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Biomedical subjects

H Nakae

Publications and source records attributed to H Nakae.

At least 19 recordsLinked to original sources
PubMed2006

Extravascular lung water measured using single transpulmonary thermodilution reflects perioperative pulmonary edema induced by esophagectomy.

Pulmonary edema is the most frequent postoperative complication following esophagectomy for thoracic esophageal cancer. We enrolled 23 patients who underwent esophagectomy with extended lymph node dissection for thoracic esophageal cancer in a prospective observational clinical trial. We used the PiCCO device to measure extravascular lung water with the aim of determining whether it correlates with the respiratory index and whether it is predictive of pulmonary complications. Based on constant criteria, the tracheal tubes of 11 patients were removed on the morning of postoperative day 1 (extubation group), while 12 patients remained intubated (intubation group). These two groups significantly differed in that all patients in the extubation group recovered without any pulmonary complications, whereas 4 patients (33%) in the intubation group developed pulmonary complications. The extravascular lung water measured using PiCCO correlated significantly with the respiratory index. In the intubation group, both extravascular lung water and respiratory index were elevated 12 h after surgery and were even higher 24 h after surgery. The extravascular lung water measured using PiCCO reflects the level of postoperative pulmonary edema and predicts the pulmonary complications induced by esophagectomy with extended lymph node dissection.

Aged↗
PubMed2006

Cytokines differentially regulate ICAM-1 and VCAM-1 expression on human gingival fibroblasts.

The expression of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) on human gingival fibroblasts (HGF) may be important for migration and retention of inflammatory cells in periodontally diseased tissue. This study aimed to assess which cytokines regulate ICAM-1 and VCAM-1 expression on HGF. Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma enhanced both ICAM-1 and VCAM-1 expression on HGF. Interleukin (IL)-1beta mainly up-regulated ICAM-1 expression. On the other hand, IL-4 and IL-13 enhanced only VCAM-1 expression on HGF. IL-10 did not modulate both ICAM-1 and VCAM-1 expression. Transforming growth factor (TGF)-beta1 enhanced ICAM-1 expression. However, TGF-beta1 inhibited the VCAM-1 expression induced by TNF-alpha or IL-4. Both ICAM-1 and VCAM-1 expression by HGF was inhibited by nuclear factor-kappaB (NF-kappaB) activation inhibitor (MG-132). Mitogen-activated protein kinases (MAPK) inhibitors did not influence ICAM-1 expression induced by TNF-alpha. Interestingly, VCAM-1 expression was enhanced by MEK inhibitor (PD98059) and c-Jun NH2-terminal kinase (JNK) inhibitor (SP600125). These results mean that the balance of cytokines in periodontally diseased tissue may be essential for control of ICAM-1 and VCAM-1 expression on HGF, and the balance of ICAM-1 and VCAM-1 expression might be important for regulation of leucocytes infiltration and retention in periodontally diseased tissue.

Cells, Cultured↗
PubMed2006

Proinflammatory effects of tumour necrosis factor-like weak inducer of apoptosis (TWEAK) on human gingival fibroblasts.

Tumour necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), a member of the TNF family, is a multi-functional cytokine that regulates cellular proliferation, angiogenesis, inflammation and apoptosis. In this study, we investigated TWEAK expression in periodontally diseased tissues and the effect of TWEAK on human gingival fibroblasts (HGF). Reverse transcription-polymerase chain reaction (RT-PCR) analysis and immunohistochemistry revealed that TWEAK and the TWEAK receptor, fibroblast growth factor-inducible 14 (Fn14), mRNA and protein were expressed in periodontally diseased tissues. HGF expressed Fn14 and produced interleukin (IL)-8 and vascular endothelial growth factor (VEGF) production upon TWEAK stimulation in a dose-dependent manner. The IL-8 and VEGF production induced by TWEAK was augmented synergistically by simultaneous stimulation with transforming growth factor (TGF)-beta1 or IL-1beta. IL-1beta and TGF-beta1 enhanced Fn14 expression in a dose-dependent manner. Moreover, TWEAK induced intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression on HGF in a dose-dependent manner. The ICAM-1 expression induced by TWEAK was augmented by TGF-beta1. On the other hand, the TWEAK-induced VCAM-1 expression was inhibited by TGF-beta1. Phosphatidylinositol 3-kinase (PI3K) and nuclear factor-kappaB (NF-kappaB) inhibitor inhibit both ICAM-1 and VCAM-1 expression induced by TWEAK. However, mitogen-activated protein kinase (MEK) and c-Jun NH2-terminal kinase (JNK) inhibitor enhanced only VCAM-1 expression on HGF. These results suggest that TWEAK may be involved in the pathophysiology of periodontal disease. Moreover, in combination with IL-1beta or TGF-beta1, TWEAK may be related to the exacerbation of periodontal disease to induce proinflammatory cytokines and adherent molecules by HGF.

