Nearly full‐length genome characterization of canine parvovirus strains circulating in Nigeria

Canine parvovirus type 2 (CPV‐2) emerged suddenly in the late 1970s as pathogen of dogs, causing a severe and often fatal gastroenteric disease. The original CPV‐2 was replaced by three antigenic variants, CPV‐2a, CPV‐2b and CPV‐2c, which to date have gained a worldwide distribution with different relative proportions. All previous studies conducted in Africa were based on partial VP2 gene sequences. The aim of this study was to provide a genome analysis to characterize the CPV strains collected in Nigeria, Africa. Rectal swab samples (n = 320) were collected in 2018 and tested by means of an immunochromatographic assay. Among the 144 positive samples, 59 were selected for further analyses using different molecular assays. The results revealed a high prevalence of CPV‐2c (91.5%) compared to the CPV‐2a variant (8.5%). The VP2 gene sequences showed a divergence from the strains analysed in 2010 in Nigeria and a closer connection with CPV strains of Asian origin. The non‐structural gene analysis evidenced amino acid changes never previously reported. The molecular analysis based on genomic sequences evidenced a geographical pattern of distribution of the analysed strains, suggesting a potential common evolutionary origin with CPV of Asian origin. This study represents the first CPV molecular characterization including all the encoding gene sequences conducted in the African continent and contributes to define the current geographical spread of the CPV variants worldwide.     

A post-streptococcal pathogenesis in children with tic disorders is suggested by a color Doppler echocardiographic study.

BACKGROUND: A post-streptococcal autoimmune mechanism, similar to that of rheumatic fever or Sydenham's chorea, has been hypothesized in some cases of neuropsychiatric disorder (tics and/or obsessive-compulsive disorders). A few studies on the involvement of other organs, outside the central nervous system, have been performed in these patients. AIM: To evaluate a possible post-streptococcal pathogenesis in the children affected by tic disorders and showing sign of streptococcal exposure. METHODS: A case-control study was performed at the Outpatient Division of the Child Neurology and Psychiatry, and Paediatrics Departments of the University "La Sapienza" of Rome, from September 1, 2000, to February 28, 2005. Forty-eight subjects affected by tic disorder, aged 4-16 years, with signs of a recent or intercurrent exposure to streptococcal antigens, and 18 age-matched patients affected by tic disorder but without evidence of streptococcal exposure were examined by Color doppler echocardiography. RESULTS: The rate of echocardiographic abnormalities was significantly higher (p<0.001) in the patients with sign of streptococcal exposure. In 28 out of 48 patients (58.3%), the color Doppler echocardiography showed abnormalities: 26 patients (54,3%) had a mitral regurgitation, 1 (2%) a mitral valve prolapse and finally 1 (2%) showed a kinking of the anterior mitral valve leaflet. In the control group, four children (22.2%) showed a mitral regurgitation. All of these abnormalities were not hemodynamically significant, and in many cases decreased with time. CONCLUSIONS: The higher rate of echocardiographic abnormalities observed in patients with tic disorder and exposure to group A beta-haemolytic streptococcal antigens, together with their decrease with time, suggest a post-streptococcal pathogenesis.     

Calcium-induced calcium release contributes to action potential-evoked calcium transients in hippocampal CA1 pyramidal neurons

Calcium-induced calcium release (CICR) is a mechanism by which local elevations of intracellular calcium (Ca2+) are amplified by Ca2+ release from ryanodine-sensitive Ca2+ stores. CICR is known to be coupled to Ca2+ entry in skeletal muscle, cardiac muscle, and peripheral neurons, but no evidence suggests that such coupling occurs in central neurons during the firing of action potentials. Using fast Ca2+ imaging in CA1 neurons from hippocampal slices, we found evidence for CICR during action potential-evoked Ca2+ transients. A low concentration of caffeine enhanced Ca2+ transient amplitude, whereas a higher concentration reduced it. Simultaneous Ca2+ imaging and whole-cell recordings showed that membrane potential, action potential amplitude, and waveform were unchanged during caffeine application. The enhancement of Ca2+ transients by caffeine was not affected by the L-type channel blocker nifedipine, the phosphodiesterase inhibitor IBMX, the adenylyl cyclase activator forskolin, or the PKA antagonist H-89. However, thapsigargin or ryanodine, which both empty intracellular Ca2+ stores, occluded this effect. In addition, thapsigargin, ryanodine, and cyclopiazonic acid reduced action potential-evoked Ca2+ transients in the absence of caffeine. These results suggest that Ca2+ release from ryanodine-sensitive stores contributes to Ca2+ signals triggered by action potentials in CA1 neurons.     

Neuronal functionality assessed by magnetoencephalography is related to oxidative stress system in acute ischemic stroke

The hypoxic brain damage induced by stroke is followed by an ischemia–reperfusion injury modulated by oxidative stress. Magnetoencephalographic (MEG) recording of rest and evoked cortical activities is a sensitive method to analyse functional changes following the acute ischemic damage. We aimed at investigating whether MEG signals are related to oxidative stress compounds in acute stroke.Eighteen stroke patients and 20 controls were enrolled. All subjects underwent MEG assessment to record background activity and somatosensory evoked responses (M20 and M30) of rolandic regions, neurological examination assessed by National Institute of Health Stroke Scale (NIHSS) and plasmatic measurement of copper, iron, zinc, ceruloplasmin, transferrin, total peroxides and Total Anti-Oxidant Status. Magnetic Resonance was performed to estimate the lesion site and volume.Delta power and M20 equivalent current dipole (ECD) strength in the affected hemisphere (AH) correlated with NIHSS scores (respectively, rho = .692, p = .006 and rho = − .627, p = .012) and taken together explained 67% of NIHSS variability (p = .004). Higher transferrin and lower peroxides levels correlated with better clinical status (respectively, rho = − .600, p = .014 and rho = .599, p = .011). Transferrin also correlated with AH M20 ECD strength (rho = .638 p = .014) and inversely with AH delta power (rho = − .646 p = .023) and the lesion volume, especially in cortico-subcortical stroke (p = .037).Our findings strengthen MEG reliability in honing the evaluation of neuronal damage in acute ischemic stroke also demonstrating an association between the MEG parameters most representing the clinical status and the oxidative stress compounds. Our results meet at a possible protective role of transferrin in limiting the oxidative damage in acute stroke.     

