American palm ethnomedicine: A meta-analysis

<p>Abstract</p> <p>Background</p> <p>Many recent papers have documented the phytochemical and pharmacological bases for the use of palms (<it>Arecaceae</it>) in ethnomedicine. Early publications were based almost entirely on interviews that solicited local knowledge. More recently, ethnobotanically guided searches for new medicinal plants have proven more successful than random sampling for identifying plants that contain biodynamic ingredients. However, limited laboratory time and the high cost of clinical trials make it difficult to test all potential medicinal plants in the search for new drug candidates. The purpose of this study was to summarize and analyze previous studies on the medicinal uses of American palms in order to narrow down the search for new palm-derived medicines.</p> <p>Methods</p> <p>Relevant literature was surveyed and data was extracted and organized into medicinal use categories. We focused on more recent literature than that considered in a review published 25 years ago. We included phytochemical and pharmacological research that explored the importance of American palms in ethnomedicine.</p> <p>Results</p> <p>Of 730 species of American palms, we found evidence that 106 species had known medicinal uses, ranging from treatments for diabetes and leishmaniasis to prostatic hyperplasia. Thus, the number of American palm species with known uses had increased from 48 to 106 over the last quarter of a century. Furthermore, the pharmacological bases for many of the effects are now understood.</p> <p>Conclusions</p> <p>Palms are important in American ethnomedicine. Some, like <it>Serenoa repens </it>and <it>Roystonea regia</it>, are the sources of drugs that have been approved for medicinal uses. In contrast, recent ethnopharmacological studies suggested that many of the reported uses of several other palms do not appear to have a strong physiological basis. This study has provided a useful assessment of the ethnobotanical and pharmacological data available on palms.</p

In situ immune response and mechanisms of cell damage in central nervous system of fatal cases microcephaly by Zika virus

Abstract Zika virus (ZIKV) has recently caused a pandemic disease, and many cases of ZIKV infection in pregnant women resulted in abortion, stillbirth, deaths and congenital defects including microcephaly, which now has been proposed as ZIKV congenital syndrome. This study aimed to investigate the in situ immune response profile and mechanisms of neuronal cell damage in fatal Zika microcephaly cases. Brain tissue samples were collected from 15 cases, including 10 microcephalic ZIKV-positive neonates with fatal outcome and five neonatal control flavivirus-negative neonates that died due to other causes, but with preserved central nervous system (CNS) architecture. In microcephaly cases, the histopathological features of the tissue samples were characterized in three CNS areas (meninges, perivascular space, and parenchyma). The changes found were mainly calcification, necrosis, neuronophagy, gliosis, microglial nodules, and inflammatory infiltration of mononuclear cells. The in situ immune response against ZIKV in the CNS of newborns is complex. Despite the predominant expression of Th2 cytokines, other cytokines such as Th1, Th17, Treg, Th9, and Th22 are involved to a lesser extent, but are still likely to participate in the immunopathogenic mechanisms of neural disease in fatal cases of microcephaly caused by ZIKV

Sepsis-surviving mice are more susceptible to a secondary kidney insult

Objective: It is well known that sepsis causes damage in different organs, including kidneys. However, few studies have been conducted on the magnitude of the long-term effects of sepsis on the surviving population, in particular, in relation to kidney disease. In this study, we examined the impact of long-term effects of sepsis on a second kidney insult. Design: Prospective experimental study. Setting: University research laboratory. Interventions: Wild-type mice were subjected to the cecal ligation and puncture sepsis model. Control animals underwent identical laparotomy but without ligation and cecum puncture. On days 0, 7, and 14 after surgery, the ratio between urinary protein and creatinine was measured. Fifteen days after surgery, surviving mice were subjected to a second kidney insult through intraperitoneal injections of bovine serum albumin for 7 days. On day 22 after surgery, urinary protein and creatinine, γ-glutamyl transpeptidase, lactate dehydrogenase, histologic parameters, macrophage infiltration, apoptotic cell, renal and plasmatic cytokines were determined. Measurements and Main Results: On days 7 and 14 after surgery, the urinary protein and creatinine observed in the septic animal group were higher than those observed in the control group. On day 22 after surgery, sepsis-surviving animals that were subjected to a second kidney insult showed more severe tubular injury compared with controls. This process seems to involve an immunosuppressive state because the concentrations of some renal cytokines, such as tumor necrosis factor-α, interleukin 6, interferon-γ and chemokine ligand 2, were decreased and leukocyte numbers were increased. Conclusions: These results suggest that sepsis induces long-term effects in kidney structure aggravating tubule damage in a second kidney insult

