Microbial contamination of a disinfectant-soaked unwoven cleaning cloth.

In December 2009, a 76-year-old male patient developed pneumonia due to Burkholderia cepacia whilst in an intensive care unit at a Japanese university hospital. During the subsequent environmental investigation to find the source, B. cepacia with an identical DNA type was found in his denture storage solution. Open packets of unwoven rayon cloths soaked in 0.2% alkyldiaminoethylglycine hydrochloride, used for environmental cleaning, were shown to be contaminated with B. cepacia, Alcaligenes xylosoxidans, Pseudomonas fluorescens and Pseudomonas aeruginosa. B. cepacia of a different DNA type was found in five of 42 samples from sealed packets of cloths.

SAR analysis of the improved resonant cavity applicator with electrical shield and water bolus for deep tumors by a 3-D FEM.

This paper discusses the improvements of the re-entrant resonant cavity applicator, such as an electromagnetic shield and a water bolus for concentrating heating energy on deep tumors in an abdominal region of the human body. From our previous study, it was found that the proposed heating system using the resonant cavity applicator, was effective for heating brain tumors and also for heating other small objects. However, when heating the abdomen with the developed applicator, undesirable areas such as the neck, arm, hip and breast were heated. Therefore, we have improved the resonant cavity applicator to overcome these problems. First, a cylindrical shield made of an aluminum alloy was installed inside the cavity. It was designed to protect non-tumorous areas from concentrated electromagnetic fields. Second, in order to concentrate heating energy on deep tumors inside the human body, a water bolus was installed around the body. Third, the length of the lower inner electrode was changed to control the heating area. In this study, to evaluate the effectiveness of the proposed methods, specific absorption rate (SAR) distributions were calculated by FEM with the 3-D anatomical human body model reconstructed from MRI images. From these results, it was confirmed that the improved heating system was effective to non-invasively heat abdominal deep tumors.

Neurotrophin-3 and neurotrophin receptor immunoreactivity in peptidergic enteric neurons.

In the rat small intestine, neurotrophin-3 immunoreactivity was identified in ganglion cells and in processes mostly innervating the mucosa and occasionally the muscle layer and vasculature. The vast majority of neurotrophin-3 immunoreactive neurons contained vasoactive intestinal polypeptide (VIP), but not substance P or related tachykinin (SP/TK). Neurotrophin receptors visualized by pan-trk immunoreactivity were found in numerous ganglion cells of both plexuses and in nerve processes in the intestinal wall. Pan-trk submucosal neurons contained VIP (36%) or SP/TK-IR (47%). Pan-trk myenteric neurons contained VIP-IR (57%) or SP/TK (27%). Our data suggest that neurotrophin-3 and neurotrophin receptors may be involved in the maintenance of enteric neuronal circuits, transmission and phenotypic expression.

[Clinical features and outcomes of mechanically ventilated patients with acute respiratory failure during treatment with immunosuppressive drugs].

We examined clinical features and outcomes of mechanically ventilated patient (n = 11) retrospectively who had developed acute respiratory failure during treatments with immunosuppressive drugs. The mean APACHE II score was 22.6, and the mean lung injury score was 2.9. In eight patients chest X-ray and computed tomography showed interstitial pneumonia. Fungus and/or cytomegalovirus were isolated most often from patients with interstitial pneumonia. Observed mortality (72.7%) was significantly (P < 0.001) higher than predicted mortality (45.1%) in the APACHE II score. Patients, who were complicated with septic shock caused by fungus infection, showed poor mortality. These results suggest that the fungus and cytomegalovirus infections might be associated with poor prognosis in patients with acute respiratory failure during treatment with immunosuppressive drugs.

Effect of 5-(N,N-Dimethyl)-amiloride, a specific inhibitor of Na(+)/H(+) exchanger, on the palmitoyl-L-carnitine-induced mechanical and metabolic derangements in the isolated perfused rat heart.

The present study was carried out to determine the effect of 5-(N, N-dimethyl)-amiloride (DMA), a specific inhibitor of the Na(+)/H(+) exchanger, on the cardiac mechanical and metabolic derangements induced by palmitoyl-L-carnitine (PALCAR). Rat hearts were perfused aerobically at a constant flow according to the Langendorff technique, while being paced electrically. PALCAR (5 micromol/l) increased the left-ventricular end-diastolic pressure, decreased the left ventricular developed pressure (i.e. mechanical dysfunction), decreased the tissue level of ATP and increased the tissue level of AMP (i.e. metabolic change). DMA (10 or 20 micromol/l) attenuated the mechanical and metabolic alterations induced by PALCAR in a concentration-dependent way. Nevertheless, DMA (10 or 20 micromol/l) did not affect the mechanical function or energy metabolism in the normal (PALCAR-untreated) heart. These results suggest that inhibition of the Na(+)/H(+) exchanger with DMA is effective in attenuating the PALCAR-induced mechanical and metabolic derangements in the heart.

