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Biomedical subjects

A Nonaka

Publications and source records attributed to A Nonaka.

At least 19 recordsLinked to original sources

Clinical assessment of oral malodor by the electronic nose system.

A recently developed electronic nose has not yet been clinically applied to evaluations of oral malodor. This investigation sought to determine whether an electronic nose could clinically assess oral malodor. Twenty-nine healthy adults and 49 patients were assessed by results of an actual organoleptic test, a score representing malodor strength with an electronic nose in "top-note" mode (top-note score), and measurements of volatile sulfur compound (VSC) concentrations. The correlation coefficient between top-note and actual organoleptic scores (r = 0.71) was comparable with the log VSC and actual organoleptic scores (r = 0.63). However, the area under the receiver-operating characteristic plots for top-note score was significantly larger than that for log VSC. In logistic regression analyses with top-note score as a dependent variable, probing depth, tongue coating, and plaque control record each had independent associations. Our findings suggest that the top-note score from an electronic nose examination may be useful for the clinical evaluation of oral malodor.

Adult↗

Suppressive effects of selectin inhibitor SKK-60060 on the leucocyte infiltration during endotoxin induced uveitis.

BACKGROUND: It is well known that selectin is involved in the development of endotoxin induced uveitis (EIU), and has a major role in leucocyte infiltration. Recently, a novel selectin inhibitor (SKK-60060) that can block P and L selectins in vitro has been developed. This study was designed to investigate the anti-inflammatory effects of SKK-60060 on the inflammatory reaction during EIU in rats by studying leucocyte-endothelium interactions. METHODS: EIU was induced in Lewis rats by footpad injection of lipopolysaccharide (LPS). SKK-60060 was administered 15 minutes before LPS injection, and its suppressive effects on inflammatory leucocyte behaviour were evaluated in vivo with acridine orange digital fluorography; the diameters of retinal arteries and veins were also measured. After these studies, aqueous humour was collected to evaluate leucocyte infiltration and protein leakage. RESULTS: After LPS injection, rolling leucocytes were observed in major retinal veins, followed by leucocyte infiltration into the vitreous cavity. Following treatment with SKK-60060, leucocyte rolling was significantly inhibited in the retinal veins (p <0.01), and subsequent leucocyte infiltration into the vitreous cavity was also significantly suppressed (p <0.01). Retinal vasodilation was also substantially suppressed in SKK-60060 treated rats (p <0.01). Similarly, leucocyte infiltration and protein leakage into the aqueous humour were reduced significantly by SKK-60060 (p <0.01). CONCLUSIONS: SKK-60060 treatment significantly inhibited the inflammatory reaction induced by LPS. Its inhibitory effects on P and L-selectin resulted in suppression of leucocyte infiltration and the subsequent inflammatory reaction caused by accumulated leucocytes. The current findings suggest that SKK-60060 may be useful in the management of uveitis.

Animals↗

Up-regulation by clarithromycin of alpha(1)-acid glycoprotein expression in liver and primary cultured hepatocytes.

alpha(1)-Acid glycoprotein (AGP) is the major transport protein for cationic drugs, endogenous ligands, and some anionic drugs in plasma. Hepatic synthesis and secretion of AGP are altered during acute inflammation as well as by a number of drugs. This alteration could influence the binding of drugs and its biological function. Macrolide antibiotics are widely used in the treatment of a variety of infectious diseases. The effects of macrolide antibiotics have been studied with respect to rat AGP expression in vivo. After the individual administration of six macrolides to rats, with the exception of oleandomycin, five increased AGP levels in serum. Of these five, clarithromycin (CAM) was the most potent inducer of AGP, which reached a maximum level between 3 to 7 days after administration. CAM increased the steady-state level of AGP mRNA in liver as well as protein level in serum in a dose-dependent manner. In addition, CAM increased AGP mRNA levels in primary cultured hepatocytes. In the luciferase promoter assay, CAM potentiated dexamethasone-increased promoter activity of the AGP gene, which contained the glucocorticoid response element, in cultured rat hepatocytes, although CAM itself had no effect on its activity. The effect of CAM and dexamethasone was diminished by glucocorticoid response element deletion or mutation or by adding the antiglucocorticoid, RU486. Further, in the mouse mammary tumor virus (MMTV) promoter containing functional glucocorticoid response element, CAM potentiated dexamethasone-increased promoter activity. In the adrenalectomized rats, CAM did not increase AGP levels in serum. These findings suggest that CAM may cause transcriptional induction of AGP, at least in part, via a glucocorticoid-mediated mechanism.

