Antiparasitic drugs: in vitro tests against nematophagous fungi.

The use of biological agents has been intensified in recent years against eggs and larvae of gastrointestinal nematodes as an alternative control method in pasture plant health management, with the concomitant use with antiparasitic drugs still occurring. The aim of this study was to test the in vitro activity of the following antiparasitic drugs: Ivermectin and albendazole against the following nematophagous fungi: Paecilomyces fumosoroseus, Paecilomyces lilacinus and Paecilomyces variotii. The agar diffusion test was performed using an initial concentration of 0.0016g/mL of each drug, after solidification of the culture medium containing the drug concentration each nematophagous fungi was inoculated. The results showed that in a concentration of 80µg/mL, the fungal growth decreased, however, with the concentration of 160µg/mL, there was no fungal growth in both drugs, compared to the control, which indicates an inhibition in the development of the nematophagous fungi studied when they come in contact with ivermectin and albendazole.

Alpha-melanocyte-stimulating hormone stimulation of aldosterone secretion in hypophysectomized rats.

Intact and hypophysectomized male rats on low and high sodium diets were treated with sc infused ACTH and alpha MSH, and the levels of aldosterone and corticosterone were determined in truncal blood. Plasma aldosterone levels were lower in hypophysectomized animals on the low sodium diet than in intact animals on the low sodium diet. Alpha MSH (8 micrograms/day) restored plasma levels of aldosterone to normal in hypophysectomized rats on the low sodium diet. ACTH (6 micrograms/day) did not cause significant changes in plasma levels of aldosterone in hypophysectomized animals. ACTH restored plasma corticosterone to normal in hypophysectomized rats, whereas alpha MSH had no effect on corticosterone. Alpha MSH did not increase plasma aldosterone levels in intact rats. These data suggest that alpha MSH may be important in the regulation of aldosterone secretion in the rat and that zona glomerulosa responsiveness to alpha MSH in vivo is increased by hypophysectomy. The mechanisms of alpha MSH action on glomerulosa cells are different from those of ACTH.

Bmf upregulation through the AMP-activated protein kinase pathway may protect the brain from seizure-induced cell death.

Prolonged seizures (status epilepticus, SE) can cause neuronal death within brain regions such as the hippocampus. This may contribute to impairments in cognitive functioning and trigger or exacerbate epilepsy. Seizure-induced neuronal death is mediated, at least in part, by apoptosis-associated signaling pathways. Indeed, mice lacking certain members of the potently proapoptotic BH3-only subfamily of Bcl-2 proteins are protected against hippocampal damage caused by status epilepticus. The recently identified BH3-only protein Bcl-2-modifying factor (Bmf) normally interacts with the cytoskeleton, but upon certain cellular stresses, such as loss of extracellular matrix adhesion or energy crisis, Bmf relocalizes to mitochondria, where it can promote Bax activation and mitochondrial dysfunction. Although Bmf has been widely reported in the hematopoietic system to exert a proapoptotic effect, no studies have been undertaken in models of neurological disorders. To examine whether Bmf is important for seizure-induced neuronal death, we studied Bmf induction after prolonged seizures induced by intra-amygdala kainic acid (KA) in mice, and examined the effect of Bmf-deficiency on seizures and damage caused by SE. Seizures triggered an early (1-8 h) transcriptional activation and accumulation of Bax in the cell death-susceptible hippocampal CA3 subfield. Bmf mRNA was biphasically upregulated beginning at 1 h after SE and returning to normal by 8 h, while again being found elevated in the hippocampus of epileptic mice. Bmf upregulation was prevented by Compound C, an inhibitor of adenosine monophosphate-activated protein kinase, indicating Bmf expression may be induced in response to bioenergetic stress. Bmf-deficient mice showed normal sensitivity to the convulsant effects of KA, but, surprisingly, displayed significantly more neuronal death in the hippocampal CA1 and CA3 subfields after SE. These are the first studies investigating Bmf in a model of neurologic injury, and suggest that Bmf may protect neurons against seizure-induced neuronal death in vivo.

Antiparasitic drugs: in vitro tests against nematophagous fungi / Antiparasitários: teste in vitro contra fungos nematófagos

Abstract The use of biological agents has been intensified in recent years against eggs and larvae of gastrointestinal nematodes as an alternative control method in pasture plant health management, with the concomitant use with antiparasitic drugs still occurring. The aim of this study was to test the in vitro activity of the following antiparasitic drugs: Ivermectin and albendazole against the following nematophagous fungi: Paecilomyces fumosoroseus, Paecilomyces lilacinus and Paecilomyces variotii. The agar diffusion test was performed using an initial concentration of 0.0016g/mL of each drug, after solidification of the culture medium containing the drug concentration each nematophagous fungi was inoculated. The results showed that in a concentration of 80μg/mL, the fungal growth decreased, however, with the concentration of 160μg/mL, there was no fungal growth in both drugs, compared to the control, which indicates an inhibition in the development of the nematophagous fungi studied when they come in contact with ivermectin and albendazole.