Inhibition of Na+ channel or Na+/H+ exchanger attenuates the hydrogen peroxide-induced derangements in isolated perfused rat heart.

The effect of tetrodotoxin, a specific inhibitor of the Na+ channel, and 5-(N,N-dimethyl)-amiloride, a specific inhibitor of the Na+/H+ exchanger, on the mechanical and metabolic derangements induced by hydrogen peroxide (H2O2) was studied in the isolated perfused rat heart. The isolated rat heart was perfused aerobically at a constant flow rate and driven electrically. H2O2 (600 microM) decreased the left ventricular developed pressure and increased the left ventricular end-diastolic pressure (i.e. mechanical dysfunction), decreased the tissue levels of adenosine triphosphate and adenosine diphosphate (i.e. metabolic derangement), and increased the tissue level of malondialdehyde (i.e. lipid peroxidation). These mechanical and metabolic derangements induced by H2O2 were significantly attenuated by tetrodotoxin (3 microM) or 5-(N,N-dimethyl)-amiloride (15 microM). Neither tetrodotoxin nor 5-(N,N-dimethyl)-amiloride modified the tissue malondialdehyde level, which was increased by H2O2. In the normal (H2O2-untreated) heart, neither tetrodotoxin nor 5-(N,N-dimethyl)-amiloride affected the mechanical function and energy metabolism. These results suggested that inhibition of the Na+ channel or Na+/H+ exchanger was effective in attenuating the H2O2-induced mechanical dysfunction and metabolic derangements in the isolated perfused rat heart.

Surgical/tourniquet pain accelerates blood coagulability but not fibrinolysis.

Tissue damage during surgery induces coagulation factors and activates platelets. Surgical pain may provoke release of catecholamines, leading to hypercoagulability. We have investigated the effect of surgical pain on blood coagulability and fibrinolysis in orthopaedic operations using tourniquets in 22 patients undergoing total knee replacement. Patients were allocated to one of two groups to receive extradural anaesthesia (EA; n = 11) or general anaesthesia (GA; n = 11). The EA group received lumbar extradural block with lidocaine. The GA group received only general anaesthesia, maintained with 1.5-2.5% sevoflurane and 66% nitrous oxide in oxygen. Using a thrombelastogram technique, blood coagulability and fibrinolysis were measured. Mean maximum amplitude (MA), which reflects coagulability, increased after tourniquet inflation (11%) in group GA whereas MA in group EA did not change. After tourniquet deflation, MA values in both GA and EA groups increased significantly (10% and 20%, respectively) (P < 0.05), and there was also a significant difference in MA between groups (P < 0.05). The fibrinolytic rate did not change in either group during tourniquet inflation, but increased significantly (160%) after tourniquet deflation. There was no significant difference in fibrinolytic rate between the groups. We conclude that the hypercoagulability seen in group GA could have been caused by surgical or tourniquet pain, or both, and that extradural anaesthesia is a useful technique to prevent hypercoagulability.

[The effect of scalp infiltration with bupivacaine on blood coagulability and fibrinolysis in neurovascular surgery].

We investigated the effect of scalp infiltration with bupivacaine on blood coagulability and fibrinolysis in neurovascular surgery. Patients were randomly divided into two groups: scalp infiltration group (who received scalp infiltration with 0.5% bupivacaine prior to surgical incision, n = 7) and control group (n = 6). The blood coagulability and fibrinolysis were measured before and after surgical incision using a thromboelastogram (Thromboelastograph C-3000, Haemoscope). In the control group, the reaction and coagulation times were significantly shortened (30% and 23%, respectively, P < 0.05) and the maximum amplitude, which reflects coagulability, increased significantly (21%, P < 0.01) compared to each presurgical value. The scalp infiltration prior to the surgical incision prevented these reactions (P < 0.05). The fibrinolytic rate did not change in either group. We conclude that scalp infiltration prior to surgical incision is beneficial for attenuating an increase in blood coagulability, which could induce perioperative complications due to associated systemic diseases (i.e. hypertension, diabetes, ischemic heart disease, etc.).

Propofol improves functional and metabolic recovery in ischemic reperfused isolated rat hearts.