Potential role of fetal cardiac evaluation with magnetic resonance imaging: preliminary experience

OBJECTIVE: To report our experience with magnetic resonance imaging (MRI) in fetal heart evaluation. METHOD: Two radiologists examined 31 MRI of fetuses with no ultrasound (US) evidence of cardio-thoracic anomalies. T2-weighted half-Fourier single-shot turbo spin-echo sequences were acquired for anatomic evaluation; fast imaging with steady-state free precession (TrueFISP) and cine-MR sequences with real-time steady-state free precession oriented like standard fetal echocardiographic projections were acquired for the characterization of cardiovascular morphology and function. RESULTS: In every case, MRI assessed the viscero-atrial situs. The four-chamber view and the short-axis view of the left ventricle were obtained in all fetuses, the long-axis view of the aortic arch in 28, the long-axis view of the ductus arteriosus in 17, the five-chamber view in 12, the long-axis of the left ventricle in 9, the three-vessel view in 7, the tricuspid-aortic view in 3, and the transverse view of the aortic arch and the angulated view of the arch and the ductus arteriosus simultaneously in 2 fetuses. CONCLUSION: Our preliminary experience demonstrates the feasibility to visualize the fetal heart with routine fetal MRI protocols in particular, by means of acquisition of TrueFISP imaging (morphological study) and real-time cine-MRI (dynamic study), potentially making MRI a second-level tool to add to fetal echocardiography in the prenatal study of congenital cardiac malformations.     

A randomized,assessor‐blind,parallel‐group,multicentre, phase IV comparative trial of a suffocant compared with malathion in the treatment of head lice in children

Background/Objectives: There are concerns about the effectiveness of head lice treatments because of increasing resistance and safety. This trial compared the safety and efficacy of a suffocant‐based head lice treatment to malathion in children. Methods: The trial used strict entry criteria, standardized treatment and assessment regimens, sibling treatment where appropriate and a primary efficacy end‐point defined as the absence of live head lice. Results: A total of 216 children were enrolled. One hundred and sixty‐nine were per‐protocol. The suffocant was significantly more effective than malathion for the intention‐to‐treat population (53.9% vs 40.4% louse‐free, unadjusted P = 0.052; adjusted P = 0.024), as well as for the per‐protocol population (57.8% vs 43.0% louse‐free, unadjusted P = 0.054; adjusted P = 0.045). Adverse events were limited to itching or stinging and there were no serious or systemic adverse events. Repeat insult patch testing with the suffocant resulted in no adverse reactions. In vitro tests confirmed that the suffocant is a potent ovicide and pediculicide with 100% mortality of eggs and lice following a 20‐min contact time. Conclusions: The suffocant is shown to be significantly more effective in eliminating head lice than malathion in children, while being associated with a low incidence of mild, transient adverse events.     

Effect of repetitive transcranial magnetic stimulation on serum brain derived neurotrophic factor in drug resistant depressed patients

BACKGROUND: Depression has been associated with low brain-derived neurotrophic factor (BDNF) serum levels, while antidepressant drugs appear to mend this alteration. The purpose of this study was to assess BDNF serum levels in drug resistant depressed patients before and after repetitive Transcranial Magnetic Stimulation (rTMS) antidepressant treatment. METHODS: BDNF levels were measured in serum of 16 resistant depressed patients using the ELISA technique. RESULTS: BDNF baseline levels showed a negative correlation with illness severity measured by HDRS scores (R = -0.517, p = 0.04) and a significant increase of serum BDNF was found after rTMS treatment (t = -2.549, df = 15, p = 0.022). CONCLUSIONS: Our findings support the relationship between decreased serum BDNF and depression symptomatology and suggest a normalizing effect of rTMS antidepressant treatment. Further replications in larger samples will help to clarify the relevance of this preliminary data in the rTMS mechanism of action.     

ATP7B Variants as Modulators of Copper Dyshomeostasis in Alzheimer’s Disease

To understand the role of the key copper-regulating gene, ATP7B, in copper dyshomeostasis associated with Alzheimer’s disease (AD), we analyzed the serum levels of copper, ceruloplasmin and ‘free’ (i.e., non-ceruloplasmin bound) copper in 399 patients with AD and 303 elderly healthy controls. We also performed analyses of informative variants of ATP7B. AD patients had higher levels of copper and free copper than controls. Individuals with free copper levels higher than 1.6 μmol/L (the upper value of the normal reference range) were more frequent among cases (p < 0.001). Among these individuals, those who were carriers of the ATP7B variants accounted for a large proportion of the free copper levels, specifically in the AD group (p < 0.01). Our results suggest the existence of a ‘copper dysfunction’ phenotype of sporadic AD which has a genetic basis. They also suggest that free copper is a risk factor for this disorder, modulating additional pathways leading to the disease cascade.