5' Untranslated Regions↗

Suppressive effects of histamine H1 receptor antagonist diphenhydramine on the leukocyte infiltration during endotoxin-induced uveitis.

Histamine has been shown to play an important role in the step of leukocyte rolling, the initial step to leukocyte infiltration into an inflamed region. We investigated the roles of histamine in the leukocyte recruitment during endotoxin-induced uveitis (EIU) in vivo using acridine orange digital fluorography. An injection of histamine into the vitreous cavity of a Lewis rat induced leukocyte rolling along the major retinal veins. In other experiments, EIU was induced in Lewis rats by footpad injection of lipopolysaccharide (LPS). Leukocyte rolling was also observed in the retinal veins of EIU rats. To block the histamine H1 receptor, diphenhydramine (DPH) was administered intraperitoneally 15 min before the LPS injection. DPH significantly inhibited leukocyte rolling along the major retinal veins of EIU rats, suppressing leukocyte infiltration into the vitreous cavity. The vasodilation in EIU was also significantly suppressed with DPH. Moreover, leukocyte infiltration into aqueous humor was significantly suppressed in DPH-treated rats. Although the inhibitory effects of DPH was less obvious at later time points, addition of DPH every 12 hr showed prolonged anti-inflammatory effects up to 48 hr after LPS injection. In contrast, protein leakage into the aqueous humor was not suppressed as much as leukocyte infiltration with DPH. These results suggest that histamine would play a pivotal role in leukocyte recruitment during EIU in rats. Blocking the histamine H1 receptor might help to prevent or minimize leukocyte infiltration in uveitis.

Animals↗

Atypical form of dural graft associated Creutzfeldt-Jakob disease: report of a postmortem case with review of the literature.

A postmortem case of an atypical form of dural graft associated Creutzfeldt-Jakob disease (CJD) is described. A 42 year old man developed progressive spastic paresis 163 months after a cadaveric dura mater graft. He presented with no myoclonus and very late occurrence of periodic synchronous discharges on EEG. The prion protein (PrP) gene was homozygous for methionine at the polymorphic codon 129. Neuropathological examination disclosed plaque-like PrP deposits with atypical distribution of synaptic PrP accumulations in the brain. This patient represents an atypical form of dural graft associated CJD characterised by unusual clinicopathological features.

Adult↗

Effects of propofol on ischemia and reperfusion in the isolated rat heart compared with thiamylal.

The aim of the present study was to investigate whether clinical doses of propofol and thiamylal affect oxygen free radical production and intracellular calcium concentration ([Ca2+]i) in the post-ischemic reperfused heart. Forty-eight rat hearts were perfused with a Langendorff system and loaded with Fura-2 / AM as a [Ca2+]i marker. The hearts were divided into 6 groups as follows (each group: n = 8); Group S (saline), Group TL (thiamylal 100 microM), Group TH (thiamylal 300 microM), Group I (Intralipid), Group PL (propofol 3 microM), and Group PH (propofol 10 microM). All hearts were initially perfused for 5 min as control aerobic perfusion. Afterwards, no-flow ischemia was induced for 15 min, followed by reperfusion for 20 min. The formation of hydroxyl radicals in the coronary effluent was measured with high performance liquid chromatography using salicylic acid. At the beginning of the ischemia and reperfusion periods, increases in systolic and diastolic [Ca2+]i were observed in all groups except Group TH. The high dose of thiamylal significantly suppressed this initial increase in cytosolic [Ca2+]i (Group S 1.30+/-0.15; Group TL 0.99+/-0.17; Group TH 0.70+/-0.09, at 1 min after reperfusion; systolic [Ca2+]i : p < 0.05). Total DHBAs in the coronary effluent of all groups increased significantly 1 min after reperfusion, however, there were no significant differences among the groups. Clinical doses of propofol had no significant effect on myocardial function and [Ca2+]i before and after ischemia, whereas thiamylal suppressed the increase in [Ca2+]i during ischemia and reperfusion. However, free radical formation during reperfusion was unaffected by thiamylal and propofol.