Adult↗
PubMed2005

Expression of fractalkine (CX3CL1) and its receptor, CX3CR1, in periodontal diseased tissue.

The regulatory role of chemokines and chemokine receptors on specific leucocyte recruitment into periodontal diseased tissue is poorly characterized. We observed that leucocytes infiltrating inflamed gingival tissue expressed marked levels of CX3CR1. In periodontal diseased tissue, the expression of fractalkine and CX3CR1 mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) and further, fractalkine was distributed mainly on endothelial cells, as shown by immunohistochemistry. Moreover, we can detect CX3CR1-expressing cells infiltrated in periodontal diseased tissue by immunohistochemical staining. Furthermore, fractalkine production by human umbilical vein endothelial cells (HUVEC) was up-regulated by pathogen-associated molecular patterns (PAMPs), including Porphyromonas gingivalis lipopolysaccharide (LPS). Thus, these findings suggested that CX3CR1 and the corresponding chemokine, fractalkine may have an important regulatory role on specific leucocyte migration into inflamed periodontal tissue.

Antigens, Bacterial↗
PubMed2005

CXCL12 and CXCR4 expression by human gingival fibroblasts in periodontal disease.

CXCL12 is a CXC chemokine that is related to lymphocyte infiltration and angiogenesis in inflammatory sites such as arthritis. However, the expression and roles of CXCL12 in periodontal disease are uncertain. The aim of this study was to assess the expression of CXCL12 and its receptor, CXCR4, in periodontal tissue and to investigate the properties of CXCL12 and CXCR4 expression by human gingival fibroblasts (HGF). RT-PCR analysis revealed that CXCL12 and CXCR4 mRNA were expressed in both normal gingival tissues and periodontal diseased tissues. Immunohistochemistry disclosed that CXCL12 was expressed and CXCR4 positive cells were found in both normal and periodontal diseased gingival tissues. Our in vitro experiments elucidated that HGF constitutively produced CXCL12, and the levels were enhanced by stimulation with tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), regulated upon activation normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein 3(alpha) (MIP-3(alpha)). On the other hand, heat killed Porphyromonas gingivalis (P. gingivalis) and P. gingivalis LPS reduced the CXCL12 production by HGF. Flow cytometry analysis clarified that CXCR4 was highly expressed on HGF, and CXCR4 expression was abrogated by TNF-alpha, IFN-gamma and P. gingivalis LPS. Moreover, CXCL12 induced vascular endothelial growth factor (VEGF) production by HGF. Our results demonstrated that CXCL12 might be related to CXCR4+ cells infiltration and angiogenesis both in normal periodontal tissues and periodontal diseased tissue. P. gingivalis, a known periodontal pathogen, inhibits the production of CXCL12 and the expression of CXCR4 by HGF. This fact means that P. gingivalis may inhibit CXCR4+ cells infiltration and neovascularization in periodontal tissue and escape from the immune response.

Cells, Cultured↗
PubMed2005

Increase of CCL20 expression by human gingival fibroblasts upon stimulation with cytokines and bacterial endotoxin.

We have demonstrated recently that CCL20 was expressed in periodontal diseased tissues and abundant CCR6 positive T cells infiltrated in periodontally diseased tissue. However, it is uncertain which cells can elicit CCL20 production. In the present study, we examined the properties of CCL20 production by human gingival fibroblasts (HGF) culture. Here, we report that interleukin-1 beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and Escherichia coli lipopolysaccharide (LPS) can significantly induce the production of CCL20 by HGF. We found that TNF-alpha and E. coli LPS enhanced the production of CCL20 by HGF treated with IL-1beta. In contrast, interferon-gamma (IFN-gamma) dramatically diminished CCL20 production induced by IL-1beta. Moreover, we demonstrated that nuclear factor-kappaB (NF-kappaB), p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK) play an important role in mediating the production of CCL20 induced by IL-1beta and TNF-alpha. On the other hand, we found that not only NF-kappaB, p38 MAPK and ERK but also c-Jun NH2-terminal kinase (JNK) are involved in CCL20 production induced by E. coli LPS. Finally, we found that HGF express CCR6, CCL20 receptor, and CCL20 induced vascular endothelial growth factor (VEGF) by HGF. Taken together, these findings that HGF will be a source of CCL20 in periodontal tissue, and the CCL20 production will be controlled by proinflammatory cytokine and bacterial LPS in periodontally diseased tissue. Thus, CCL20 by HGF might be involved in inflammatory cells infiltration, and promote the progression of periodontal disease.

