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Copyright of Brazilian Journal of Biology is the property of Instituto Internacional de Ecologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Brazilian Journal of Biology is the property of Instituto Internacional de Ecologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cladocerans are a diverse group of species that show rapid responses to changes in environmental conditions. This adaptive capacity has important implications for egg production and life cycle, especially in transitory environments such as temporary waterbodies. The present study investigated the life history and egg production of Alona gutatta Sars, 1862 (Crustacea, Cladocera), an abundant and frequent species from a high-altitude temporary pond (Lagoa Seca, Minas Gerais, Brazil). Newly hatched neonates were monitored in relation to time of maturation, number of eggs produced per female and time of survival. Neonates required a mean of 8 days to mature. A. guttata survived for a mean of 30.9 ± 8.1 days and produced 2 eggs per brood, generating a mean of 10.95 ± 6.41 neonates during the entire life cycle. The rapid development, short time to produce eggs and long life cycle are important adaptations to the adverse environmental conditions of temporary aquatic environments, which can contribute to the rapid colonization of Alona guttata in transitory ecosystems.

Objectives: To describe an outbreak of acute myalgia accompanied by elevated levels of muscle enzymes that occurred in the northeast region of Brazil from December 2016 through to May 2017., Methods: Clinical data were analysed and laboratory tests were performed in 86 specimens obtained from 52 individuals with suspected acute myalgia. A broader reactive enterovirus real-time RT-PCR followed by a semi-nested PCR amplification of partial VP1 gene were performed to identify the causative agent., Results: Eighty-six clinical samples were received in our laboratory during the myalgia outbreak. Median age of individuals was 39 years. Sudden acute myalgia and dark urine were the most common symptoms. Creatine phosphokinase levels were elevated with mean value ∼16 893 U/L. Human enterovirus was detected in 67% (58/86) of the patient's specimens (urine, serum, faeces and rectal swab). The enterovirus positivity per patient was 82.7% (43/52). Echovirus 30 (E-30) (82% of the typed specimens, 18/22; 76.4% (13/17) of the typed specimens per patient) was the main enterovirus identified. In addition to E-30, CV-A16 (1/22) and E-6 (3/22) were detected in 4% and 14% of the typed specimens, respectively. No deaths occurred., Conclusion: The 2016-2017 outbreak of acute myalgia that occurred in the northeast region of Brazil can be associated with E-30. Despite the clinical manifestations, a favourable outcome was observed for all patients., (Copyright © 2018 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved.)

Objective: We evaluated the effects of sodium hyaluronate (HY) and carbon nanotubes functionalized with HY (HY-CNT) on bone repair in the tooth sockets of diabetic rats., Materials and Methods: Diabetes was induced by streptozotocin (50 mg kg(-1) i.v.), and the sockets were divided into normal control, diabetic control, diabetic treated with HY (1%), and diabetic treated with HY-CNT (100 μg ml(-1)) groups. The sockets were analyzed according to the percentage of bone formation and the number of cell nuclei., Results: The percentage of bone trabeculae was lower in diabetic control animals (11.16 ± 5.10% vs 41.92 ± 6.34% in normal animals) after 14 days. Treating diabetic animals with HY or HY-CNT significantly increased the percentage of neoformed trabeculae (HY: 29.43 ± 3.29%; HY-CNT: 36.90 ± 3.07%). Moreover, the sockets of diabetic animals had an increased number of cell nuclei and HY or HY-CNT reduced this parameter., Conclusion: Our results indicate that HY and HY-CNT restore bone repair in the tooth sockets of diabetic rats, suggesting that these biomaterials are potential adjuvant therapies for the management of diabetes., (© 2012 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Development of RNA interference (RNAi) technology utilizing short interfering RNA sequences (siRNA) has focused on creating methods for delivering siRNAs to cells and for enhancing siRNA stability in vitro and in vivo. Here, we describe a novel approach for siRNA cellular delivery using siRNA coiling into carboxyl-functionalized single-wall carbon nanotubes (SWCNTs). The CNT-siRNA delivery system successfully demonstrates nonspecific toxicity and transfection efficiency greater than 95%. This approach offers the potential for siRNA delivery into different types of cells, including hard-to-transfect cells, such as neuronal cells and cardiomyocytes. We also tested the CNT-siRNA system in a non-metastatic human hepatocellular carcinoma cell line (SKHep1). In all types of cells used in this work the CNT-siRNA delivery system showed high efficiency and apparent no side effects for various in vitro applications.

