19 research outputs found
Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry.
BACKGROUND: The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry. METHODS AND RESULTS: A total of 52,014 patients with newly diagnosed AF were enrolled globally; of these, 1388 patients were recruited from 26 sites within India (2012-2016). In India, the mean age was 65.8 years at diagnosis of NVAF. Hypertension was the most prevalent risk factor for AF, present in 68.5% of patients from India and in 76.3% of patients globally (P < 0.001). Diabetes and coronary artery disease (CAD) were prevalent in 36.2% and 28.1% of patients as compared with global prevalence of 22.2% and 21.6%, respectively (P < 0.001 for both). Antiplatelet therapy was the most common antithrombotic treatment in India. With increasing stroke risk, however, patients were more likely to receive oral anticoagulant therapy [mainly vitamin K antagonist (VKA)], but average international normalized ratio (INR) was lower among Indian patients [median INR value 1.6 (interquartile range {IQR}: 1.3-2.3) versus 2.3 (IQR 1.8-2.8) (P < 0.001)]. Compared with other countries, patients from India had markedly higher rates of all-cause mortality [7.68 per 100 person-years (95% confidence interval 6.32-9.35) vs 4.34 (4.16-4.53), P < 0.0001], while rates of stroke/systemic embolism and major bleeding were lower after 1 year of follow-up. CONCLUSION: Compared to previously published registries from India, the GARFIELD-AF registry describes clinical profiles and outcomes in Indian patients with AF of a different etiology. The registry data show that compared to the rest of the world, Indian AF patients are younger in age and have more diabetes and CAD. Patients with a higher stroke risk are more likely to receive anticoagulation therapy with VKA but are underdosed compared with the global average in the GARFIELD-AF. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01090362
Morphometric analysis of brain lesions in rat fetuses prenatally exposed to low-level lead acetate: correlation with lipid peroxidation
The effect of prenatal lead acetate exposure
was studied microscopically together with the
concentration of lead and lipid fluorescent products
(LFP) in the brain of rat fetuses. Wistar rats were
intoxicated with a lead solution containing either 160 or
320 ppm of lead acetate solution during 21 days through
drinking water. The control group (ten rats) received
deionized water for the same period. The rats were killed
on gestation day 21 and fetuses were obtained; the
placenta, umbilical cord and parietal cortex (Cx),
striatum (St), thalamus (Th) and cerebellum (Ce) were
collected for measuring tissue lead concentration, LFP as
an index of lipid peroxidation and histopathologic
examination. Lead contents were increased in placenta,
umbilical cord, St, Th and Cx in both lead-exposed
groups. Lead exposure increased (LFP) in placenta and
umbilical cord, St, Th and Ce as compared to the control
group. Histopathological examination showed severe
vascular congestion in placenta, the Cx, St, Th and Ce
with hyperchromatic and shrunken cells. Interstitial
oedema was found in all regions studied of both lead
exposed groups. The morphometric evaluation of the
studied brain regions showed an absolute decrease in
total cell number and increased number of damaged cells and interstitial oedema. Our results show that
morphological changes in rat brain are correlated with
increased lipid peroxidation, and the lead levels of the
umbilical cord, however it is not clear whether oxidative
stress is the cause or the consequence of these
neurotoxic effects of lead
Taenia solium: Development of an Experimental Model of Porcine Neurocysticercosis.
Human neurocysticercosis (NC) is caused by the establishment of Taenia solium larvae in the central nervous system. NC is a severe disease still affecting the population in developing countries of Latin America, Asia, and Africa. While great improvements have been made on NC diagnosis, treatment, and prevention, the management of patients affected by extraparenchymal parasites remains a challenge. The development of a T. solium NC experimental model in pigs that will allow the evaluation of new therapeutic alternatives is herein presented. Activated oncospheres (either 500 or 1000) were surgically implanted in the cerebral subarachnoid space of piglets. The clinical status and the level of serum antibodies in the animals were evaluated for a 4-month period after implantation. The animals were sacrificed, cysticerci were counted during necropsy, and both the macroscopic and microscopic characteristics of cysts were described. Based on the number of established cysticerci, infection efficiency ranged from 3.6% (1000 oncospheres) to 5.4% (500 oncospheres). Most parasites were caseous or calcified (38/63, 60.3%) and were surrounded by an exacerbated inflammatory response with lymphocyte infiltration and increased inflammatory markers. The infection elicited specific antibodies but no neurological signs. This novel experimental model of NC provides a useful tool to evaluate new cysticidal and anti-inflammatory approaches and it should improve the management of severe NC patients, refractory to the current treatments
Histopathological classification of the inflammatory reaction (Experiment 2).
<p>SA: subarachnoid. IM: intramuscular.</p><p>Histopathological classification of the inflammatory reaction (Experiment 2).</p
Expression of inflammatory and non-inflammatory cytokines.
<p>Six-micrometer sections of pig brain tissues proximal to installed parasites and sections of an equivalent region from sham-operated pigs (40X) were incubated with antibodies against inflammatory cytokines (IL-17, TNF-α, and IL6), the non-inflammatory cytokine IL-10 and a Th2-prototype cytokine. Arrows indicate regions where cytokines were expressed.</p
Expression of vimentin.
<p>The immunohistochemical analysis of vimentin expression showed that immature astrocytes were more frequently found in areas proximal to the parasite (A) than in tissues distal to the parasite (B) (40X).</p
Macroscopic examination of cysticerci recovered after implantation of activated oncospheres in brain and muscle (Experiment 2).
<p>SA: subarachnoid. IM: intramuscular. Co/Cs: colloidal/caseous.</p><p>Macroscopic examination of cysticerci recovered after implantation of activated oncospheres in brain and muscle (Experiment 2).</p
Microscopic examination (HE, 4x) of a cysticercus recovered from brain.
<p>Lymphocyte Aggregates are observed in the parasite periphery. Parasite structures are not visible. A grade-4 inflammatory reaction is shown.</p
Expression of inflammatory cell markers in brain tissues.
<p>Six-micrometer sections of pig brain tissues proximal to installed parasites and sections of an equivalent region from sham-operated pigs (40X) were incubated with antibodies against inflammatory cell markers (CD106, CD80, CD54, and CD69). Non-immunized rabbit serum (control) showed no reaction. Arrows indicate regions where inflammatory markers are expressed. CD106 was expressed in brain microvessels, while CD80 was expressed in microglia cells.</p
Macroscopic aspect of cysticerci recovered from brain.
<p>Vesicular (white arrows) and colloidal/caseous (black arrows) parasites are shown.</p