Analysis of Variance↗

[Anesthetic management for mitral valve replacement in a patient with idiopathic hypereosinophilic syndrome].

We have experienced anesthetic management for mitral valve replacement in a 48-year-old female with idiopathic hypereosinophilic syndrome. Preoperative examination showed mild biventricular dysfunction. Anesthesia was induced and maintained with meticulous administration of fentanyl and midazolam in 66% oxygen. Administration of dopamine, dobutamine and prostaglandin E1 contributed to reducing afterload and maintaining cardiac output. The operative and postoperative courses were uneventful. Hypereosinophilic syndrome is one of the identified causes of restrictive cardiomyopathy. Anesthesia for patients with hypereosinophilic syndrome must be carried out carefully, because heart or respiratory failure is the most dangerous complication. In patients with hypereosinophilic syndrome requiring general anesthesia, perioperative steroid cover is advisable. This may reduce or prevent serious lung complications.

Anesthesia, General↗

Inhibitory effects of antithrombin III against leukocyte rolling and infiltration during endotoxin-induced uveitis in rats.

PURPOSE: This study was designed to investigate the suppressive effects of antithrombin (AT)III on inflammatory reactions during endotoxin-induced uveitis (EIU) in rats by studying leukocyte-endothelium interactions. METHODS: EIU was induced in Lewis rats by footpad injection of lipopolysaccharide (LPS). ATIII was administered immediately after or at 6 hours after LPS injection. Its suppressive effects on inflammatory leukocyte behavior were evaluated in vivo with acridine orange digital fluorography. Clinical signs of inflammation were also examined, and aqueous humor (AH) was collected to evaluate leukocyte infiltration and protein leakage. In a separate experiment, P-selectin mRNA expression was studied in the iris-ciliary body (ICB) and the retina. RESULTS: After treatment with ATIII, leukocyte rolling was substantially inhibited along the retinal veins, suppressing subsequent leukocyte infiltration into the vitreous cavity. Similarly, leukocyte infiltration and protein leakage into the AH were significantly reduced with ATIII treatment. The clinical grade of EIU was substantially lower in ATIII-treated rats. In addition, delayed administration of ATIII after EIU induction significantly attenuated these inflammatory reactions. The levels of P-selectin mRNA expression in both ICB and retina, which were upregulated after LPS injection, were substantially lower in the ATIII-treated rats. CONCLUSIONS: ATIII treatment significantly inhibited inflammatory reactions induced with LPS. Its suppressive effects on P-selectin expression could contribute to the attenuation of leukocyte infiltration, possibly by inhibiting leukocyte rolling. The current findings suggest that ATIII may have a role in the management of patients with uveitis.

Animals↗

In vivo evaluation of platelet--endothelial interactions after transient retinal ischemia.

