The Parker Flex-Tip tube for nasotracheal intubation: the influence on nasal mucosal trauma.

We tested our hypothesis that use of the Parker Flex-Tip tracheal tube could reduce the incidence of nasal mucosal trauma during nasotracheal intubation when compared with a conventional tip tracheal tube. One hundred and two patients, who were scheduled for elective oral surgery in which nasotracheal intubation was indicated to optimise the surgical approach, were recruited into this study. Either a Flex-Tip tracheal tube or a conventional tip tracheal tube was chosen randomly for each nasotracheal intubation. The incidence of epistaxis using the Flex-Tip tracheal tube (6 (11.8%)) was significantly lower than that with the conventional tip tracheal tube (18 (35.3%); p = 0.009). Nasal pain due to intubation, rated on a 100-mm visual analogue scale, was less intense with the Flex-Tip tracheal tube (median, (10th-90th percentile) 19 (12-28) mm compared with the conventional tip tracheal tube (30 (22-35) mm; p < 0.001). The Flex-Tip tracheal tube thus appeared to reduce the incidence of nasal mucosal trauma during nasotracheal intubation and the incidence of post-intubation nasal pain, compared with the conventional tip tracheal tube.

O2R, a novel regulatory element mediating Rox1p-independent O(2) and unsaturated fatty acid repression of OLE1 in Saccharomyces cerevisiae.

Fatty acid desaturation catalyzed by fatty acid desaturases requires molecular oxygen (O(2)). Saccharomyces cerevisiae cells derepress expression of OLE1 encoding Delta9 fatty acid desaturase under hypoxic conditions to allow more-efficient use of limited O(2). It has been proposed that aerobic conditions lead to repression of OLE1 by well-established O(2)-responsive repressor Rox1p, since putative binding sequences for Rox1p are present in the promoter of OLE1. However, we revealed in this study that disruption of ROX1 unexpectedly did not affect the O(2) repression of OLE1, indicating that a Rox1p-independent novel mechanism operates for this repression. We identified by promoter deletion analysis the 50-bp O(2)-regulated (O2R) element in the OLE1 promoter approximately 360 bp upstream of the start codon. Site-directed mutagenesis of the O2R element showed that the putative binding motif (5'-GATAA-3') for the GATA family of transcriptional factors is important for O(2) repression. Anaerobic derepression of OLE1 transcription was repressed by unsaturated fatty acids (UFAs), and interestingly the O2R element was responsible for this UFA repression despite not being included within the fatty acid-regulated (FAR) element previously reported. The fact that such a short 50-bp O2R element responds to both O(2) and UFA signals implies that O(2) and UFA signals merge in the ultimate step of the pathways. We discuss the differential roles of FAR and O2R elements in the transcriptional regulation of OLE1.

The E-box DNA binding protein Sgc1p suppresses the gcr2 mutation, which is involved in transcriptional activation of glycolytic genes in Saccharomyces cerevisiae.

Glycolytic gene expression is mediated by the Gcr1p-Gcr2p transcriptional activation complex. A screen for multicopy suppressors of gcr2 yielded SGC1. SGC1's suppression activity was specific to gcr2, it did not extend to gcr1. Disruption of SGC1 moderately affected glycolytic enzyme activities, although no growth defect was evident. Sgc1p exhibits a bHLH motif which is characteristic of E-box DNA-binding proteins. DNA footprinting experiments demonstrated Sgc1p's ability to bind at an E-box. However, its binding specificity was less than 10-fold, which is also characteristic of E-box binding proteins. LexA fusion experiments demonstrated that Sgc1p has weak intrinsic activating activity independent of GCR1 and GCR2. We propose that Sgc1p binds at E-boxes of glycolytic genes and contributes to their activation.

A series of protein phosphatase gene disruptants in Saccharomyces cerevisiae.

Thirty-two protein phosphatase (PPase) genes were identified in the genome nucleotide sequence of Saccharomyces cerevisiae. We constructed S. cerevisiae disruptants for each of the PPase genes and examined their growth under various conditions. The disruptants of six putative PPase genes, i.e. of YBR125c, YCR079w, YIL113w, YJR110w, YNR022c and YOR090c, were created for the first time in this study. The glc7, sit4 and cdc14 disruptants were lethal in our strain background. The remaining 29 PPase gene disruptants were viable at 30 degrees C and 37 degrees C, but only one disruptant, yvh1, showed intrinsic cold-sensitive growth at 13 degrees C. Transcription of the YVH1 gene was induced at 13 degrees C, consistent with an idea that Yvh1p has a specific role for growth at a low temperature. The viable disruptants grew normally on nutrient medium containing sucrose, galactose, maltose or glycerol as carbon sources. The ppz1 disruptant was tolerant to NaCl and LiCl, while the cmp2 disruptant was sensitive to these salts, as reported previously, and none of the other viable PPase disruptants exhibited the salt sensitivity. When the viable disruptants were tested for sensitivity to drugs, i.e. benomyl, caffeine and hydroxyurea, ppz1 and ycr079w disruptants exhibited sensitivity to caffeine.

