Invasive rhinomaxillary mucormycosis: a case report with a review of the literature

Mucormycosis is a rare, often fatal disease that is caused by zygomycetes, which are common fungi frequently found in the soil and decaying vegetation. Diabetes mellitus, malnutrition, and an immunocompromised state favor the growth of various microorganisms, including zygomycetes and the normal flora of the oral cavity, which are otherwise nonpathogenic, leading to opportunistic infections. Here we report a case of mucormycosis presenting with extensive necrosis of the maxilla along with rhinocerebral involvement in a 60-year-old patient suffering from uncontrolled diabetes with ketoacidosis.     

Acetaminophen toxicity up-regulates MRP2 expression in the liver of cats: an old story with new vision

This study was conducted to clarify the role of efflux transporter MRP₂ in acetaminophen-induced hepatotoxicity in cats. Sixteen mixed bred male cats and four liver samples from mixed breed male dogs were used. The cats were assigned into four groups (n?=?4), received saline and 2, 10 and 50?mg/kg doses of acetaminophen orally for 14 days. Unlike the intact dogs, the MRP₂ was not detectable in control cats. MRP₂ at mRNA level was expressed in the liver of cats, which received the medium and high doses. Data suggest that the MRP₂ expression may involve in the acetaminophen-induced hepatotoxicity in cats.     

EEG bei Janz-Syndrom (juvenile myoklonische Epilepsie) und anderen generalisierten Epilepsien

Clinical Epileptology - Die Elektroenzephalographie (EEG) ist die spezifischste technische Methode in der Evaluation von Epilepsien. Die typischen Befunde bei den sog. genetischen (idiopathischen)...     

Nitric oxide synthase inhibitors affect nitric oxide synthesis in normoxic but not in ischemic organs during intestinal ischemia and early reperfusion

Inhibition of endogenous nitric oxide (NO) synthesis during early intestinal ischemia/reperfusion (I/R(i)) enhances remote organ damage related to I/R(i). However, the effects of NO synthase (NOS) inhibitors on NO formation in various organs have not yet been specified. We therefore investigated the effects of N-G-monomethyl-L-arginine (L-NMMA), a nonspecific NOS inhibitor, and L-arginine, the NOS substrate, on NO formed in ischemic intestine versus normoxic remote organs (lung and liver). We used electron paramagnetic resonance spectroscopy and a specific NO trap to assay NO in blood, intestine, lung, and liver of rats subjected to local I/R(i), with and without L-NMMA and L-arginine supplementation. We found that I/R(i) increased NO levels in the intestine and blood, but not in the remote organs lung and liver. Administration of L-NMMA before I/R(i) decreased I/R(i)-independent basal NO levels in normoxic lung and liver without influencing I/R(i)-induced increase in NO levels in intestinal tissue or in blood. L-arginine supplementation increased circulating levels of NO, with sensitivity to L-NMMA, without affecting NO levels in normoxic or ischemic tissue. Our data suggest that NOS activity controls the NO generated in normally perfused remote organs during early I/R(i). Hence NOS inhibitors, when administered during I/R(i), decrease physiological NO levels in normoxic remote organs without affecting increased NO levels originating from ischemic intestine. This may explain the harmful effect of nonspecific NOS inhibitors during early I/R(i). In addition, the generation of NO in remote organs is not limited by tissue L-arginine concentrations and, therefore, not influenced by exogenous L-arginine. The protective effect of L-arginine supplementation during I/R(i) is probably related to increasing intravascular NO formation.     

Neuron-specific-enolase is increased in plasma after hemorrhagic shock and after bilateral femur fracture without traumatic brain injury in the rat

Neuron-specific enolase (NSE) is an acknowledged marker of traumatic brain injury. Several markers originally considered reliable in the setting of traumatic brain injury have been challenged after having been studied more extensively. The aim of our experimental study was to determine whether NSE is a reliable marker of traumatic brain injury early after trauma. Hemorrhagic shock was achieved by bleeding anesthetized rats to a mean arterial pressure (MAP) of 30-35 mmHg through a femoral catheter until incipient decompensation. MAP was maintained at 30-35 mmHg until 40% of shed blood had been administered as Ringer's solution and was then increased and maintained at 40-45 mmHg for 40 min by further administration of Ringer's solution, mimicking the phase of inadequate preclinical resuscitation. Blood samples were drawn at the end of the 40-min period of inadequate resuscitation. Femur fracture was achieved in anesthetized rats by bilateral application of forceps. Blood samples were drawn 30 and 60 min after fracture. Hemorrhagic shock caused NSE increase versus laboratory controls at the end of inadequate resuscitation (P < 0.01). Bilateral femur fracture caused NSE increase versus laboratory controls 30 min after fracture, which was significant 60 min after fracture (P < 0.01). During femur fracture, MAP remained at a level that is not associated with shock in rats. Our findings show for the first time that NSE increases after hemorrhagic shock as well as after femur fracture without hemorrhagic shock in rats. From a clinical point of view, these findings indicate that NSE cannot be considered a reliable marker of traumatic brain injury early after trauma in cases associated with hemorrhagic shock and/or femur fracture.     

Hemorrhage- and resuscitation-related alterations in gastrointestinal circulation: effect of a low dose of L-NMMA

The gastrointestinal tract, including its mucosal barrier, is most sensitive to ischemic insults. The present study was conducted to evaluate hemorrhage- and resuscitation-related regional alterations in gastrointestinal circulation in presence or absence of a low dose of N(G)-monomethyl-L-arginine (L-NMMA), a nonspecific nitric oxide synthase inhibitor. Organ-specific circulation was studied using the colored microsphere technique in rats subjected to prolonged hemorrhagic shock (180 min) followed by resuscitation with or without L-NMMA (2 mg/kg body weight) treatment at the end of resuscitation. We found an initial distal gradient in the intestinal blood flow with the highest rate in duodenum followed by jejunum, ileum, and colon. Hemorrhage resulted in the highest decrease in gastric blood flow. Resuscitation restored circulation in the intestinal tract to baseline levels except for gastric blood flow. L-NMMA treatment after completion of resuscitation did not deteriorate gastrointestinal blood flow. Our data show (a) a distal gradient in the intestinal blood flow from duodenum to colon, (b) that hemorrhage and resuscitation cause different degrees of alteration in gastric and intestinal blood flow, (c) that gastric perfusion does not recover after resuscitation, predisposing to further organ damage, and (d) that a low dose of L-NMMA does not deteriorate intestinal circulation in rats subjected to hemorrhage and resuscitation.     

Ictal asystole mimicking seizure deterioration in temporal lobe epilepsy

We report on a patient with temporal lobe epilepsy, secondary to a left lateral temporal cavernoma, in whom the change in seizure semiology suggested recurrence of secondary generalized seizures. Anticonvulsive medication previously controlled secondary generalized seizures over a period of years but focal seizures continued at a lower rate. Continuous video‐EEG monitoring revealed ictal asystole associated with myoclonic syncope and falls during focal seizures arising from the left temporal lobe. After implantation of a cardiac pacemaker, no more falls occurred during the focal seizures. In conclusion, recurrence of seizure‐associated falls is typically attributed to recurrence of secondary generalized seizures, however, ictal asystole should be considered in selected epilepsy patients as a differential diagnosis of falls. [Published with video sequence]