PURPOSE: Accumulating evidence suggests that platelets play an important role in ischemia-reperfusion injury. To fulfill that role, platelets flowing in the bloodstream would have to interact with retinal endothelial cells and to accumulate in the postischemic retina. This study was designed to investigate quantitatively platelet-endothelial interactions in postischemic retina after transient retinal ischemia. METHODS: Transient retinal ischemia was induced in Long-Evans rats for 60 minutes by temporal ligation of the optic nerve. Isolated platelet samples labeled with carboxyfluorescein diacetate succinimidyl ester were administered intravenously to recipient rats after various reperfusion periods. Platelet-endothelial interactions in postischemic retina were evaluated in vivo with a scanning laser ophthalmoscope. Anti-P-selectin monoclonal antibody (mAb) was administered 5 minutes before the injection of labeled platelets. P-selectin gene expression in the postischemic retina was studied by semiquantitative polymerase chain reaction. RESULTS: Under basal conditions, infused platelets showed minimal interactions with retinal endothelial cells. In contrast, postischemic retinas showed active platelet-endothelial interactions. Many platelets were observed rolling along and adhering to the major retinal veins. The number of rolling and adhering platelets reached a peak (555 +/- 65/mm per min and 25.8 +/- 3.2/mm(2)) 12 hours after reperfusion. However, the interactions between platelets and postischemic retinal endothelial cells were substantially inhibited by neutralizing P-selectin expressed on endothelial cells. In addition, P-selectin gene expression in postischemic retina corresponded with the time course of platelet-endothelial interactions during the reperfusion period. CONCLUSIONS: This study demonstrated that platelets actively interacted with retinal endothelial cells in the postischemic retina through P-selectin expressed on the retinal endothelial cells.

Animals↗

Inhibitory effect of ischemic preconditioning on leukocyte participation in retinal ischemia-reperfusion injury.

PURPOSE: Recent reports have shown that ischemic preconditioning induces strong protection against retinal damage by subsequent prolonged ischemia and that this protection is mediated by mechanisms involving the adenosine A1 receptor. This study was designed to evaluate quantitatively the effects of ischemic preconditioning on leukocyte-mediated reperfusion injury after transient retinal ischemia and to define the role of the adenosine A1 receptor in these effects. METHODS: Transient retinal ischemia was induced in male rats by temporary ligation of the optic nerve. Ischemic preconditioning (5 minutes of ischemia) was induced 24 hours before 60 minutes of ischemia. The adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) was administered intramuscularly immediately after ischemic preconditioning. Leukocyte behavior in the retina after 60 minutes of ischemia was evaluated in vivo with acridine orange digital fluorography. RESULTS: Ischemic preconditioning inhibited leukocyte rolling. The maximum number of rolling leukocytes was reduced to 3.0% at 12 hours after reperfusion (P < 0.01). Subsequent leukocyte accumulation was also decreased with ischemic preconditioning. The maximum number of accumulated leukocytes was reduced to 22.6% at 24 hours after reperfusion (P < 0.01). These inhibitory effects were suppressed by administration of DPCPX (P < 0.0001). The numbers of rolling leukocytes at 12 hours after reperfusion and accumulated leukocytes at 24 hours after reperfusion were 102.7% (NS) and 83.4% (P < 0.01), respectively, compared with the number without ischemic preconditioning. CONCLUSIONS: The present study demonstrates the inhibitory effects of ischemic preconditioning on leukocyte rolling and subsequent leukocyte accumulation during retinal ischemia-reperfusion injury. Furthermore, the adenosine A1 receptor may play an important role in these inhibitory effects.

Acridine Orange↗

Leukocyte-endothelial cell interactions in diabetic retina after transient retinal ischemia.

Diabetes is associated with increased neural damage after transient cerebral ischemia. Recently, leukocytes, which are thought to play a central role in ischemia-reperfusion injury, have been suggested to be involved in exacerbated damage after transient ischemia in diabetic animals. The present study was designed to clarify whether the anticipated worse outcome after transient cerebral ischemia in diabetic animals was due to augmented leukocyte-mediated neural injury. Using rats with streptozotocin-induced diabetes of 4-wk duration, we investigated leukocyte-endothelial cell interactions during reperfusion after a transient 60-min period of retinal ischemia. Unexpectedly, postischemic diabetic retina showed no active leukocyte-endothelial cell interactions during reperfusion. The maximal numbers of rolling and accumulating leukocytes in diabetic retina were reduced by 73.6 and 41.2%, respectively, compared with those in nondiabetic rats. In addition, neither preischemic insulin treatment of diabetic rats nor preischemic glucose infusion of nondiabetic rats significantly influenced leukocyte-endothelial cell interactions during reperfusion. The present study demonstrated that high blood glucose concentration before induction of ischemia did not exacerbate leukocyte involvement in the postischemic retinal injury. Furthermore, diabetic retina showed suppressed leukocyte-endothelial cells interactions after transient ischemia, perhaps due to an adaptive mechanism that developed during the period of induced diabetes.

