Valuable antiviral therapeutic options for the treatment of chronic hepatitis C patients with thrombocytopenia.

Thrombocytopenia in patients with chronic hepatitis C may represent an obstacle for the initiation of antiviral treatment. The aim of this study was to evaluate factors predictive of successful pegylated interferon (PEG-IFN) α2b and ribavirin (RBV) treatment for patients with thrombocytopenia with no history of splenectomy or partial splenic embolization. One hundred and fifty-one chronic hepatitis C patients (genotype 1: n = 110, genotype 2: n = 41) with TCP (<100 × 10(9) /L) at baseline were enrolled. Pretreatment variables included interleukin 28B (IL28B) genotype (rs8099917) and homoeostasis model assessment of insulin resistance score (HOMA-IR). The kinetics of haemoglobin and platelets according to the inosine triphosphatase (ITPA) genotype (rs1127354) were investigated. Sustained virological response (SVR) was significantly more frequent in hepatitis C virus (HCV) genotype 2 (65.9%) than in genotype 1 (34.5%) patients (P < 0.0001). Multiple logistic regression analysis of HCV genotype 1 extracted IL28B TT genotype [odds ratio (OR) 5.97, P = 0.006] and HOMA-IR <2.5 (OR 7.14, P = 0.0016) as significant independent pretreatment predictors of SVR. The analyses of HCV genotype 2 showed that HOMA-IR was significantly related to SVR, but IL28B genotype was not. Patients with ITPA CC genotype showed a significant haemoglobin reduction and lower degree of platelets decrease than those with ITPA CA/AA genotypes. The most common reason for premature discontinuation of treatment was the development of hepatocellular carcinoma (n = 8, 5.3%). In conclusion, HOMA-IR is a useful predictor of SVR for patients with thrombocytopenia infected with HCV genotype 1 or 2 treated with PEG-IFNα2b and RBV. The inclusion of IL28B, ITPA genotypes and HOMA-IR adds valuable therapeutic information.

Serum pepsinogen and Helicobacter pylori infection--a Japanese population study.

The decreased ratio of serum pepsinogen (PG) I and II has good correlation with the presence of atrophic gastritis. A total of 1,540 residents aged 30-89 years were enrolled into this study to investigate which serum PG level of residents with Helicobacter pylori infection would represent an adjunct to the diagnosis and progression of atrophic gastritis. All participants received esophagogastroduodenoscopy. Serum antibody to H. pylori (anti-H. pylori) was measured by an enzyme-linked immunosorbent assay (ELISA). Serological atrophic gastritis was defined as serum PG I isozyme level ≤70 ng/ml and a PG I/II ratio of ≤3.0. Of the 1,540 participants, 923 (59.9%) were positive for anti-H. pylori. Serological atrophic gastritis was found significantly more often in anti-H. pylori-positive participants (40.8%) than in anti-H. pylori-negative participants (7.9%) (p ≤ 0.0001). The endoscopic findings of anti-H. pylori-positive participants with serological atrophic gastritis were significantly more frequent by 4.06 times for atrophic gastritis (p ≤ 0.0001) than anti-H. pylori-negative participants without serological atrophic gastritis. Eight anti-H. pylori-positive participants were diagnosed with gastric cancer, but no cancer was found in anti-H. pylori-negative participants without serological atrophic gastritis. Serum PG testing is clinically useful for the prediction of gastric lesions in H. pylori-infected persons.

Utility of glycated albumin for the diagnosis of diabetes mellitus in a Japanese population study: results from the Kyushu and Okinawa Population Study (KOPS).

AIMS/HYPOTHESIS: Glycated albumin is a measure of the mean plasma glucose concentration over approximately 2-3 weeks. We determined reference values for glycated albumin, and assessed its utility for the diagnosis of type 2 diabetes mellitus in the general population. METHODS: We studied 1,575 men and women (mean age, 49.9 years; range, 26-78 years) who participated in a periodic health examination in a suburban Japanese town. HbA(1c) and fasting plasma concentrations of glucose (FPG) and glycated albumin were measured. Participants with FPG ≥ 7.0 mmol/l or HbA(1c) ≥ 6.5% (48 mmol/mol) were diagnosed as having diabetes. In our laboratory, the glycated albumin assay had intra-assay and inter-assay CVs of 1.1% and 1.6%, respectively. RESULTS: Glycated albumin levels were significantly correlated with HbA(1c) levels (r = 0.766, p < 0.001) and FPG (r = 0.706, p < 0.001). The presence of diabetes was significantly higher in participants with glycated albumin levels between 15.0% and 15.9% (five of 276, 1.81%) than in those with glycated albumin <14% (three of 672, 0.45%) (p = 0.037), and was markedly increased in those with a glycated albumin level >16% (58 of 207, 28.0%). Receiver operating characteristic curve analysis indicated that a glycated albumin level of ≥15.5% was optimal for predicting diabetes, with a sensitivity of 83.3% and a specificity of 83.3%. CONCLUSIONS/INTERPRETATION: There is merit to further investigating the potential for glycated albumin to be used as an alternative measure of dysglycaemia for future research and clinical practice.