Enteroviruses were investigated in respiratory secretions collected from patients with acute respiratory infections (ARI) over a seven year period (1985-1991), as part of a longitudinal study of ARI aetiology. All the viruses that are most commonly associated with ARI were found in this study. Among the virus isolates, enteroviruses were only less frequent than respiratory syncytial viruses, adenoviruses and influenzaviruses. Forty five enterovirus samples were isolated from patients with either upper respiratory tract infections (URTI) or lower respiratory tract infections (LRTI). From these enterovirus isolates, thirty one samples were identified as poliovirus (n = 18) and non polio enterovirus (n = 13) by serum neutralization. Poliovirus were identified as type 1 and 2 and all of them were vaccinal strains. From thirteen non polio enterovirus, twelve were identified as echovirus serotypes 1, 2, 7, 11, 19 and 31. The remainder was identified as coxsackievirus B4.

Rhabdomyosarcoma monolayers were inoculated with enterovirus 71 (EV 71) at 73 degrees C, sampled at intervals during the replicative cycle, and examined in thin sections by electron microscopy, using routine and immunoelectronmicroscopy with polyclonal antibodies against EV 71. The location of EV 71 or its precursors was followed during the viral replicative cycle. The earliest samples (3 h postinoculation) showed a cell shape change, from elongated to rounded. At 6 h postinoculation, the presence of early virus-induced vesicles developing within the cytoplasm was pointed out, although no virus particles were observed at these stages. At 12 and 20 h postinoculation, virus particles appeared in the cytoplasm. They were found free or in clusters in the cytoplasmic matrix, between the virus-induced vesicles. EV 71 particles were also occasionally observed in the form of paracrystalline arrays situated in the vesiculated areas. The immunolabel (gold beads) was found, initially, over dense cytoplasmic areas and in more advanced process at the vesiculated area and over the virus particles. Therefore the main cellular alterations observed in this infection were the shape change of the cell and the appearance of electron-dense areas (viroplasm) and smooth walled vesicles which are probably the site of the virus replication.

Delayed response to medical treatment sometimes leads to unnecessary liver transplantation in patients with severely decompensated Wilson disease. We report the course of five patients (mean age 13.4 years, range 11 to 15 years) with severely decompensated Wilson disease who were successfully treated medically. Prothrombin time improved after a minimum of 1 month and returned to normal within 3 months to 1 year or more.

This study reports a type 1 poliovirus strain isolated in Brazil from a case classified as vaccine-associated paralytic poliomyelitis (VAPP). After serotyping of the viral isolate with hyperimmune equine sera, PCR and molecular hybridization techniques characterized the strain as P1/Sabin-derived. The isolate was partially sequenced to identify mutations at nucleotides 480, 525 and 6203, which are important for reversion of the P1/Sabin strain to neurovirulence. In a recent study, a P1/Sabin-derived strain isolated from the central nervous system of a VAPP case did not mutate at these positions, but maintained 480-G and 525-U (and 6203-C), suggesting that these mutations are not essential for the occurrence of disease (Georgescu et al., (1994), Journal of Virology, 68: 8089-8101). Although the Brazilian strain also maintained 480-G and 525-U (and 6203-C) and was isolated from the stool, the possibility that this isolate invaded the central nervous system after replicating in the gut, causing the paralysis, cannot be ruled out. This is the first report of a type 1 VAPP case in Brazil, although some cases caused by type 2 and type 3 strains have been described.

Twenty strains of P2/Sabin-related polioviruses isolated in Brazil were analyzed; ten from persistent paralytic poliomyelitis cases, three from suspected polio cases with transient paralysis, and seven from healthy contacts. The serotypes of the viral isolates were identified by the neutralization test with hyperimmune equine sera. The relationship of the isolates to the P2/Sabin strain was demonstrated by molecular hybridization and polymerase chain reaction (PCR). Partial sequencing demonstrated mutations at nucleotide 481 in the 5' noncoding region and at amino acid 143 of the capsid protein VP1 in most of these isolates from vaccine-associated cases in Brazil. These data support previous studies on the importance of mutations at these attenuated determinants in the establishment of the disease. However, the existence of isolates without mutations at these positions suggests that they are not essential. The results also strengthen the possibility of the participation of a mutation at nucleotide 398 in the establishment of the disease, and suggest that a mutation at nucleotide 491 or 500 may also be involved in this process. The isolates from healthy contacts presented the same mutations as the isolates from vaccine-associated cases with which they were in contact. This strengthens the observation that, although mutations in the genome of the P2/Sabin strain are important for the establishment of the disease, host factors are also involved.