Isolation and sequence of the GCR3 homologue from Candida albicans by complementation of (delta)gcr3 strain of Saccharomyces cerevisiae.

To study the function of GCR3, a gene involved in the expression of glycolytic genes in Saccharomyces cerevisiae, a Candida albicans gene which complements the growth defect of the (delta)gcr3 mutant was isolated. Transformants of this gene also recovered the glycolytic enzyme activities. Its DNA sequencing predicted an 886 amino acid protein with 30.4% identity to the Gcr3p of S. cerevisiae.

Isolation and characterization of mutations affecting expression of the delta9- fatty acid desaturase gene, OLE1, in Saccharomyces cerevisiae.

Expression of the delta9- fatty acid desaturase gene, OLE1, of Saccharomyces cerevisiae is negatively regulated transcriptionally and post-transcriptionally by unsaturated fatty acids. In order to isolate mutants exhibiting irregulation of OLE1 expression, we constructed an OLE1p-PHO5 fusion gene as a reporter consisting of the PHO5 gene encoding repressible acid phosphatase (rAPase) under the control of the OLE1 promoter (OLE1p). By EMS mutagenesis, we isolated three classes of mutants, pfo1, pfo2 and pfo3 positive regulatory factor for OLE1) mutants, which show decreased rAPase activity under derepression conditions (absence of oleic acid). Analysis of the transcription of OLE1 in these pfo mutants revealed that pfo1 and pfo3 mutants have a defect in the regulation of OLE1 expression at the transcriptional level while pfo2 mutants were suggested to have a mutation affecting OLE1 expression at a post-transcriptional step. In addition, four other classes of mutants, nfo1, nfo2, nfo3 and nfo4 (negative factor for OLE1) mutants that have mutations causing strong expression of the OLE1p-PHO5 fusion gene under repression conditions (presence of oleic acid), were isolated. Results of Northern analysis of OLE1 as well as OLE1p-PHO5 transcripts in nfo mutants suggested that these mutations occurred in genes encoding global repressors. We also demonstrated that TUP1 and SSN6 gene products are required for full repression of OLE1 gene expression, by showing that either tup1 or ssn6 mutations greatly increase the level of the OLE1 transcript.

Scanning electron microscopic studies of the palatine mucosa and its microvascular architecture in the rat.

Detailed observations were made on the structure and microvasculature of the palatine mucosa of the rat by means of microvascular corrosion casts and epithelium-digested specimens using scanning electron microscopy. The rat palate was divided into four regions according to the characteristics of the palatine plicae. In the atrial region, no transverse palatine plicae were present, but there were longitudinal ridges and folds in the median area. These structures contribute to the transportation of rough and grainy foods with the assistance of the hairy buccal part. Capillary loops in the ridge and folds appeared as continuous, sagittally elongated loops. In the palatine fissure or antemolar region, only three typical transverse palatine plicae contribute to the regurgitation of food. Capillary loops appeared in variant forms on the top, and the anterior and posterior slopes of the plicae. Venous palatine plexus was observed only in the palatine fissure region. In the intermolar region, each of the five transverse plicae was composed of many wedges arranged sagittally. These plicae contribute to the transportation of food toward the larynx. Capillary loops in the plica were in the shape of complicated villi. Filiform protrusions or papillae were aggregated immediately posterior to the last plica. The capillary loops appeared as typical hairpins. They contribute to swallowing of food with active assistance from the epithelial eminence of the lingual dorsum. Palatine plicae showed considerable local differences, which may contribute to the prehension, transportation, and mashing of food.

Effect of cerebral venous congestion on the pressure-volume index in the evaluation of intracranial pressure dynamics.