Milrinone improves lung compliance in patients receiving mechanical ventilation for cardiogenic pulmonary edema.

BACKGROUND: Cardiogenic pulmonary edema is a frequent cause of respiratory failure. We investigated whether milrinone improved lung compliance. METHODS: We selected 10 patients with respiratory failure due to severe cardiogenic pulmonary edema to receive mechanical ventilation. Patients were administered a bolus injection of milrinone (50 microg kg-1) over 10 min, followed by continuous intravenous infusion (0.5 microg kg-1 min-1). Lung compliance, blood gas values, hemodynamic parameters, and sample plasma milrinone levels were assessed over 120 min after the onset of the continuous infusion of milrinone. RESULTS: Ten min following milrinone infusion, dynamic compliance (Cdyn) and static compliance (Cst) increased from 37 +/- 12 to 42 +/- 12 ml cmH2O-1 and from 40 +/- 13 to 45 +/- 12 ml cmH2O-1, respectively (P < 0.01). Plasma milrinone levels reached a therapeutic level for vasodilator and positive inotropic effect at 10 min after milrinone infusion. A significant decrease in mean pulmonary artery pressure and pulmonary artery wedge pressure occurred simultaneously with an increase in respiratory system compliance. However, an increase in cardiac index was observed later than these changes. There were significant correlations between the mean pulmonary artery pressure and Cdyn (r = -0.39, P < 0.01) and Cst (r = -0.38, P < 0.01). CONCLUSIONS: Milrinone-induced improvement in lung compliance along with an improvement of hemodynamics was found together with an inverse relationship between compliance and mean pulmonary artery pressure.

A new method for evaluating the bitterness of medicines by semi-continuous measurement of adsorption using a taste sensor.

We describe a new method for the evaluation of the bitterness of medicines by semi-continuous measurement of adsorption using a multichannel taste sensor or 'electric tongue'. The bitterness of 10 basic medicines was evaluated by both the taste sensor and in human gustatory sensation tests with 11 volunteers. The sensor part of the taste sensor consists of eight electrodes made of lipid/polymer membranes. Three variables were obtained from the taste sensor data: sensor output (S), the change of membrane potential caused by adsorption, corresponding to aftertaste (C), and the ratio C/S. These variables were used to predict an estimated bitterness score in multiple regression analysis. Semi-continuous measurement of C (every 30 s up to 150 s) was adopted as an additional explanatory variable, and the attenuation rate of C was defined as C'. These data were also subjected to multiple regression analysis. The correlation coefficient (r) estimated for the bitterness score predicted by the taste sensor, using C' for channel 2 and C/S for channel 4, and the score obtained by human gustatory sensation, was 0.824. This value was greater than that obtained using C/S for both channels 2 and 4 (0.734). The method described in the present study seems to offer good predictability for the evaluation of bitterness.

Effects of Pseudomonas aeruginosa endotoxin on vasodilation in the intact spinotrapezius muscle.