UNLABELLED: Propofol attenuates mechanical dysfunction, metabolic derangement, and lipid peroxidation by exogenous administration of H2O2 in the Langendorff rat heart. In this study, we examined the effects of propofol on mechanical and metabolic changes, as well as on lipid peroxidation induced by ischemia-reperfusion, in isolated, working rat hearts. Rat hearts (in control-modified Krebs-Henseleit bicarbonate buffer) were treated with two doses (25 microM and 50 microM) of propofol in an intralipid vehicle. In the first protocol, propofol was administered during the preischemic and reperfusion period, whereas in the second, it was only administered during the reperfusion period. Ischemia (15 min) decreased peak aortic pressure (PAOP), heart rate (HR), rate-pressure product (RPP), coronary flow (CF), and tissue concentrations of adenosine triphosphate (ATP) and creatine phosphate. After postischemic reperfusion (20 min), the CF and tissue concentration of ATP recovered incompletely; however, PAOP, HR, and RPP did not. Ischemia-reperfusion also increased the tissue concentration of malondialdehyde (MDA). In both protocols, both doses of propofol enhanced recovery of PAOP, HR, RPP, CF, and tissue concentration of ATP during reperfusion, and inhibited the tissue accumulation of MDA. These results indicate that propofol improves recovery of mechanical function and the energy state in ischemic reperfused isolated rat hearts, and the mechanism may involve the reduction of lipid peroxidation during postischemic reperfusion. IMPLICATIONS: We evaluated the possible cardioprotective effects of propofol in isolated, working rat hearts subjected to 15-min ischemia, followed by 20-min reperfusion. We observed that propofol attenuated mechanical dysfunction, metabolic derangement, and lipid peroxidation during reperfusion. This latter finding seems to be one mechanism for cardioprotective effects of propofol.

Flow injection analysis of potassium using an all-solid-state potassium-selective electrode as a detector.

The concentration of potassium was determined by a combination of flow injection analysis (FIA) with an all-solid-state potassium sensor detection. The all-solid-state potassium-selective electrode possessing long-term potential stability was fabricated by coating an electroactive polypyrrole/poly(4-styrenesulfonate) film electrode with a plasticized poly(vinyl chloride) membrane containing valinomycin. The simple FIA system developed in this laboratory demonstrated sensitivity identical to that in the batch system and achieved considerably rapid assay (150 samples h(-1)). Analyses of soy sauce and control serum samples by this FIA system yielded results in good agreement with those obtained by conventional measurements.

Lidocaine attenuates mechanical and metabolic derangements induced by palmitoyl-L-carnitine in the isolated perfused rat heart.

The effect of lidocaine on the palmitoyl-L-carnitine (PALCAR)-induced mechanical and metabolic derangements was studied in Langendorff rat hearts, perfused aerobically at a constant flow rate and paced electrically. PALCAR (5 mumol/l) increased the left ventricular end-diastolic pressure, decreased the left ventricular developed pressure (i.e., mechanical dysfunction), and decreased the tissue levels of adenosine triphosphate and creatine phosphate (i.e., metabolic change). These mechanical and metabolic alterations induced by PALCAR were concentration-dependently attenuated by lidocaine (20, 50 or 100 mumol/l). Nevertheless, lidocaine (20, 50 or 100 mumol/l) did not affect the mechanical function and energy metabolism of the normal (PALCAR-untreated) heart. These results indicate that lidocaine has a cardioprotective action against the PALCAR-induced mechanical and metabolic derangements.

Beneficial effects of dilazep on the palmitoyl-L-carnitine-induced derangements in isolated, perfused rat heart: comparison with tetrodotoxin.

The present study was carried out to determine the effect of dilazep, having an inhibitory effect on the Na+ channel, on the mechanical dysfunction and metabolic derangements induced by palmitoyl-L-carnitine in isolated rat heart and to compare the effect of dilazep with that of tetrodotoxin, a specific inhibitor of the Na+ channel. Rat hearts were perfused aerobically at a constant flow according to Langendorff's technique and paced electrically. Palmitoyl-L-carnitine (5 microM) decreased the left ventricular developed pressure and increased the left ventricular end diastolic pressure (i.e., it produced mechanical dysfunction), decreased the tissue level of adenosine triphosphate and increased the tissue level of adenosine monophosphate (i.e., it produced metabolic derangements). These mechanical and metabolic alterations induced by palmitoyl-L-carnitine were attenuated by either dilazep (1 microM) or tetrodotoxin (3 microM). On the other hand, neither dilazep nor tetrodotoxin modified the mechanical function and energy metabolism of the normal (palmitoyl-L-carnitine-untreated) heart. These results suggest that inhibition of the Na+ channel with dilazep or tetrodotoxin is responsible, at least in part, for attenuating the palmitoyl-L-carnitine-induced mechanical dysfunction and metabolic derangements in the heart.

Cellular localization of Pan-trk immunoreactivity and trkC mRNA in the enteric nervous system.

