Blood cell alterations in Colossoma macropomum juveniles caused by silver nanoparticles.

This study evaluated the median lethal concentration of silver nanoparticles and their effects in fish tambaqui Colossoma macropomum. Therefore, an acute toxicity assay was carried out in completely randomized design evaluating six different concentrations of silver nanoparticles on blood parameters of tambaqui. The silver nanoparticles were produced by chemical reduction with polyvinyl alcohol (AgNP-PVA). The lethal concentration 50% (LC50) was estimated using probit regression. The blood was collected, analyzed and the data were submitted to T-test (dying x surviving fish) and Tukey test (surviving fish). An increase in glucose, hematocrit, total plasma protein, hemoglobin, erythrocytes, leukocytes, monocytes, and neutrophils as well as reduced MCV (mean corpuscular volume) in dying fish compared to surviving fish were observed. Survived fish exposed to 187.5 µg/L showed an increase in hematocrit, MCV, and MCH and a reduction in erythrocytes, total numbers of leukocyte, thrombocyte, lymphocyte, and neutrophil. The fish exposed to concentrations below 125 µg/L, had returned the blood parameter to baselines compared to control. The estimated LC50 was 165.09 µg/L and was classified as highly toxic for the fish tambaqui. In higher concentrations, it causes an acute respiratory toxicity, but in concentrations below 125 µg/L, the fish can adapt to the stressing agent.

Mechanism for increase in expression of cerebral diazepam binding inhibitor mRNA by nicotine: involvement of L-type voltage-dependent calcium channels.

We investigated the mechanisms underlying the increase in diazepam binding inhibitor (DBI) and its mRNA expression induced by nicotine (0.1 microM) exposure for 24 h using mouse cerebral cortical neurons in primary culture. Nicotine-induced (0.1 microM) increases in DBI mRNA expression were abolished by hexamethonium, a nicotinic acetylcholine (nACh) receptor antagonist. Agents that stabilize the neuronal membrane, including tetrodotoxin (TTX), procainamide (a Na(+) channel inhibitor), and local anesthetics (dibucaine and lidocaine), dose-dependently inhibited the increased expression of DBI mRNA by nicotine. The nicotine-induced increase in DBI mRNA expression was inhibited by L-type voltage-dependent Ca(2+) channel (VDCC) inhibitors such as verapamil, calmodulin antagonist (W-7), and Ca(2+)/calmodulin-dependent protein kinase II (CAM II kinase) inhibitor (KN-62), whereas P/Q- and N-type VDCC inhibitors showed no effects. In addition, nicotine exposure for 24 h induced [3H]nicotine binding to the particulate fractions of the neurons with an increased B(max) value and no changes in K(d). Under these conditions, the 30 mM KCl- and nicotine-induced 45Ca(2+) influx into the nicotine-treated neurons was significantly higher than those into non-treated neurons. These results suggest that the nicotine-stimulated increase in DBI mRNA expression is mediated by CAM II kinase activation resulting from the increase in intracellular Ca(2+) through L-type VDCCs subsequent to the neuronal membrane depolarization associated with nACh receptor activation.

Removal of hydroxyl radical facilitates Ca2+-dependent [3H]GABA release by peroxynitrite.

We investigated mechanisms for enhancement of peroxynitrite (OONO-; 5 microM)-evoked [3H] gamma-aminobutyric acid (GABA) release. Hydroxyl radical scavengers such as N,N'-dimethylthiourea (DMTU), mannitol, and uric acid, significantly increased OONO--evoked [3H]GABA release, whereas urea showed no effects on the release. Removal of Ca2+ from incubation buffer abolished the enhancement of the release by DMTU, although DMTU showed no effects on the basal release with and without Ca2+ in extracellular space. These results indicate that hydroxyl radical scavengers facilitate OONO--evoked [3H]GABA release dependent on Ca2+.

Suppression of Ca2+ influx through L-type voltage-dependent calcium channels by hydroxyl radical in mouse cerebral cortical neurons.

