From 1992 to 1995, 688 accidents by venomous snakes (mean of 192 cases/year) have been notified to the Health Ministry of the State of Ceará, with an incidence between 0.9 and 5.8/100.000 inhabitants. Among 473 cases, 88.3% were of the genus. Bothrops, 10.7% Crotalus, 0.8% Micrurus and 0.2% Lachesis. The highest incidence occurred from April to September. Male (75.6%) predominated with ages from 10 to 49 years old (72.3%). The more frequently bitten anatomical region were the lower limbs (81.9%) and upper limbs (14.7%). The attendance at health unit which notified the accident took place within 6 hours in 66.9% of the cases. Lethality was 0.7%. The afflicted people were mainly peasants (62.7%), and most of the accidents took place in their own work place. The authors emphasize that the snake bites in the state of Ceará may be considered work accidents, concern mainly peasants and constitute a cause of death.
The complex of porcine seminal plasma heterodimers I and II (PSP-I/PSP-II), which are heterodimers of glycosylated spermadhesins, is the major component of porcine seminal fluid. The proinflammatory and immunostimulatory activities of this spermadhesin complex suggest its participation in modulation of the uterine immune activity that may ensure reproductive success. Spermadhesin PSP-I/PSP-II induced the migration of neutrophils into the peritoneal cavity of rats via activation of resident cells. In the present study, we have investigated the involvement of macrophages and mast cells in the neutrophil chemotactic activity of PSP-I/PSP-II and the underlying mechanism. Macrophages and mast cells were isolated, cultured, and stimulated with purified PSP-I/PSP-II. Pharmacological modulation was performed using the glucocorticoid dexamethasone, indomethacin (cyclooxygenase inhibitor), MK886 (leukotriene inhibitor), and the supernatant of spermadhesin-stimulated mast cells. Macrophages stimulated with PSP-I/PSP-II released into the culture supernatant a neutrophil chemotactic substance. This activity was partly inhibited by both dexamethasone (85%) and the supernatant of spermadhesin-stimulated mast cells (74%) but not by indomethacin and MK886. An anti-tumor necrosis factor (TNF) alpha antibody neutralized (by 68%) the neutrophil chemotactic activity of PSP-I/PSP-II-stimulated macrophages. An anti-interleukin (IL)-4 antibody blocked the inhibitory activity of spermadhesin-stimulated mast cells on release of a neutrophil chemotactic substance by PSP-I/PSP-II-stimulated macrophages. As a whole, these data indicate that the neutrophil migration-inducing ability of spermadhesin PSP-I/PSP-II involves the release of the inflammatory cytokine TNFalpha by stimulated macrophages and that this activity is modulated by the lymphokine IL-4 liberated by mast cells. The balance between these two cytokines may control onset of the local inflammatory reaction, avoiding excessive neutrophil recruitment that would lead to tissue damage.
Rats are commonly used in anaphylaxis models, mainly in intestinal anaphylaxis. Hypersensitivity mechanisms are complex and they are not clearly defined. Ovalbumin (OVA) is commonly used for studies on the hypersensitivity mechanism. However, the potential pro-inflammatory mediators induced by this antigen in the model of paw oedema in immunized rats are still not completely understood. This work examines the pharmacological modulation of several mediators involved in rat hind paw immune oedema induced by OVA. Wistar rats were previously immunized (14-18 days) with OVA (30 microg, intraperitoneally) or sham-sensitized with aluminum hydroxide (control). The paw volumes were measured before the antigenic stimuli and 1, 2, 3 and 4 h after the intraplantar injection of OVA (10 microg/paw). Subcutaneous injection of dexamethasone, diphenhydramine, cyproheptadine, chlorpromazine or methysergide significantly inhibited (p < 0.05) the allergic paw oedema. The dual inhibitor of cyclooxygenase and lipoxygenase (NDGA), the cyclooxygenase inhibitor (indomethacin), the lipoxygenase inhibitor (MK-886), the PAF antagonist (WEB 2086), the mast cell stabilizer (ketotifen), and the anti-histamine (meclizine) did not inhibit the immune oedema. In addition, thalidomide and pentoxifylline (anti-tumour necrosis factor drugs) were ineffective against OVA-induced oedema. The fact that indomethacin, MK-886, NDGA and WEB 2086 are unable to inhibit this allergic oedema indicates that the dexamethasone action seems not to be via phospholipase A2, but possibly due to the synthesis and/or the inhibitory activity of cytokines. The paw oedema inhibition by diphenhydramine, but not by meclizine, may suggest a different mechanism, which is independent of the effect of histamine. These data indicate that allergic oedema is more sensitive to anti-serotonin drugs, mainly anti-5-HT2, suggesting that the principal mediator of this inflammatory response is serotonin.