Adult↗
PubMed2001

Failure to clear casts and secretions following inhalation injury can be dangerous: report of a case.

A 27-year-old man suffered smoke inhalation during a fire. Three days later, he complained of respiratory difficulty and was admitted to our hospital. Bronchoscopy revealed a very large buildup of sputum mixed with soot extending from the left main bronchus to the bifurcation of the upper and lower lobe bronchi and causing both pulmonary atelectasis and pneumonia. The debris was successfully removed the next day with basket forceps via bronchoscopy. The patient's airway pressure dropped significantly, enabling extubation almost immediately. Because of the possibility for respiratory failure caused by viscous secretion, it is important to perform initial bronchoscopy in cases of suspected inhalation injury.

Adult↗
PubMed2001

Soluble products from Eikenella corrodens stimulate oral epithelial cells to induce inflammatory mediators.

In the inflammatory response elicited by bacterial colonization in periodontal pockets, pocket epithelial cells not only serve as a barrier to isolate the pocket microenvironment from external stimuli but also regulate the functions of neighboring cells including fibroblasts and inflammatory cells. To elucidate this mechanism, we characterized the effects of periodontopathic bacterium Eikenella corrodens 1073 components on the production of some inflammatory mediators in a human oral epithelial cell line (KB). In enzyme-linked immunosorbent assay (ELISA), the E. corrodens supernatant induced interleukin-6 (IL-6), IL-8 and prostaglandin E2 but not interferon-gamma (IFN-gamma) production by KB cells. After incubation with E. corrodens supernatant, KB cells showed a marked increase in the levels of IL-6, IL-8 and PG G/H synthase (cyclooxygenase)-2, but not IFN-gamma, gene expression by reverse-transcriptase polymerase chain reaction. All these E. corrodens products responsible for production of these inflammatory mediators resisted freezing and boiling and were present in a 10-kDa filtrate. These results imply that these soluble small-molecular-mass products from E. corrodens stimulate various inflammatory mediator productions by human oral epithelial cells and may play a role in the initiation of periodontal inflammation and subsequently perpetuate the inflammatory response during chronic infection.

Bacterial Adhesion↗
PubMed2001

Effectiveness of combining plasma exchange and continuous hemodiafiltration (combined modality therapy in a parallel circuit) in the treatment of patients with acute hepatic failure.

Plasma exchange has gained widespread acceptance as an effective mode of blood purification in patients suffering from acute hepatic failure. However, it is still undetermined whether a single use of plasma exchange is capable of removing inflammatory cytokines completely or of preventing the development of citrate toxicity inherent with fresh frozen plasma. To clarify these issues we developed combined plasma exchange and continuous hemodiafiltration (CHDF) modality in which CHDF is performed in an opposite direction to plasma exchange. This study was designed to assess the effectiveness of combined modality therapy. Fifteen patients with acute hepatic failure were treated with plasma exchange (plasma exchange group) or plasma exchange and CHDF (plasma exchange + CHDF group), and various biochemical parameters were determined before and after treatment. Although citrate levels increased significantly after treatment compared with pretreatment levels in both the plasma exchange group and the plasma exchange + CHDF group, the percentage of the increase in citrate levels was significantly higher in the plasma exchange group than in the plasma exchange + CHDF group. Bilirubin levels were significantly lower after treatment in both the plasma exchange and plasma exchange + CHDF groups. There were no significant differences in tumor necrosis factor-alpha levels before and after treatment in the plasma exchange group, but they were significantly lower after treatment in the plasma exchange + CHDF group. Interleukin-6 (IL-6) levels increased significantly after treatment in the plasma exchange group, but there were no significant differences in the IL-6 levels before and after treatment in the plasma exchange + CHDF group. Interleukin-8 levels increased significantly after treatment in the plasma exchange group while decreasing significantly after treatment in the plasma exchange + CHDF group. These results indicate that combining plasma exchange and CHDF in a parallel circuit is an effective modality for suppressing the elevation of blood citrate levels and for removing inflammatory cytokines. This finding may have important implications for the development of an effective treatment for patients with acute hepatic failure.

Citrates↗
PubMed2001

Soluble Fas and soluble Fas ligand levels in patients with acute hepatic failure.