Resumo O uso de agentes biológicos que atuam em ovos e larvas de nematódeos gastrintestinais como uma alternativa para o manejo de pastagens de saúde tem se intensificado nos últimos anos, bem como o uso concomitante com outros medicamentos antiparasitários. O objetivo deste estudo foi testar o efeito in vitro dos fármacos Ivermectina e Albendazol em fungos nematófagos Paecilomyces fumosoroseus, Paecilomyces lilacinus e Paecilomyces variotii. Foi utilizada a técnica de difusão em agar, sendo preparado a partir de uma concentração inicial de 0,0016g/mL de cada uma das drogas e diluídas em meio de cultura, com posterior semeadura dos fungos nematófagos. Os resultados mostraram que na concentração de 80μg/mL, o crescimento diminuiu, no entanto, com a concentração de 160μg/mL de ambas as drogas, não houve crescimento de fungos durante o período de estudo, em comparação com o controle, indicando a inibição do desenvolvimento dos fungos nematófagos estudados quando em contato com a Ivermectina e Albendazol.

Suppression of aldosterone by cyproheptadine in idiopathic aldosteronism.

To study the role of serotonin in regulating the release of aldosterone, we gave single, oral doses of cyproheptadine, an antiserotoninergic agent, to five normal volunteers with high aldosterone levels secondary to sodium deprivation and to 14 patients with aldosteronism (six with idiopathic aldosteronism due to bilateral adrenal hyperplasia and eight with adrenal adenoma). A diet containing 150 mmol of sodium was given to the patients with spontaneous aldosteronism, and one containing 10 mmol of sodium was given to the normal subjects, for three days before treatment and throughout the study. All subjects received dexamethasone, 2 mg daily. Serum aldosterone was measured with the subject in the recumbent position before cyproheptadine administration and at 30-minute intervals for two hours afterward. Serum aldosterone fell significantly (P less than 0.025) from the basal level in the patients with idiopathic aldosteronism due to hyperplasia. No fall was observed in the normal subjects or in the patients with adenoma. No changes were seen in renin activity, cortisol, sodium, or potassium, in any group after cyproheptadine. Suppression of aldosterone with cyproheptadine suggests a serotonin-mediated aldosterone-stimulating system. Hyperactivity of this system may be the cause of idiopathic aldosteronism associated with adrenal hyperplasia.

Detecting residual bcr-abl transcripts in chronic myeloid leukaemia patients using coupled reverse transcriptase-polymerase chain reaction with rTth DNA polymerase.

The bcr-abl fusion gene is the hallmark of chronic myeloid leukaemia (CML) and presumably the cause of its development. Accordingly, long-term disappearance of the bcr-abl gene after intensive therapy suggests that a patient is probably cured of CML. The diagnostic protocol based on coupling of two enzymatic reactions, reverse transcription (RT) and nested polymerase chain reaction (nPCR), for the detection of bcr-abl transcripts in peripheral blood provides a powerful tool for minimal residual CML detection. We have developed a new detection protocol using rTth DNA polymerase as the only enzyme catalysing both reactions for simplifying CML diagnosis. We demonstrate its efficacy investigating residual leukaemic cells in the peripheral blood of 10 patients. This assay offers several advantages over the use of conventional RT-PCR, being more sensitive, faster, less prone to false positives since no opening of the tube is required between the two reactions and requires no special oils or waxes. Our simple assay for bcr-abl chimeric transcripts detection is a practical addition to the diagnostic evaluation of the patient with chronic myeloid leukaemia.

Enfermedad de Hansen: a propósito de un caso / Hansen`s disease: a purpose of a case

La lepra o enfermedad de Hansen es una enfermedad infecto contagiosa producida por el bacilo Mycobacterium leprae. Presenta dos tipos principales: la lepra tuberculoide, que produce grandes manchas hiperestésicas posteriormente anestésicas, y la lepra lepromatosa, que origina grandes nódulos en la piel. El tratamiento, hoy en día, varía entre seis meses y dos años, y se basa en la administración de sulfonas. Presentamos caso de masculino de 25 años de edad ingresado en el servicio de Medicina Interna del Hospital Sor Juana Inés de la Cruz con el diagnóstico de lepra lepromatosa confirmado posterior a reporte de biopsia de piel.