Epidemic of jungle yell fever in Brazil, 2000: implications of climatic alterations in disease spread

Ministério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Ministério da Saúde. Fundação Nacional de Saúde. Centro Nacional de Epidemiologia. Brasília, DF, Brazil.Ministério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Ministério da Saúde. Fundação Nacional de Saúde. Centro Nacional de Epidemiologia. Brasília, DF, Brazil.Ministério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Ministério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Secretaria de Saúde do Estado da Bahia. Salvador, BA, Brazil.Ministério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Pan American Health Organization. Division of Vaccines and Immunization. Washington, DCMinistério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Ministério da Saúde. Fundação Nacional de Saúde. Centro Nacional de Epidemiologia. Brasília, DF, Brazil.Ministério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Ministério da Saúde. Fundação Nacional de Saúde. Centro Nacional de Epidemiologia. Brasília, DF, Brazil.Ministério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Ministério da Saúde. Fundação Nacional de Saúde. Centro Nacional de Epidemiologia. Brasília, DF, Brazil.Ministério da Saúde. Fundação Nacional de Saúde. Instituto Evandro Chagas. WHO Collaborating Center for Arbovirus Reference and Research. Belém, PA, Brasil.Seventy-seven human cases of sylvatic yellow fever were reported in Brazil during the period January–June 2000. The first cases were reported 1 week after New Year's day and originated at Chapada dos Veadeiros, a tourist canyon site in Goiás state, near Brasília, the Brazilian capital. The laboratory procedures used for diagnoses included serology with an IgM capture assay and plaque reduction neutralization test, virus isolation in suckling mice and C6/36 cells, and immunohistochemistry. All cases were diagnosed by at least two different laboratory procedures, with the exception of the first three fatal cases, which were diagnosed on the basis of clinical and epidemiological information. The cases were reported in eight Brazilian states as follows: Goiás with 64.9% (50 cases); Amazonas (1); Bahia (10); Distrito Federal (1); Mato Grosso (4); Minas Gerais (2); Pará (1); São Paulo (2); and Tocantins (6). Patient ages were within the following ranges: 13–74 years old (mean 34.3), 64 (84.4%) were male, especially agricultural workers (n = 30), but tourists (n = 11), carpenters (n = 4), fishermen (n = 4), students (n = 3), truck drivers (n = 3), and other people (n = 22) were also sickened. The case fatality rate was 50.6% (39/77). In Bahia state, a serologic survey that was carried out has suggested a symptomatic/asymptomatic coefficient of 1:4. Field studies developed in Distrito Federal, Goiás, and São Paulo states showed that Haemagogus janthinomys was the mosquito species associated with the transmission. A single strain was also obtained from Aedes scapularis in Bahia. Epizootic occurrence (monkey mortality) was observed in 49 municipalities mainly in Goiás state, where 40 municipalities made reports, 21 of which also diagnosed human cases. Data obtained by the National Institute of Meteorology in Brazil showed an increase in temperature and rain in December 1999 and the first 3 months of 2000 in Goiás and surrounding states, which perhaps has contributed to the intense and widespread transmission of the yellow fever virus. The relatively small number of cases probably reflects the extensive use of yellow fever 17D-vaccine during the last 3 years, in which about 45 million doses were used. During the last months of 1999, 16 and 11 yellow fever cases were reported in Tocantins and Goiás states, respectively. It is noteworthy that the last reported autochthonous cases of sylvatic yellow fever in São Paulo and Bahia, both states outside the endemic/enzootic area, had occurred in 1953 and 1948, respectively