Translocation of cerebrospinal fluid (CSF) between the intracranial and spinal subarachnoid space was blocked by ligating the cervical spinal core in eight cats under pentobarbital and nitrous oxide anesthesia, and the effects of cerebral venous congestion on the pressure-volume index (PVI), a measure relating the change in intracranial volume, and the logarithm of intracranial pressure (ICP) were evaluated. The changes in the volume-pressure response (VPR), a measure of intracranial elastance, were calculated simultaneously. Cerebral venous congestion was induced by lowering the head relative to the level of the heart by tilting the trunk of the animals to 20 degrees below horizontal. The presence of venous congestion was confirmed by an increase in the sagittal sinus pressure (SSP). The body position was shifted from horizontal prone (H1 group) to head-down tilt (D1 group) in four animals (group 1) and from head-down tilt (D2 group) to horizontal prone (H2 group) in the other four animals (group 2), and PVI and VPR were determined in each group. The changes in ICP and SSP with change of body position in group 1 were not significantly different from those in group 2, with both pressures changing by 7-8 mm Hg. PVI showed no significant differences between the H1 group and H2 group or between the D1 group and D2 group. The mean (+/- SEM) PVI for all measurements in the head-down tilt position (D1 and D2 groups) was significantly higher (0.50 +/- 0.02 ml; p < 0.01) than in the horizontal position (H1 and H2 groups; 0.35 +/- 0.02 ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Microvascular architecture of the filiform papillae in primates and insectivores.

The microvascular architecture of filiform papillae was investigated under a scanning electron microscope in man, Japanese monkeys, common squirrel monkeys, common marmosets, common tree shrews, large Japanese moles and dwarf shrews utilizing microvascular corrosion casts. Filiform papillae were circularly arranged in primates, and each of them was supplied by a hairpin capillary loop. These papillae sometimes were aggregated. The filiform papillae of Japanese monkeys exhibited markedly locational differences on the lingual dorsum and were supplied by circularly arranged capillary loops or by an intrapapillary capillary network. Small filiform papillae were located on an epithelial eminence in the lingual radix, each of them supplied by a low and simple hairpin capillary loop. The aggregated filiform papillae of common squirrel monkeys were less frequent without any locational differences. Low filiform papillae of common marmosets and tree shrews were simpler in form, being arranged in a circle and supplied by a simple hairpin capillary loop. The filiform papillae of insectivores were not arranged in a circle. The filiform papillae of dwarf shrews were supplied by an incomplete capillary ring without a loop. With respect to species differences, the circularly arranged capillary loops in man were most complicated and highly developed. Microvascular architecture of the filiform papillae of insectivores was much simpler, different from those observed in primates.

[Mathematical simulation of intracranial condition--Part 1. Linear model stimulation].

We developed a linear mathematical model of the intracranial vessels, which reflects changes of the pulse wave (pulse pressure) of intracranial pressure after ligation of the internal jugular vein. The model composed of eight major variables: 1. resistance of arteries, 2. resistance of small arteries and capillary vessels, 3. resistance of veins, 4. resistance of internal jugular and vertebral veins, 5. compliance of arteries, 6. compliance of small arteries and capillary vessels, 7. compliance of veins and 8. intracranial compliance. All variables are presumed to have linear elements and replaced with electrical elements. The model of neck dissection is expressed as the change of resistance of the internal jugular and vertebral veins. Intracranial condition is expressed as the pulse wave (pulse pressure) of intracranial pressure and driving pressure. After unilateral ligation of the internal jugular vein, the pulse wave of intracranial pressure increased 24% and, after bilateral ligation of the internal jugular vein, it increased 55%. After unilateral ligation of the internal jugular vein, the pulse wave of intracranial pressure increased 27%, and, after bilateral ligation, it increased 79%. When intracranial compliance is normal, the respective ratios of pulse wave of intracranial pressure and driving pressure to cross-sectional area decreased, whereas those after increase of intracranial compliance increased.

[Effects of sevoflurane on intracranial pressure and formation and absorption of cerebrospinal fluid in cats].

The effects of sevoflurane on intracranial pressure (ICP) and the formation and absorption of cerebrospinal fluid (CSF) were examined in cats. Changes in ICP and superior sagittal sinus pressure (SSSP) were studied for 180 minutes during anesthesia with 1MAC sevoflurane (2.6%, inspired) and 50% N2O in O2. ICP increased significantly immediately after the start of anesthesia. The level remained for the subsequent 120 minutes, but increased significantly again 140 minutes after the start of anesthesia. There was no change in SSSP. The rate of CSF formation (Vf) was examined using the open ventriculocisternal perfusion method during anesthesia for 180 minutes with 1MAC sevoflurane or 1MAC enflurane (2.4%, inspired) and 50% N2O in O2. During sevoflurane administration, Vf decreased significantly 30 minutes after the start of anesthesia. In contrast, during enflurane administration, Vf increased significantly 10 minutes after the start of anesthesia. Finally, Vf and the rate of CSF absorption (Va) were measured under 1MAC sevoflurane or 1MAC enflurane and 50% N2O in O2 anesthesia, or under 50% N2O in O2 anesthesia. They were compared with ICP level. Vf decreased significantly when ICP level increased in all groups. The increase in Va when ICP level increased, was greater in the N2O group than in those anesthetized with sevoflurane or enflurane. The delayed increase of ICP under sevoflurane may have resulted in part from the cranial accumulation of CSF due to increased resistance to CSF absorption.