Eight strains of P3/Sabin-related polioviruses were analyzed; four from persistent paralytic poliomyelitis cases classified as vaccine associated, one from a transient paralysis case classified as transverse myelitis, one from a transient paralysis case classified as Guillain-Barré syndrome, one from a transient facial paralysis case, and one from a healthy vaccine. The serotypes of the viral isolates were identified by the neutralization test with hyperimmune equine sera and the relationship of the isolates with the P3/Sabin strain was demonstrated by molecular hybridization of the viral RNA of the isolates with a P3/Sabin-specific probe. The P3/Sabin relationship was confirmed by PCR, using a pair of specific primers for P3/Sabin-related isolates. The available data indicate that a U-->C mutation at nucleotide 472 in the 5' noncoding region of the genome of the type 3 Sabin strain increases the neurovirulence of this strain and this mutation was observed in all type 3 isolates from vaccine-associated cases. These eight P3/Sabin-related isolates were partially sequenced in the 5' noncoding region and seven presented a U-->C mutation at nucleotide 472, except the isolate from a transient paralysis case classified as transverse myelitis, that maintained a U at nucleotide 472. Although this virus maintaining U at nucleotide 472 may not be the etiological agent of the disease, the possibility that the virus was the causative agent of the disease could not be ruled out.

Eight strains of P1/Sabin-derived polioviruses isolated in Brazil from paralysis cases were analyzed. The serotypes of the viral isolates were identified by neutralization test with hyperimmune equine sera. The relationship of the isolates to the P1/Sabin strain was demonstrated by molecular hybridization and PCR. The isolates were partially sequenced with the objective of finding mutations at nucleotides (nt) 480 and 525 of the 5'-noncoding region (5' NCR) and at nt 6203 of the 3Dpol coding region (3Dpol), which are important for reversion towards neurovirulence. Four isolates from paralysis cases classified as Guillain Barré Syndrome (GBS; three with sequels) were analyzed; one presented G-->A (480) and C-->U (6203) mutations, one G-->A (480) mutation, one G-->A (480) and U-->C (525) mutations, and one did not mutate at the analyzed positions. Two isolates from transient facial paralysis cases were analyzed; one presented U-->C (525) mutation and the other G-->A (480) mutation. One isolate from a transient paralysis case classified as a neuroviral disease and one isolate from a paralysis case with sequels were analyzed and none mutated at the analyzed positions. Although the isolates may not be the causative agent of the disease, a temporal association between the isolation of the P1/Sabin-derived isolates and the disease was observed. The possibility that GBS and the facial paralysis were caused by these isolates could not be excluded.

This study analyzed 3129 fecal samples derived from 1626 patients with sudden onset acute flaccid paralysis clinically compatible with poliomyelitis. The samples were collected in the period ranging from January 1990 to September 1993 in all regions of Brazil. Among the 1626 cases studied, 196 had isolation of poliovirus. Nevertheless, it was observed that some factors influenced the isolation rate and the intratypic characterization of these polioviruses. No cases of acute flaccid paralysis has been found to be etiologically related with wild polioviruses.