PURPOSE: The Fas ligand (FasL)/Fas system is an apoptosis induction system that plays an important role in homeostasis and biophylaxis. We measured tumor necrosis factor alpha (TNF-alpha), soluble FasL (sFasL), and soluble Fas (sFas) in patients with acute hepatic failure to determine the relation between such failure and apoptosis. MATERIALS AND METHODS: We assayed 21 blood samples from patients with acute hepatic failure and 8 from patients with sepsis but without acute hepatic failure. Serum TNF-alpha, sFas, and sFasL levels were determined by enzyme-linked immunosorbent assay. RESULTS: sFasL levels were significantly higher in the patients with acute hepatic failure than in the patients with sepsis (0.68 +/- 0.42 ng/mL vs. 0 ng/mL, P =.0001). No significant differences were observed in sFas levels between the two groups. A significant correlation was observed between TNF-alpha and sFas levels (r = 0.657, P =.0008); a negative correlation was observed between TNF-alpha and sFasL levels (r = 0.454, P =.038). CONCLUSIONS: Our results suggest that pathologic aggravation of acute hepatic failure are related to changes in the FasL/Fas system and that TNF-alpha and sFasL, in particular, may play hepatoprotective roles.

Aged↗
PubMed2001

Are proinflammatory cytokine concentrations reduced by plasma exchange in patients with severe acute hepatic failure?

We studied citric acid levels and proinflammatory cytokines (TNF-alpha, IL-6, and IL-8) before and after plasma exchange in 8 patients with acute liver failure. Plasma exchange was performed over a 6 to 7-hour period. At each session, 3.6 to 4.0 1 of plasma was exchanged for the same volume of fresh frozen plasma (FFP). The concentrations of citric acid were significantly increased after plasma exchange above concentrations before exchange (p<0.0001). There were no significant differences in TNF-alpha, IL-6, or IL-8 concentrations (p=0.7222, p=0.9357, p=0.6394, respectively). Thus, plasma exchange with FFP alone may not effectively remove cytokines.

Adult↗
PubMed2000

Nitrite/nitrate (NOx) levels and hemodynamics during septic shock.

Nitric oxide (NO) acts as a vasorelaxant. We investigated the relationship between nitrite/nitrate (NOx), which are the final metabolites of NO, and hemodynamics during septic shock. We also examined tumor necrosis factor alpha (TNF-alpha), interleukin-8 (IL-8), and endotoxin. A significant negative correlation was observed between NOx levels and pulmonary capillary wedge pressure (PCWP; r = -0.6075, P = 0.0028). A significant positive correlation was noted between NOx levels and the cardiac index (CI; r = 0.5934, P = 0.0038). A significant negative correlation was found between NOx levels and the systemic vascular resistance index (SVRI; r = -0.4354, P = 0.0485). A significant positive correlation was observed between NOx levels and the stroke volume index (SVI; r = 0.5040, P = 0.0186). A significantly close positive correlation was also observed between TNF-alpha levels and NOx levels (r = 0.7848, P < 0.0001). These findings suggest that NOx levels are closely associated with hemodynamics during septic shock, resulting in a vascular relaxing effect.

Adult↗
PubMed2000

Are nitrite/nitrate (NOx) levels elevated by inhalation injury?

The relationship between airway burn and nitric oxide (NO) levels in the early burn stage was investigated by quantifying nitrite/nitrate (NOx), which are the final metabolites of NO, in 22 burn patients. Although total body surface area (TBSA) and burn index (BI) were significantly higher in patients with airway-burn than in patients without airway burn (P=0.0347 and 0.0422, respectively), no significant difference in NOx levels was observed between the two groups (P=0.6196). The NOx levels were found to correlate significantly with TBSA (r=0.4775, P=0.0246). A significant correlation was also noted between the NOx levels and BI (r=0.4391, P=0.0409). These results suggest that NO reflects the intensity of inflammation in the early burn stage, but that excessive NO formation is unlikely to be induced by stress, such as that caused by airway burn.

Adult↗
PubMed2000

Hyperemia of the intraperitoneal organs associated with scald burn.

A 65-year-old man with a history of cerebral infarction sustained scald burns over 54% of the body surface. In spite of adequate fluid therapy, respiratory management with an artificial ventilator, and continuous hemodiafiltration, the patient died on day 5 post-admission. Autopsy revealed necrotic change on the surface of the liver, and necrosis and perforation of the ileum. Histologic examination showed necrosis of the hepatocytes lining the surface and necrosis of the hepatocytes and congestion in the central area of the liver. We speculated that systemic responses to the extensive burn resulted in hyperemia of the intraperitoneal organs, thereby inducing acute liver failure and the subsequent development of multiple organ failure.