The purpose of this study was to determine whether short-term exposure to clinically relevant concentrations of Pseudomonas aeruginosa lipopolysaccharide (LPS) impairs vasoreactivity of resistance arterioles in the intact spinotrapezius muscle microcirculation and, if so, to determine the mechanisms mediating this response. Using intravital microscopy, we found that 60-min suffusion of P. aeruginosa LPS (0.03-3.0 microg/ml) on the in situ hamster spinotrapezius muscle elicited an immediate, profound, and prolonged concentration-dependent vasodilation (P < 0.05). This response was reversible once suffusion of P. aeruginosa LPS was stopped. Pretreatment with N(G)-nitro-L-arginine methyl ester (10.0 microM), a nonselective nitric oxide (NO) synthase inhibitor, but not N(G)-nitro-D-arginine methyl ester, abrogated P. aeruginosa LPS-induced vasodilation and elicited a small, albeit significant, vasoconstriction. Indomethacin had no significant effects on P. aeruginosa LPS-induced responses. P. aeruginosa LPS had no significant effects on acetylcholine- and nitroglycerin-induced vasodilation in the spinotrapezius muscle. Collectively, these data indicate that short-term exposure to clinically relevant concentrations of P. aeruginosa LPS evokes an immediate, potent, prolonged, and reversible NO-dependent, prostaglandin-independent vasodilation in skeletal muscles in vivo. We suggest this response could play an important role in the pathophysiology of the profound vasomotor dysfunction observed in the peripheral circulation of patients with P. aeruginosa sepsis syndrome.

PGH(2)-TxA(2)-receptor blockade restores vasoreactivity in a new rodent model of genetic hypertension.

The purpose of this study was to determine whether activation of prostaglandin H(2)-thromboxane A(2) (PGH(2)-TxA(2)) receptors impedes vasodilation in the in situ peripheral microcirculation of spontaneously hypertensive hamsters, a new rodent model of high-renin genetic hypertension. Using intravital microscopy, we found that vasodilation elicited by suffusion of acetylcholine and vasoactive intestinal peptide (VIP), two neurotransmitters localized in perivascular nerves in the peripheral circulation, on the in situ cheek pouch was significantly attenuated in spontaneously hypertensive hamsters relative to age- and genetically matched normotensive hamsters (P < 0.05). However, nitroglycerin-induced vasodilation was similar in both groups. Pretreatment with SQ-29548, a selective and potent PGH(2)-TxA(2)-receptor antagonist, restored acetylcholine- and VIP-induced vasodilation in spontaneously hypertensive hamsters. SQ-29548 had no significant effects on resting arteriolar diameter and on nitroglycerin-induced vasodilation in both groups. SQ-29548 slightly but significantly potentiated VIP- but not acetylcholine-induced vasodilation in normotensive hamsters. Collectively, these data indicate that activation of PGH(2)-TxA(2) receptors impedes agonist-induced vasodilation in the in situ cheek pouch of spontaneously hypertensive hamsters. We suggest that this model is suitable for studying the role of prostanoids in mediating vasomotor dysfunction observed in genetic hypertension.

Tyrosine kinase inhibitors modulate agonist-induced vasodilation in the hamster cheek pouch.

The purpose of this study was to determine whether inhibitors of tyrosine kinase attenuate vasodilation elicited by endogenously elaborated and exogenously applied nitric oxide in the in situ peripheral microcirculation. Using intravital microscopy, we found that pretreatment with genistein (1.0 microM) and tyrphostin 25 (10.0 microM), two structurally unrelated tyrosine kinase inhibitors, significantly attenuated acetylcholine-, bradykinin- and nitroglycerin-induced dilation of second-order arterioles (51 +/- 1 microm) in the in situ hamster cheek pouch (P < 0.05). Both inhibitors nearly abrogated acetylcholine-induced responses but only partially blocked bradykinin- and nitroglycerin-induced vasodilation. Genistein and tyrphostin 25 alone had no significant effects on resting arteriolar diameter and on adenosine-induced vasodilation in the cheek pouch. On balance, these data indicate that tyrosine kinase inhibitors attenuate endogenously elaborated and exogenously applied nitric oxide-induced vasodilation in the in situ hamster cheek pouch. However, the extent of tyrosine kinase inhibitor-sensitive pathway involvement in this response appears to be agonist dependent.

Dexamethasone attenuates acute macromolecular efflux increase evoked by smokeless tobacco extract.

The purpose of this study was to determine whether dexamethasone attenuates the acute increase in macromolecular efflux from the oral mucosa elicited by an aqueous extract of smokeless tobacco (STE) in vivo, and, if so, whether this response is specific. Using intravital microscopy, we found that 20-min suffusion of STE elicited significant, concentration-related leaky site formation and an increase in clearance of fluorescein isothiocyanate-labeled dextran (FITC-dextran; mol mass 70 kDa) from the in situ hamster cheek pouch (P < 0.05). This response was significantly attenuated by dexamethasone (10 mg/kg iv). Dexamethasone also attenuated the bradykinin-induced leaky site formation and the increase in clearance of FITC-dextran from the cheek pouch. However, it had no significant effects on adenosine-induced responses. Dexamethasone had no significant effects on baseline arteriolar diameter and on bradykinin-induced vasodilation in the cheek pouch. Collectively, these data indicate that dexamethasone attenuates, in a specific fashion, the acute increase in macromolecular efflux from the in situ oral mucosa evoked by short-term suffusion of STE. We suggest that corticosteroids mitigate acute oral mucosa inflammation elicited by smokeless tobacco.