RESUMOObjetivo: estudar a mortalidade materna por hipertensão na gestação, estimando a razão de mortalidade e o perfil das pacientes que foram a óbito por esta causa. Métodos: estudo retrospectivo dos óbitos maternos devidos à hipertensão ocorridos na Maternidade-Escola Assis Chateaubriand da Universidade Federal do Ceará -MEAC/UFC, no período de 1981 a 2003. Foram avaliadas as razões de mortalidade materna geral (RMM) e específica para hipertensão e, nesta população de hipertensas, os dados epidemiológicos e clínicos. Resultados: registraram-se 296 casos de óbitos maternos e 184.672 nascidos vivos (NV), resultando em RMM de 160,28/100.000 NV. A causa de óbito mais freqüente foi hipertensão (41,2%), com 122 casos e média anual de 5,3 óbitos e RMM para hipertensão de 60,10/100.000 NV. Analisando-se o grupo de mortes por hipertensão verificou-se que a idade materna variou de 13 a 42 anos, com média de 26 anos. A maioria das pacientes originou-se do interior do estado. As mortes aconteceram principalmente nas primeiras 24 horas após a admissão hospitalar (50,9%). Houve predomínio de mortes em primigestas (40,3%) e na faixa entre 31 e 38 semanas (48,2%). A eclâmpsia ocorreu em 73 pacientes (64,1%), sendo mais prevalente durante a gestação (53,4%). Aconteceram 101 óbitos no período puerperal. Houve predomínio de cesárea (62,3%) e de anestesia geral (45,1%). A assistência pré-natal não foi realizada em 61,4% das pacientes. Conclusões: as razões de mortalidade materna geral e por hipertensão foram elevadas, sendo a hipertensão a principal causa de óbito materno em nossa maternidade. PALAVRAS-CHAVE:Hipertensão/mortalidade; Gravidez/metabolismo; Complicações na gravidez; Mortalidade materna; Cuidado pré-natal; Estudos retrospectivos ABSTRACT Purpose: to study maternal mortality caused by hypertension during pregnancy, determining the mortality rate and the profile of those patients. Methods: a retrospective study of maternal mortality caused by hypertension at the Maternidade Escola Assis Chateaubriand of the Universidade Federal do Ceará, from 1981 to 2003. General maternal mortality rate (MMR) and specific maternal mortality rate due to hypertension were evaluated, as well as these patients' epidemiological and clinical data. Results: two hundred and ninety six cases of maternal death and 184,672 of live births were recorded, with a MMR of 160.28/100.000 live births. The most frequent cause of death was hypertension (41.2%); with 122 cases and an annual average of 5.3 deaths, and hypertension MMR of 60.10/100,000 live births. The women's age range varied from 13 to 42 years with an average of 26 years. Most of the patients came from the interior of the state. Deaths occurred predominantly in the first 24 hours after admission to the hospital (50.9%). Deaths were predominant in the first pregnancy (40.3%) and in women with 31 to 38 weeks gestational age (48.2%). Eclampsia occurred in 73 patients (64.1%) and was predominant along the gestational period (53.4%). There were 101 deaths in the puerperium. Cesarean section (6...
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