Effect of sevoflurane on intracranial pressure, sagittal sinus pressure, and the intracranial volume-pressure relation in cats.

The effect of sevoflurane on intracranial pressure (ICP), sagittal sinus pressure (SSP), and the intracranial volume-pressure (V-P) relation was examined in cats. In experiment 1, on nine cats, changes in ICP and SSP were studied for 180 min during anesthesia with 1 MAC sevoflurane (2.6%, inspired) and 50% nitrous oxide (N2O) in oxygen (O2). ICP significantly (p <0.01) increased from 8.4 +/- 3.8 cm H2O (mean +/- SD), the control level to 10.6 +/- 5.1 cm H2O immediately after the administration of sevoflurane. ICP was unchanged for the subsequent 120 min but then increased significantly (p <0.05) 140 min after administration, being 15.5 +/- 9.0 cm H2O at 180 min. There were no changes in SSP or blood gases. In experiment 2, the rapid injection technique of mock cerebrospinal fluid was used to determine the intracranial V-P relation in ten cats. Measures of V-P relationships included (a) ICP before volume injection (Po), (b) peak ICP caused by volume injection (Pp), (c) intracranial compliance (C) calculated as the ratio of change of intracranial volume Delta V) to change of ICP (Delta P), and (d) the pressure volume index (PVI) calculated as the ratio of Delta V to log Pp/Po. The subjects were divided into two groups, one administered 2.6% sevoflurane and 50% N2O in O2 (n = 6) and the other 50% N2O in O2 (n = 4). Each cat in both groups was given two bolus injections into the lateral ventricle at 180 min after the start of anesthesia. Then, C and PVI were calculated. C and PVI in the group treated with sevoflurane were significantly (p <0.05) lower than in the other group. These findings suggest that prolonged use of sevoflurane increases the intracranial elastance.

Effects of bilateral jugular vein ligation on intracranial pressure and cerebrospinal fluid outflow resistance in cats.

In order to study the effect of jugular venous outflow obstruction on intracranial pressure and cerebrospinal fluid (CSF) reabsorption capability, changes in epidural pressure (EDP) and CSF outflow resistance (Ro) were examined following bilateral jugular vein ligation in cats. EDP increased significantly (P less than 0.01) immediately after ligation from the control value of 4.9 +/- 0.5 mmHg (mean +/- SEM) to 15.9 +/- 0.9 mmHg. Thereafter, EDP gradually decreased back toward the control value. The pressure level had decreased to 6.7 +/- 0.5 mmHg by 20 minutes after ligation. The mean Ro was significantly (P less than 0.01) higher in the ligation group (200.4 +/- 9.7 mmHg/ml/min) that in the non-ligation group (120.0 +/- 9.9 mmHg/ml/min). These results suggest that bilateral jugular vein ligation impairs CSF reabsorption.

Effect of head-down tilt on intracranial pressure and sagittal sinus pressure during general anesthesia in cats.

The effect of head-down tilt during general anesthesia on intracranial pressure (ICP) dynamics was examined in eight cats. Changes in lateral ventricular pressure (LVP), sagittal sinus pressure (SSP), and effective CSF pressure (ECSFP), which is the driving pressure of cerebrospinal fluid (CSF) absorption, were studied in association with a shift from the horizontal prone position to the 20 degrees head-down tilt position. Both LVP and SSP values were significantly (P < 0.01) increased at 10 min in the head-down tilt position as compared with the control position, remained elevated during the next 110 min, and returned to baseline when the horizontal position was restored. However, ECSFP (expressed by LVP - SSP) was not significantly different from the control value, because changes in LVP and SSP were similar. These results suggest that head-down tilt does not impair CSF absorption.

[Influence of location for jugular venous blood sampling to cerebral circulatory index (CCI)].

When cerebral circulatory index (CCI) expressed as inverse of arterial-jugular venous oxygen content difference is measured, venous sampling at the internal jugular bulb needs to be done in order to avoid mixture with extra-cerebral perfusion blood. To estimate the validity of this point, difference of values calculated with blood obtained simultaneously at the jugular superior bulb, the inferior region and the cerebral sinus were examined in monkeys. As a result, no significant differences were found to result from location of the sampling, and significant correlation between PaCO2 and CCI was recognized. These findings supported the idea that CCI reflects the cerebral blood flow due to PaCO2 changes.