The surface of the syncytial epithelium of the human parasite, Schistosoma mansoni, consists of an apical plasma membrane (APM) and an overlying envelope (En). The rapid turnover of these membranes is an adaptation to parasitism and is influenced by ambient signals emanating from the host's immune system. The third component of complement (C3) has been shown to stimulate the synthesis of the En via a C3-binding protein (C3bp) and a Ca(2+)-dependent signal transduction mechanism. Using ELISA the C3bp was found to be restricted to the En. In addition, cross-linking of iodinated C3 to En proteins with the homobifunctional noncleavable disuccinimidyl suberate reagent yielded a receptor-C3 complex in excess of 250 kDa, and SDS-PAGE analysis of solubilized En proteins that were radiolabeled and chromatographed on C3-Sepharose revealed a 130-kDa protein that specifically bound to the C3 beads. In further experiments, using a photoactivatable radiolabeled cross-linker, the Denny-Jaffe reagent, C3 transferred the radiolabel to a 130-kDa En protein. Metabolic labeling experiments have demonstrated that this C3bp is synthesized by the parasite and, more importantly, antibodies raised against the C3bp blocked En synthesis in vivo. Also, the surface localization of the C3bp was demonstrated using immunolabeling electron microscopy. The data presented herein strongly suggest that the 130-kDa schistosome En protein is a C3bp responsible for renewal of the En in response to C3 binding.

Background: After thrombolytic therapy for patients with acute myocardial infarction (MI), percutaneous transluminal coronary angioplasty (PTCA) is frequently performed because of the presence of a "significant" infarct vessel stenosis demonstrated at predischarge coronary angiography. Several studies have shown PTCA performed early after thrombolysis to be unnecessary or even harmful. However, PTCA in these trials was generally performed 1-3 days after MI, when the milieu in the infarct artery may be unsuited for PTCA, and the incidence of major ischemic complications was high. To date, no trial has assessed whether delayed PTCA (4-14 days) should be performed in patients without evidence of ischemia on stress testing., Methods and Results: To test the hypothesis that delayed PTCA might provide clinical benefit compared with medical therapy alone, 87 patients treated within 6 hours of chest pain onset with thrombolytic therapy and with negative functional test were randomized between PTCA to be performed 4-14 days after MI versus no PTCA. Both groups received medical therapy. Patients with postinfarct angina or prior Q wave infarction in the infarct distribution were excluded. The primary study end point was increase in left ventricular ejection fraction with exercise measured by radionuclide studies 6 weeks after MI, a parameter known from other studies to correlate inversely with future ischemic events. Clinical outcome was also monitored for 12 months. There were no differences between the study groups for any prerandomization variable recorded. Mean age was 57 +/- 10 years, 84% of patients were male, 21% had prior MI, 36% had anterior MI, 7% had multivessel disease, and the infarct stenosis measured 70 +/- 17% before randomization. PTCA was successful in 38 of 42 patients (88%) but resulted in non-Q wave MI due to acute closure of the treated site in three of 42 (9.5%). There was no difference in 6-week resting ejection fraction or increase in ejection fraction with exercise between the two groups (47 +/- 12% and 6 +/- 8%, respectively, in the PTCA group; 49 +/- 10% and 5 +/- 9% in the no-PTCA group; p = NS for both.) There were no deaths in either group. Actuarial 12-month infarct-free survival was 97.8% in the no-PTCA group and 90.5% in the PTCA group (p = 0.07)., Conclusions: There was no functional or clinical benefit from routine late PTCA after MI treated with thrombolytic therapy in this relatively low-risk cohort of patients. These data strongly suggest that patients with an uncomplicated MI after thrombolytic therapy, even if they have a "significant" residual stenosis of the infarct vessel, should be treated medically if they are without evidence of ischemia on stress testing before hospital discharge.

Synthetic oligodeoxynucleotide probes, 21-23 nucleotides in length, were prepared which specifically hybridize to the genomes of the wild type 1 and 3 polioviruses currently endemic to the northeastern region of Brazil. The probes are complementary to sequences near the 5'-terminus of the VP1 gene that differ substantially among genetically distant polioviruses but are largely conserved among related isolates. The probes have been routinely used in the laboratory surveillance of poliomyelitis cases in Brazil, permitting direct, rapid identification of the indigenous wild polioviruses by dot-blot hybridization.

The nucleotide sequences encoding the capsid protein VP1 were determined for the wild polioviruses of serotypes 1 and 3 endemic to the northeastern region of Brazil. Compared with the corresponding Sabin vaccine strain sequences, the wild isolates differed at 20% (type 1) and 22% (type 3) of their nucleotide positions, and in 7% (type 1) and 11% (type 3) of their amino acid residues. The highest degree of amino acid heterogeneity occurred within the amino-terminal residues of the VP1 proteins. Intratypic amino acid differences also occurred in VP1 surface residues that form parts of antigenic sites for neutralizing antibodies.