In the present study, we investigated the effect of hydroxyl radical (.OH) produced by the Fenton reaction with FeSO(4) to H(2)O(2) on Ca2+ influx by measuring [(45)Ca2+] influx into mouse cerebral cortical neurons in primary culture.OH formed from 3 microM FeSO(4) and 0.01 microM H(2)O(2) significantly reduced 30 mM KCl-induced [(45)Ca2+] influx and this reduction was abolished by .OH scavengers such as N,N'-dimethylthiourea and mannitol. Nifedipine (1 microM), an inhibitor for L-type voltage-dependent Ca2+ channels (VDCCs) showed no additive effect on the reduction of the 30 mM KCl-induced [(45)Ca2+] influx, while the inhibitors for P/Q- and N-type VDCCs showed further suppression of the KCl-induced [(45)Ca2+] influx even in the presence of .OH. Bay k 8644, an activator of L-type VDCCs, dose-dependently stimulated [(45)Ca2+] influx, and this stimulation disappeared in the presence of nifedipine. Similarly, .OH also suppressed significantly [(45)Ca2+] influx induced by Bay k 8644. These inhibitory actions of .OH on the KCl- and Bay k 8644-induced [(45)Ca2+] influx were completely abolished by .OH scavengers. These results indicate that .OH has the activity to suppress Ca2+ influx through L-type VDCCs.

Enhancement of peroxynitrite-evoked acetylcholine release by hydroxyl radical scavengers from mouse cerebral cortical neurons.

We investigated the effects of hydroxyl radical scavengers on peroxynitrite (OONO-)-evoked acetylcholine (ACh) release from mouse cerebral cortical neurons. N,N'-dimethylthiourea, a hydroxyl radical scavenger, dose-dependently increased OONO(-)-evoked ACh release. Other hydroxyl radical scavengers such as uric acid and mannitol, also enhanced OONO(-)-evoked ACh release, although these enhancing effects were not found in the absence of OONO-. In addition, OONO(-)-induced [45Ca2+]influx was significantly facilitated by the scavengers, whereas no effects of the scavengers on [45Ca2+]influx was observed in the absence of OONO-. These results indicate that hydroxyl radical scavengers enhance OONO(-)-evoked ACh release via the facilitation of OONO(-)-induced [45Ca2+]influx.

Multiple milia localized to the vulva.

Milia are most commonly observed on the cheeks and eyelids. We studied a case of multiple milia localized to the vulva in a 64-year-old female. A review of English and Japanese literature for the last 20 years failed to uncover any reports of milia limited to this area. We describe this case in detail and provide a short review of the literature on cysts of the genitalia.

Continuous treatment with morphine increases diazepam binding inhibitor mRNA in mouse brain.

Effects of acute and chronic morphine treatment on the expression of diazepam binding inhibitor (DBI) mRNA in the mouse brain were examined. Cerebral DBI mRNA expression significantly increased in morphine-dependent mice, and this increase is more remarkable in morphine-withdrawn mice, whereas a single administration of morphine (50 mg/kg) produced no changes in the expression. Simultaneous administration of naloxone (3 mg/kg) with morphine completely abolished the increase in cerebral DBI mRNA expression observed in morphine-dependent and -withdrawn mice. These results indicate that a chronic functional interaction between morphine and opioid receptors has a critical role in increases in DBI mRNA expression.

Peroxynitrite affects Ca2+ influx through voltage-dependent calcium channels.

The effect of peroxynitrite (OONO-) on voltage-dependent Ca2+ channels (VDCCs) was examined by measuring [45Ca2+] influx into mouse cerebral cortical neurones. OONO- time- and dose-dependently increased [45Ca2+] influx and this increase was abolished by manganese (III) tetrakis (4-benzoic acid) porphyrin, a scavenger for OONO-. Inhibition of cyclic GMP (cGMP) formation did not alter the OONO(-)-induced [45Ca2+] influx. OONO-, as well as 30 mm KCl, significantly increased fluorescence intensity of cell-associated bis-(1,3-dibutylbarbituric acid) trimethine oxonol (bis-oxonol). Tetrodotoxin and membrane stabilizers such as lidocaine dose-dependently suppressed OONO(-)-induced [45Ca2+] influx. Although each of 1 microM nifedipine and 1 microM omega-agatoxin VIA (omega-ATX) significantly inhibited the OONO(-)-induced [45Ca2+] influx and the concomitant presence of these agents completely abolished the influx, 1 microM omega-conotoxin GVIA (omega-CTX) showed no effect on the influx. On the other hand, OONO- itself reduced 30 mM KCl-induced [45Ca2+] influx to the level of [45Ca2+] influx induced by OONO- alone, and the magnitude of this reduction was as same as that of KCl-induced [45Ca2+] influx by omega-CTX. These results indicate that OONO- increases [45Ca2+] influx into the neurones through opening P/Q- and L-type VDCCs subsequent to depolarization, and inhibits the influx through N-type VDCCs.