Aged↗
PubMed2000

Bound and soluble adhesion molecule and cytokine levels in patients with severe burns.

We measured endotoxins, inflammatory cytokines and soluble adhesion molecules in the blood of 17 severe burn patients to determine the involvement of these factors in the pathophysiology of severe burns. All seventeen patients had burns with a total burn surface area of 20% or more and a burn index of 15% or more. Endotoxin was measured by an endotoxin-specific assay and tumor necrosis factor-alpha, interleukin 6 and interleukin 8 and soluble adhesion molecules were measured by enzyme-linked immunosorbent assay. CD11a, CD11b and CD18, measured by flow cytometry, were elevated in the non-surviving group, the septic shock group and the multiple organ dysfunction syndrome group, suggesting a close connection between these adhesion molecules and burns complicated by infection. Soluble adhesion molecules were found to indirectly reflect the level of endothelial cell adhesion molecules, suggesting that inflammatory cytokines may also be involved in their production.

Adult↗
PubMed2000

Tumor necrosis factor-alpha and tumor necrosis factor receptor I, II levels in patients with severe burns.

Tumor necrosis factor alpha (TNF-alpha) and tumor necrosis factor receptor I and II (TNFRI and TNFRII) were studied in 24 burn patients who had a total burn surface area (TBSA) of 50.2 +/- 20.4%. Immediately after the injury, both the TNFRI and TNFRII levels correlated significantly with TBSA (r = 0.7344, P < 0.0001; r = 0.6074, P = 0.0012). The TNFRI and TNFRII levels immediately after the injury were significantly higher in the 11 patients who later died of their burns than in the 13 patients who survived (0.8 +/- 0.4 ng/ml vs. 1.8 +/- 0.7 ng/ml, P = 0.0002; 2.3 +/- 1.1 ng/ml vs. 4.5 +/- 1.6 ng/ml, P = 0.0009). The TNF-alpha levels immediately after the injury did not differ significantly between the group that survived and the group that died. The TNFRI and TNFRII values for the entire follow-up period also correlated significantly with TBSA. Peak TNFRI and TNFRII levels were significantly higher in the group that died than in the group that survived (6.0 +/- 4.7 ng/ml vs. 14.1 +/- 7.8 ng/ml, P = 0.0009; 7.0 +/- 5.1 ng/ml vs. 16.7 +/- 5.2 ng/ml, P = 0.0003). The TNF-alpha levels correlated significantly with both the TNFRI and the TNFRII levels. The TNFRI and TNFRII levels thus closely reflected the severity of the burns in both the acute postburn period and the subsequent follow-up period. In other words, these parameters well reflected the severity and outcome of the burns, irrespective of the presence or absence of accompanying infection.

Adult↗
PubMed2000

Red blood cells attenuate sinusoidal endothelial cell injury by scavenging xanthine oxidase-dependent hydrogen peroxide in hyperoxic perfused rat liver.

AIMS/BACKGROUND: Rat liver perfused with an oxygenated buffered solution alone results in degenerative changes even when the perfusion flow is accelerated to give a sufficient oxygen supply. On the other hand, perfusion media supplemented with red blood cells (RBCs) preserve the viability of the liver. The present study was conducted to clarify how RBCs protect the isolated perfused liver. METHODS: The liver was perfused with and without RBCs in a perfusate equilibrated with supra-physiological oxygen tension at regulated inflow pressures, and controlled hepatic oxygen consumption. We examined alanine aminotransferase and purine nucleoside phosphorylase activity in the perfusate as specific markers of liver cells injury. Hydrogen peroxide (H2O2) production and morphological changes were determined using cerium electron microscopy. Apoptosis was detected by measuring CPP 32 protease activity and using TdT-mediated dUTP-digoxigenin nick end-labeling. RESULTS: When the liver was perfused with RBC-free buffer, H2O2 production and consequent injury progressing to apoptosis were initiated in the sinusoidal endothelial cells (SECs). After SECs were injured, H2O2 appeared in the hepatocytes. H2O2 production and associated degenerative changes were attenuated both morphologically and enzymatically by the addition of RBCs, a specific xanthine oxidase (XOD) inhibitor and the H2O2 radical scavenger, catalase. CONCLUSIONS: In the liver perfused with RBC-free buffer, H2O2 production and consequent injury were initiated in SECs. RBCs attenuate liver injury by scavenging XOD-dependent H2O2.

Alanine Transaminase↗