Exogenous calmodulin potentiates vasodilation elicited by phospholipid-associated VIP in vivo.

The purpose of this study was to determine whether exogenous calmodulin potentiates vasoactive intestinal peptide (VIP)-induced vasodilation in vivo and, if so, whether this response is amplified by association of VIP with sterically stabilized liposomes. Using intravital microscopy, we found that calmodulin suffused together with aqueous and liposomal VIP did not potentiate vasodilation elicited by VIP in the in situ hamster cheek pouch. However, preincubation of calmodulin with liposomal, but not aqueous, VIP for 1 and 2 h and overnight at 4 degrees C before suffusion significantly potentiated vasodilation (P < 0.05). Calmodulin-induced responses were significantly attenuated by calmidazolium, trifluoperazine, and NG-nitro-L-arginine methyl ester (L-NAME) but not D-NAME. The effects of L-NAME were reversed by L- but not D-arginine. Indomethacin had no significant effects on calmodulin-induced responses. Calmodulin had no significant effects on adenosine-, isoproterenol-, acetylcholine-, and calcium ionophore A-23187-induced vasodilation. Collectively, these data indicate that exogenous calmodulin amplifies vasodilation elicited by phospholipid-associated, but not aqueous, VIP in the in situ peripheral microcirculation in a specific, calmodulin active sites-, and nitric oxide-dependent fashion. We suggest that extracellular calmodulin, phospholipids, and VIP form a novel functionally coordinated class of endogenous vasodilators.

Dexamethasone attenuates grain sorghum dust extract-induced increase in macromolecular efflux in vivo.

The purpose of this study was to determine whether dexamethasone attenuates grain sorghum dust extract-induced increase in macromolecular efflux from the in situ hamster cheek pouch and, if so, whether this response is specific. By using intravital microscopy, we found that an aqueous extract of grain sorghum dust elicited significant, concentration-dependent leaky site formation and increase in clearance of FITC-labeled dextran (FITC-dextran; mol mass, 70 kDa) from the in situ hamster cheek pouch (P < 0.05). This response was significantly attenuated by dexamethasone (10 mg/kg iv). Dexamethasone also attenuated substance P-induced leaky site formation and increase in clearance of FITC-dextran from the cheek pouch but had no significant effects on adenosine-induced responses. Dexamethasone had no significant effects on arteriolar diameter in the cheek pouch. On balance, these data indicate that dexamethasone attenuates grain sorghum dust extract- and substance P-induced increases in macromolecular efflux from the in situ hamster cheek pouch in a specific fashion.

A novel formulation of VIP in sterically stabilized micelles amplifies vasodilation in vivo.

PURPOSE: To determine whether human vasoactive intestinal peptide (VIP)-poly(ethylene glycol) (PEG)-grafted distearoyl-phosphatidylethanolamine (DSPE) micelles elicit potent and stable vasodilation in vivo. METHODS: PEG-DSPE micelles were prepared by co-precipitation. VIP was loaded into micelles by incubation at room temperature. Vasoactivity of VIP in SSM was determined by monitoring changes in diameter of resistance arterioles in the in situ hamster cheek pouch using intravital microscopy. RESULTS: VIP easily undergoes self-assembly into small PEG-DSPE micelles (mean [+/-SEM] size, 18+/-1 nm) in a time-dependent fashion. This generates a potent vasoactive matrix at nanomole concentrations of VIP as manifested by approximately 3-fold potentiation and prolongation of vasodilation relative to that evoked by aqueous VIP alone (p < 0.05). This response is specific and mediated by the L-arginine/nitric oxide (NO) biosynthetic pathway. Micellar VIP dispersion remains vasoactive for at least 14 days after preparation and storage at 4 degrees C. CONCLUSIONS: A novel, self-associated, small and stable PEG-DSPE micellar formulation of VIP amplifies vasodilation in the in situ peripheral microcirculation in a specific fashion by elaborating NO. An optimized formulation could be considered for certain cardiovascular disorders associated with L-arginine/NO biosynthetic pathway dysfunction.