[Pneumonia and mortality in patients requiring prolonged mechanical ventilation].

We examined patients who required prolonged (>60 days) mechanical ventilation. A total of 31 patients were studied, 23 with pulmonary disease, 4 with neurologic disease and 4 with other conditions. Many of these patients were elderly. The survival rates one year and two years after the start of mechanical ventilation were 40% and 33%, respectively. Respiratory tract infection was the most common and most serious complication, and ventilator-associated pneumonia was the main cause of death. It is difficult but quite important to prevent these complications, especially ventilator-associated pneumonia.

[Clinical and laboratory findings associated with the severity of community-acquired pneumonia].

To clarify the clinical features of severe community-acquired pneumonia, we retrospectively studied 121 patients treated at our hospital. We divided the patients into three groups, based on the severity, of their disease. Patients were put in the "mild" group (n = 56) if they recovered after treatment with antimicrobial agents only, they were put in the "moderate" group (n = 34) if the required oxygen therapy and recovered, and they were put in the "severe" group (n = 31) if they required mechanical ventilation. Age and underlying disease were recorded, as well as signs, symptoms, and laboratory data obtained during the first 24 hours after admission. The data indicated that the following nine findings were associated with the severity of disease: age of at least 65 years, an underlying disease of (31) the respiratory or central nervous system, dyspnea, a pulse rate of at least 90 beats per minute, a respiratory rate of at least 25 breaths per minute, an albumin concentration no greater than 3.5 g/dl, a blood urea nitrogen level of at least 20 mg/dl, a PaO2 no greater than 60 mmHg or an SaO2 no greater than 90%, and a high score on a scale of the extent of roentgenographic evidence of pulmonary infiltrates. Patients in whom these are found be managed carefully.

Prevalencia de las causas que producen trombofilias hereditarias y adquiridas en una población de la Ciudad de Córdoba-Argentina / Prevalence of the cause

RESUMEN:Objetivos: Estimar la prevalencia de las causas que producen trombosis venosa, arteriales o ambas a la vez en una población de 120 pacientes provenientes de la Ciudad de Córdoba. Materiales y métodos: Los niveles de antitrombina III (AT-III) proteína C(PC), proteína S(PS), resistencia a la activada(RPCa), anticuerpos antifosfolípidos (aPL), plasminpogeno (Pg), activador tisular del plaminógeno (tPA) pre y post-oclusión venosa y de su inhibidor (PAI-1) fueron evaluados en estos pacientes quienes presentaron manifestaciones rombólicas que fueron confirmadas con distintas técnicas radiológicas. Resultaods: La prevalencia estimada fueron los siguientes: AT-III: 41 por ciento; PC: 5,8 por ciento ; RPCa: 17,5 por ciento; Pg: 0,8 por ciento, aPL: 13,3 por ciento y tPA/PAI-1: 15 por ciento. En el 35,2 por ciento de los pacientes aqui evaluados no se pudo encontrar ninguna alteración de la hemostasia. Conclusiones: Los resultados aqui obtenidos son similares a los presentados por otros autores en otros países. De acuerdo a nuestros datos, las determinaciones de AT-III, PC, PS, RPCa y aP; deberían ser incluidas como "screening" inicial en la evaluación de pacientes con trombosis. Las alteraciones de los componentes del sistema fibrinolitico deberían ser tomados con precaución como probable causa de un estado trombofílico.