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Biomedical subjects

K Sanada

Publications and source records attributed to K Sanada.

At least 19 recordsLinked to original sources
PubMed2005

Gallbladder aspiration for acute cholecystitis in average-surgical-risk patients.

We conducted a retrospective case note review to assess whether or not gallbladder aspiration can be applied as a temporary measure for the treatment of acute cholecystitis in average-surgical-risk patients. Gallbladder aspiration was performed in 79 consecutive average-surgical-risk patients with acute cholecystitis, who had no indications of emergent surgery and who complained of severe colicky pain. Elective surgery became possible in 92% of patients by gallbladder aspiration. The percentage reached 97 when percutaneous cholecystostomy was added (four patients). Emergent surgery was needed in one patient suffering bile leakage following gallbladder aspiration. Colicky pain was controlled soon after the procedure in most cases. Neither major complications nor mortalities were observed in the following surgical therapies. It is suggested that gallbladder aspiration might be applied as a temporary measure for acute cholecystitis in average-surgical-risk patients, although early surgery should remain the primary choice of therapy in such patients.

Aged↗
PubMed2004

Activation of WNT family expression and signaling in squamous cell carcinomas of the oral cavity.

The WNT family activates an oncogenic signaling mediated through beta-catenin and is up-regulated in a variety of malignant neoplasms. The signaling translocates beta-catenin into the nucleus and stimulates carcinoma cells in the epithelial-mesenchymal transition (EMT). However, WNT expression and signaling in oral carcinomas have not been examined. The present study focused on unveiling the involvement of WNTs in oral carcinomas, and showed that carcinoma cells express 11 of 19 WNT family members by reverse-transcription/PCR. WNT-expressing carcinoma cells exhibited increased beta-catenin levels in the cytoplasmic pool and translocation to the nucleus. The activation state of signaling correlated with the expression of membrane-type 1 matrix metalloproteinase, which degrades territorial matrices in carcinoma invasion. Immunohistochemistry disclosed that WNT3 expression and nuclear localization of beta-catenin were predominant in carcinoma cells at the invasive front. These results suggest that enhanced WNT expression and signaling accelerate the progression of carcinomas via activating EMTs and local invasiveness.

Carcinoma, Squamous Cell↗
PubMed2003

The LIM-only protein, LMO4, and the LIM domain-binding protein, LDB1, expression in squamous cell carcinomas of the oral cavity.

Carcinoma cells can lose their epithelial cell characteristics and dedifferentiate into a fibroblast-like cell during progression of a neoplasm. Aberrant expression of oligomeric transcriptional complexes contributes to progression of carcinomas. Although individual transcription factors initiating progression remain unknown, LIM-only protein (LMO) and LIM-domain binding protein (LDB) negatively regulate breast carcinoma cell differentiation. In this study, we investigated the expression of LMO4 and LDB in squamous cell carcinomas of the oral cavity. LMO4 mRNA was amplified in four of six carcinoma tissues and eight of 12 carcinoma cell lines, and LDB1 in three carcinoma tissues and 11 cell lines examined. Immunoprecipitation studies revealed that LMO4 and LDB1 interact with each other in the nuclear milieu of the carcinoma cells indicating the presence of an LMO4-LDB1-mediated transcription complex. Both LMO4 and LDB1 proteins were preferentially localised in the nuclei of carcinoma cells at the invasive front and the immunoreactivity was increased in less-differentiated carcinoma tissues (P<0.01). Carcinoma cells metastasised to the cervical lymph nodes with increased immunoreactivity compared to the primary site of neoplasm (P<0.05). These data suggest that the LMO4-LDB1 complexes may be involved in carcinoma progression possibly through dedifferentiation of squamous carcinoma cells of the oral cavity.

Carcinoma, Squamous Cell↗
PubMed2001

Circadian and photic regulation of MAP kinase by Ras- and protein phosphatase-dependent pathways in the chick pineal gland.

Chick pineal mitogen-activated protein kinase (MAPK) exhibits circadian activation and light-dependent deactivation at nighttime. Here we report that, in the chick pineal gland, levels of active forms of MAPK, MEK, Raf-1 and Ras exhibited synchronous circadian rhythms with peaks during the subjective night, suggesting a sequential activation of components in the classical Ras-MAPK pathway in a circadian manner. In contrast, the light-dependent deactivation of MAPK was not accompanied by any change of MEK activity, but it was attributed to the light-dependent activation of protein phosphatase dephosphorylating MAPK. These results indicate that the photic and clock signals regulate MAPK activity via independent pathways, and suggest a pivotal role of MAPK in photic entrainment and maintenance of the circadian oscillation.

Animals↗
PubMed2000

Circadian activation of bullfrog retinal mitogen-activated protein kinase associates with oscillator function.