Conformation and vasoreactivity of VIP in phospholipids: effects of calmodulin.

The purpose of this study was to determine the conformation and vasorelaxant effects of vasoactive intestinal peptide (VIP) self-associated with sterically stabilized phospholipid micelles (SSM) and whether calmodulin modulates both of these processes. Circular dichroism spectroscopy revealed that VIP is unordered in aqueous solution at room temperature but assumes appreciable a helix conformation in SSM. This conformational transition was amplified at 37 degrees C and by a low concentration of calmodulin (0.1 nM). Suffusion of VIP in SSM elicited significant time- and concentration-dependent potentiation of vasodilation relative to that elicited by aqueous VIP in the in situ hamster cheek pouch (P < 0.05). This response was significantly potentiated by calmodulin (0.1 nM). Collectively, these data indicate that exogenous calmodulin interacts with VIP in SSM to elicit conformational transition of VIP molecule from a predominantly random coil in aqueous environment to alpha helix in SSM. This process is associated with potentiation and prolongation of VIP-induced vasodilation in the in situ peripheral microcirculation.

Liposomal VIP attenuates phenylephrine- and ANG II-induced vasoconstriction in vivo.

The purpose of this study was to determine whether vasoactive intestinal peptide (VIP) modulates vasoconstriction elicited by phenylephrine and ANG II in vivo and, if so, to begin to elucidate the mechanisms underlying this phenomenon. Using intravital microscopy, we found that suffusion of phenylephrine and ANG II elicits significant vasoconstriction in the in situ hamster cheek pouch that is potentiated by VIP-(10-28), a VIP receptor antagonist, but not by VIP-(1-12) (P < 0.05). Aqueous VIP has no significant effects on phenylephrine- and ANG II-induced vasoconstriction. However, VIP on sterically stabilized liposomes (SSL), a formulation where VIP assumes a predominantly alpha-helix conformation, significantly attenuates this response. Maximal effect is observed within 30 min and is no longer seen after 60 min. Empty SSL are inactive. Indomethacin has no significant effects on responses induced by VIP on SSL. The vasodilators ACh, nitroglycerin, calcium ionophore A-23187, 8-bromo-cAMP, and isoproterenol have no significant effects on phenylephrine- and ANG II-induced vasoconstriction. Collectively, these data suggest that vasoconstriction modulates VIP release in the in situ hamster cheek pouch and that alpha-helix VIP opposes alpha-adrenergic- and ANG II-induced vasoconstriction in this organ in a reversible, prostaglandin-, NO-, cGMP-, and cAMP-independent fashion.

Vasodilation elicited by liposomal VIP is unimpeded by anti-VIP antibody in hamster cheek pouch.

The purpose of this study was to determine whether a monoclonal anti-vasoactive intestinal peptide (VIP) antibody, which binds VIP with high affinity and specificity and catalyzes cleavage of the peptide in vitro, attenuates VIP vasorelaxation in vivo and, if so, whether insertion of VIP on the surface of sterically stabilized liposomes (SSL), which protects the peptide from trypsin- and plasma-catalyzed cleavage in vitro, curtails this response. Using intravital microscopy, we found that suffusion of monoclonal anti-VIP antibody (clone c23.5, IgG2ak), but not of nonimmune antibody (myeloma cell line UPC10, IgG2ak) or empty SSL, significantly attenuates VIP-induced vasodilation in the in situ hamster cheek pouch (P < 0.05). By contrast, anti-VIP antibody has no significant effects on vasodilation elicited by isoproterenol, nitroglycerin, and calcium ionophore A-23187, agonists that activate intracellular effector systems in blood vessels that mediate, in part, VIP vasoreactivity. Suffusion of VIP on SSL, but not of empty SSL, restores the vasorelaxant effects of VIP in the presence of anti-VIP antibody. Collectively, these data suggest that VIP catalysis by high affinity and specific VIP autoantibodies displaying protease-like activity constitutes a novel mechanism whereby VIP vasoreactivity is regulated in vivo.

Mechanisms of vasodilation elicited by VIP in sterically stabilized liposomes in vivo.