The members of the trk family of tyrosine receptor kinases, trkA, trkB, and trkC, are the functional receptors for neurotrophins, a family of related neurotrophic factors. In this study, we investigated 1) the distribution of neurotrophin receptors in the developing and adult rat digestive tract with a pan-trk antibody that recognizes all known trks and 2) the cellular localization of trk-encoding mRNAs in the adult gut with single-stranded RNA probes specific for trkA, trkB, and trkC. In the developing myenteric plexus, trk immunoreactivity was present at embryonic day (ED) 14. Cells and fibers immunoreactive for trk could be visualized in the myenteric plexus at ED 16. At this age, dense staining was found in thick bundles of fibers in proximity to the myenteric plexus in the longitudinal muscle and in association with blood vessels in the mesentery. At ED 18, trk immunoreactivity was also seen in thin processes running from the myenteric plexus into the circular muscle, and in fibers and cells in intrapancreatic ganglia. By ED 20, immunoreactive staining was quite dense in both the myenteric and submucosal plexuses. At birth, virtually all enteric ganglia displayed strong trk immunoreactivity; the intensity of the staining at this age made it difficult to discern individual cells. During postnatal development, there was a decrease in cell body staining and an increase in the density of trk-containing fibers that became widely distributed to the gut wall and pancreas. The adult pattern of trk immunoreactivity was established between postnatal days 5 and 10. In adults, trk immunoreactivity was found in numerous enteric and intrapancreatic ganglion cells and in dense networks of fibers innervating all the layers of the gut, the pancreas, and vasculature. The trkC mRNA was expressed in adult enteric ganglion cells of both the myenteric and submucous plexus. By contrast, the trkA and trkB mRNAs could not be detected in enteric ganglia. All three trk mRNAs were expressed in dorsal root ganglia, which were used as positive controls. The density and wide distribution of trk immunoreactivity together with its persistence in adulthood support the concept that neurotrophins play a broad role in the digestive system from development through adult life, perhaps being involved in differentiation, phenotypic expression, and tissue maintenance. The presence of trkC mRNA in enteric neurons along with recent evidence that neurotrophin-3 plays a role in the development of the enteric nervous system suggest that trkC and neurotrophin-3 are a major neurotrophin system in the gastrointestinal tract.

[A case of emergency admission for CO2 narcosis in a patient with amyotrophic lateral sclerosis].

A 68-year-old man with severe dyspnea was admitted as an emergency case. He had no past history of any respiratory or neuromuscular diseases. Immediately after insufflation of oxygen, respiratory arrest occurred. The blood gas analysis showed hypoxemia and severe hypercapnia (PaO2; 32 mmHg, PaCO2; 127 mmHg). We diagnosed as CO2 narcosis, and he was treated with a respirator in the ICU. He showed nonflaccid bilateral diaphragmatic paralysis and muscle atrophy of the upper extremities. As the EMG showed giant spikes of neurogenic pattern, he was diagnosed as ALS. Weaning from the respirator failed because of his respiratory muscle fatigue. He was given rehabilitation during the day time and ventilatory support with the respirator during the night. We conclude that if we meet with an emergency patient with CO2 narcosis without any pulmonary disorder, we have to suspect neuromuscular diseases, e.q. ALS. In some of such cases, mechanical ventilation supports social rehabilitation.

[Continuous infusion of ketamine and midazolam for prolonged sedation in the intensive care unit].

The clinical effects and pharmacokinetics of ketamine and midazolam, administered continuously for prolonged sedation were studied in 7 critically ill patients under mechanical ventilation. Initially ketamine 1 mg.kg-1 and midazolam 0.1 mg.kg-1 were administered intravenously and these were followed by infusion at a rate of 1.0 mg.kg-1.hr-1 of ketamine and 0.05 mg.kg-1.hr-1 of midazolam. The infusion rate was changed every 30 minute with increments of 0.5 mg.kg-1.hr-1 of ketamine and 0.05 mg.kg-1.hr-1 of midazolam until the sedative score by Ramsy RAE reached rank 4 (i.e. slow response to loud verbal commands). The plasma concentrations of ketamine were analyzed using high performance liquid chromatography and those of midazolam using gas chromatography. The mean maintenance doses of ketamine and midazolam were 2.25 +/- 0.61 mg.kg-1.hr-1 and 0.11 +/- 0.05 mg.kg-1.hr-1 (mean +/- SD), respectively. There were no significant changes in blood pressure or heart rate before and after the injection of ketamine and midazolam in all the patients. The plasma concentrations of ketamine and midazolam were 2.98 +/- 0.20 micrograms.ml-1 and 494.1 +/- 66.7 ng.ml-1, respectively. The time to clear response to verbal commands after cessation of the continuous infusion was 168 +/- 109 min. The plasma concentrations of ketamine and midazolam decreased rapidly, and plasma half-life of ketamine was about 1 hour and for midazolam less than 2 hours. In conclusion, continuous infusion of ketamine and midazolam was very useful to sedate critically ill patients under mechanical ventilation, with minimal effect on the cardiovascular system and rapid recovery of consciousness.