Animals↗

Interactions between blood cells and retinal endothelium in endotoxic sepsis.

Platelets and leukocytes are thought to play a leading role in the pathogenesis of many inflammatory conditions. To recruit flowing blood cells to the inflammatory region, it would be necessary for them to interact with vascular endothelial cells. Recently, many reports have indicated the resistance of spontaneous hypertensive rats (SHR) to endotoxic sepsis. Their resistance might be derived from suppressed interaction between these blood cells and endothelial cells. Therefore, SHR and age-matched Wistar-Kyoto rats (WKY) were induced with endotoxic sepsis by intravenous injection of lipopolysaccharide (LPS). At 4, 12, 24, and 48 hours after induction, leukocyte-endothelial interactions in the retina were evaluated in vivo with acridine orange digital fluorography. Fluorescently labeled platelets were also injected to investigate platelet-endothelial interactions in the retina in endotoxic sepsis. Leukocyte rolling in SHR after LPS injection was significantly suppressed; the maximum number of rolling leukocytes was reduced by 80.1% at 12 hours after LPS injection in SHR compared with WKY. Subsequent leukocyte infiltration into the vitreous cavity was significantly inhibited in SHR. Furthermore, platelet-endothelial interactions in the retina were also suppressed in SHR treated with LPS. The maximum numbers of rolling and adherent platelets were reduced by 59.5% and 62.6%, respectively, in SHR compared with WKY. In both strains, leukocyte- and platelet-endothelial interactions were substantially inhibited by the blocking of P-selectin. These suppressed interactions could contribute to the reduction of leukocyte- and platelet-mediated tissue injury in endotoxic sepsis in SHR, resulting in their resistance to endotoxemia.

Animals↗

Administration of 17beta-estradiol attenuates retinal ischemia-reperfusion injury in rats.

PURPOSE: Accumulating evidence has suggested that 17beta-estradiol exerts protective effects against ischemic damage in various organs. In addition, leukocytes that accumulate in postischemic tissues are thought to play a central role in ischemia-reperfusion injury. This study was designed to evaluate quantitatively the inhibitory effects of 17beta-estradiol on leukocyte accumulation during ischemia-reperfusion injury and on subsequent retinal damage after transient retinal ischemia. METHODS: Transient (60 minutes) retinal ischemia was induced in male rats by temporary ligation of the optic nerve. Thirty minutes before induction of ischemia, 17beta-estradiol (0.1 mg/kg) was administered intraperitoneally. At 6, 12, 24, and 48 hours after reperfusion, leukocyte accumulation in the retina was evaluated in vivo by means of acridine orange digital fluorography. Histologic and electroretinographic (ERG) studies were carried out to evaluate retinal damage. RESULTS: Treatment with 17beta-estradiol significantly inhibited postischemic leukocyte accumulation; the maximum number of accumulating leukocytes was reduced by 35.7% at 24 hours after reperfusion (P = 0.01). Histologic examination showed that administration of 17beta-estradiol significantly reduced retinal damage, which was most obvious in the inner retina, 168 hours after reperfusion (P = 0.0001). ERG studies at 12 and 168 hours after reperfusion showed that recovery of the b-wave amplitude was significantly improved with treatment of 17beta-estradiol (P = 0.023). CONCLUSIONS: The present study demonstrated the inhibitory effects of 17beta-estradiol on leukocyte accumulation and subsequent tissue injury during retinal ischemia-reperfusion injury.

Acridine Orange↗

PKC-beta inhibitor (LY333531) attenuates leukocyte entrapment in retinal microcirculation of diabetic rats.