The purpose of this study was to begin to determine the mechanisms underlying vasodilation elicited by vasoactive intestinal peptide (VIP) in sterically stabilized liposomes (SSL) in the in situ peripheral microcirculation. Using intravital microscopy, we found that suffusion of VIP in SSL (0.42 and 0.85 nmol) onto the hamster cheek pouch for 1 h elicited significant and prolonged concentration-dependent vasodilation (P < 0.05). Suffusion of VIP in SSL (0.1 nmol) for 7 min elicited a qualitatively similar response, although its magnitude was significantly smaller than that elicited by 1 h of suffusion of VIP in SSL (P < 0.05). The VIP-receptor antagonist VIP-(10-28), but not the amino-terminal fragment VIP-(1-12), significantly attenuated and delayed the onset of VIP in SSL-induced vasodilation (P < 0.05). The nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), but not NG-nitro-D-arginine methyl ester (D-NAME), abrogated VIP in SSL-induced responses. We conclude that VIP in SSL elicits significant and prolonged vasodilation in the in situ peripheral microcirculation, which is specific, partly receptor dependent, and partly transduced by the L-arginine/NO biosynthetic pathway.

[Stereotactic radiosurgery using a linear accelerator (LINAC): simulation and positioning].

Stereotactic radiosurgery using a Gamma unit obtains good results for small intracranial diseases, arteriovenous malformation (AVM) and acoustic neurinoma. In stereotactic radiosurgery using a linear accelerator (LINAC), many fundamental problems are to be solved. 1) accuracy of a LINAC, 2) making the collimators for high energy X-ray narrow beams, 3) dosimetry for high energy X-ray narrow beams, 4) irradiation methods for stereotactic radiosurgery, 5) fixation of a patient's head and 6) simulation of a target. The usefulness of our method for simulation of a target and for positioning for radiosurgery was investigated. High energy X-ray narrow beams obtained with the collimators for narrow beams (field sizes: 9mm phi, 18mm phi and 27mm phi) satisfy clinical requirements for stereotactic radiosurgery, as indicated by dose profiles and isodose curves. No dosimetry method for high energy X-ray narrow beams has been established yet. Of the main irradiation methods for stereotactic radiosurgery, the method using multiple non-coplanar converging arcs needs no drastic reconstruction for use with LINAC. A patient's head was completely fixed by the stereotactic frame (Patil stereotaxic system or Leksell micro-stereotactic system). Simulation of a target was performed under CT scan. On CT image, the center of a target was determined and the three-dimensional coodinate on the stereotactic head frame target was settled so that the target would be reached. The three-dimensional coordinate for the target was coincided with the isocenter of a LINA by the laser beams of three-directional pointers. Afterwards, the target position was finely adjusted, by using the target positioner manipulator system.(ABSTRACT TRUNCATED AT 250 WORDS)

Multichannel taste sensor using electric potential changes in lipid membranes.

A taste sensor with a multichannel electrode was developed by using lipid membranes as a transducer of taste substances. The sensor can detect the taste in a similar manner to the human gustatory sensation by response patterns of electric potential to taste substances. The sensitivity, reproducibility and durability were superior to those of humans. The same taste as that elicited by some commercial aqueous drink was reproduced by making aqueous solution mixed from four kinds of basic taste substances, the concentrations of which were determined so that the electric-potential pattern of this mixed solution could agree well with the pattern by the drink. Different brands of beer were easily distinguished by the electric-potential patterns.

[Anesthetic management of a patient with juvenile hyaline fibromatosis: a case report].

Juvenile hyaline fibromatosis (JHF) is a rare disease of autosomal recessive heredity characterized by multiple subcutaneous nodules, hypertrophy of the gingiva, and flexural contracture of the joints including those of the cervical vertebrae and the mandibula. It has been pointed out that the clinical features render tracheal intubation profoundly difficult. We present a case of 6-year-old girl diagnosed as JHF and anesthetized for tumor resection and reconstruction of the naso-oral region. She was significantly small for her age weight 12.3 kg and lived on a wheel-chair because of flexion contracture of the extremities. However, the cervical spinal joints were not involved and the neck could be extended in our case. With extreme care and preparation, anesthetic induction and tracheal intubation were smoothly done although a tooth was damaged by the surgeon when gauze-packing was attempted into the pharynx before the operation. Anesthesia was maintained uneventfully and satisfactorily during the surgery under anesthesia with nitrous oxide, oxygen, sevoflurane, fentanyl and vecuronium. There was no prolongation of nor abnormal reaction to the effect of vecuronium observed in this patient.