote arrhythmogenesis. These overlapping
cellular and molecular alterations hinder us from distinguishing the
cause from the effect in AF pathogenesis. Yet, a plethora of therapeutic
modalities target these molecular perturbations and hold promise in
combating the AF burden. Namely, atrial selective ion channel
inhibitors, AF gene therapy, anti-fibrotic agents, AF drug repurposing,
immunomodulators, and indirect cardiac neuromodulation are discussed
here