PURPOSE: The activity of protein kinase C (PKC), preferentially beta isoform of PKC, has been shown to be elevated in the diabetic retina. Recently, LY333531, a specific inhibitor of PKC-beta, has been reported to improve the decrease of retinal blood flow in early diabetes. Increased leukocyte entrapment has been suggested to be involved in blood flow disturbances in the early diabetic retina. This study was designed quantitatively to evaluate leukocyte entrapment in the retinal microcirculation of diabetic rats and the effect of LY333531 on leukocyte entrapment. METHODS: Diabetes was induced in male Long-Evans rats by intraperitoneal injection of streptozotocin (60 mg/kg). LY333531 (0.1, 1.0, or 10.0 mg/kg/d) was administered orally during a 4-week diabetic period. Leukocyte entrapment in the retinal microcirculation was quantitatively evaluated in vivo with acridine orange digital fluorography. RESULTS: The number of leukocytes trapped in the retinal microcirculation of diabetic rats (mean +/- SEM; 14.3 +/- 1.3 cells/mm2) was significantly increased, compared with nondiabetic control rats (7.5 +/- 0.3 cells/mm2; P < 0.0001). Oral administration of LY333531 significantly decreased the number of leukocytes trapped in the retinal microcirculation of diabetic rats (10.9 +/- 0.6, 11.3 +/- 0.7, and 10.4 +/- 0.4 cells/mm2 with LY333531 0.1, 1.0, and 10.0 mg/kg/d, respectively; P < 0.05). CONCLUSIONS: Treatment with LY333531 attenuated the increase of leukocyte entrapment in the retinal microcirculation during the period of early diabetes. This effect may contribute to the improvement of abnormal retinal blood flow in early diabetes with LY333531. LY333531 might have a therapeutic efficacy in preventing microcirculatory flow disturbances by trapped leukocytes in the early diabetic retina.

Acridine Orange↗

[Effect of pre-mixed lidocaine with propofol on propofol injection pain in elderly patients].

The purpose of this study was to compare the younger and older patients in the incidence and the severity of the pain during injection of propofol. Thirty-four, elderly patients (60-80-yr-old) and 52 patients (20-40-yr-old) scheduled to undergo elective surgery were studied. We conducted a prospective, randomized and double-blinded trial. All patients were randomly allocated to one of two groups according to the agents added to 1% propofol 20 ml; Group S, normal saline 2 ml, and Group L, 2% lidocaine 2 ml. The pain on injection was rated as none, mild, moderate, or severe. Seventy percent of patients in the S group of elderly patients experienced pain, while 22% of patients experienced pain in the L group in elderly patients. The incidence of pain on injection in the S group of older patients was comparable with S group of younger patients. The severity of pain in elderly patients was significantly decreased after premixing with lidocaine. There were no significant differences between older and younger patients in the severity of propofol injection pain in both S group and L group. In conclusion, elderly patients suffered the pain on injection of propofol with the same incidence as the younger patients did. Lidocaine premixed with propofol significantly reduces the incidence and the severity of pain associated with propofol in elderly patients.

Adult↗

[Hyperkalemia after irradiated blood transfusion].

A 70-yr-old woman was scheduled for hepatectomy and colectomy. We gave general anesthesia with N2O-O2-Isoflurane and continuous epidural block. About 4.5 hours after the start of the operation, 8 units of irradiated RBC-MAP were transfused. Then elevated T waves were noted and serum potassium was increased to 5.4 mmol.l-1. The transfusion of RBC-MAP was stopped and calcium gluconate was administered immediately. Then serum potassium decreased to 4.3 mmol.l-1 and ECG returned to normal. During the operation, 10 units of irradiated RBC-MAP were transfused and 8 units of them had been stored more than 1 week after the irradiation. We suspect that hyperkalemia was induced by high concentration of potassium in RBC-MAP. Irradiation of blood products is an effective way to prevent post-transfusion graft versus host disease. However, the increase in potassium is greater in the irradiated than nonirradiated RBC-MAP. We must pay attention to the high concentration of potassium in th eplasma of RBC-MAP stored after irradiation.

Aged↗