The vertebrate retina retains a circadian oscillator, and its oscillation is self-sustained with a period close to 24 h under constant environmental conditions. Here we show that bullfrog retinal mitogen-activated protein kinase (MAPK) exhibits an in vivo circadian rhythm in phosphorylation with a peak at night in a light/dark cycle. The phosphorylation rhythm of MAPK persists in constant darkness with a peak at subjective night, and this self-sustained rhythm is also observed in cultured retinas, indicating its close interaction with the retinal oscillator. The rhythmically phosphorylated MAPK is detected only in a discrete subset of amacrine cells despite ubiquitous distribution of MAPK throughout the retinal layers. Treatment of the cultured retinas with MAPK kinase (MEK) inhibitor PD98059 suppresses MAPK phosphorylation during the subjective night, and this pulse perturbation of MEK activity induces a significant phase delay (4-8 h) of the retinal circadian rhythm in MAPK and MEK phosphorylation. These observations strongly suggest that the site-specific and time-of-day-specific activation of MAPK contributes to the circadian time-keeping mechanism of the retinal clock system.

Animals↗
PubMed2000

Role of circadian activation of mitogen-activated protein kinase in chick pineal clock oscillation.

A circadian pacemaker generates a rhythm with a period of approximately 24 hr even in the absence of environmental time cues. Several photosensitive neuronal tissues such as the retina and pineal gland contain the autonomous circadian pacemaker together with the photic-input pathway responsible for entrainment of the pacemaker to the daily light/dark cycle. We show here that, in constant darkness, chick pineal mitogen-activated protein kinase (MAPK) exhibited an in vivo circadian rhythm in tyrosine phosphorylation and in enzymatic activity with a peak during subjective night. Phosphorylated and hence activated MAPK was rapidly dephosphorylated after light illumination during the nighttime when light induces a phase-shift of the pacemaker. The circadian rhythmicity in MAPK phosphorylation was also observed in the cultured pineal gland, and importantly, MAPK kinase inhibitor treatment during subjective night not only shifted the time-of-peak of MAPK phosphorylation but also induced a remarkable phase-delay of the circadian pacemaker. These results indicate an important role of MAPK for time keeping in circadian clock systems.

Animals↗
PubMed2000

Doxorubicin preconditioning: a protection against rat hepatic ischemia-reperfusion injury.

Doxorubicin produces clinically useful responses in a variety of human cancers. However, the toxicity of doxorubicin has limited its usefulness. This side effect is mainly due to the doxorubicin-mediated free radical formation. Administration of doxorubicin (10 mg/kg body weight) to rats intravenously induces heme oxygenase-1 (HO-1) in the liver. The levels of HO-1 protein were first detected at 6 hours and peaked at about 18 to 24 hours after the injection. It is known that HO-1 plays a protective role against the oxidative injury. Therefore, we have examined the protective effect of doxorubicin preconditioning against the hepatic ischemia-reperfusion injury. Partial hepatic ischemia was produced in the left and medium lobes for 45 minutes followed by 120 minutes reperfusion. When low doses of doxorubicin (1 mg/kg body weight) was intravenously administered to rats 2 days before the ischemia, the serum alanine transaminase (ALT) levels in the preconditioning rat were clearly improved compared with those in the rat without preconditioning. Under this situation, zinc-protoporphyrin IX, a specific inhibitor of HO-1, was injected subcutaneously to rats at 3 and 16 hours before the ischemia, the ALT levels were not improved by doxorubicin preconditioning. Histopathologic examination also supported these results. Although the HO-1 protein level was fairly low 2 days after the doxorubicin administration, significant amounts of HO-1 protein were detected. Our results indicated that the induction of HO-1 played a protective role against hepatic ischemia-reperfusion injury and that doxorubicin preconditioning is more clinically useful than other preconditioning methods.

Animals↗
PubMed2000

Correlation between the expression of methionine adenosyltransferase and the stages of human colorectal carcinoma.

Methionine adenosyltransferase (MAT) catalyzes the synthesis of S-adenosylmethionine (AdoMet) from ATP and L-methionine. AdoMet is the major methyl donor in most transmethylation reactions in vivo, and it is also the propylamino donor in the biosynthesis of polyamines. In the present study, we assessed MAT activity in human colons with colorectal carcinoma and the values were compared with those of morphologically normal adjacent mucosa. Higher levels of MAT activity were observed in the colorectal carcinoma than in the normal colon. The ratio of MAT activity in tumor tissue versus normal tissue seemed to be correlated well will the stage of the colorectal tumor. Furthermore, immunoblot analysis showed that the high levels of MAT activity observed in colorectal carcinoma were due to the increased amounts of MAT protein. Immunohistochemical analysis revealed that MAT was most abundant in goblet cells, particularly in granules in the supranuclear area of these cells. In the colorectal carcinoma tissues, MAT was strongly stained in the cancerous cells and localized in granules in the supranuclear region. The results of this preliminary study suggest that determination of the relative ratio of MAT activity in both normal and tumor regions in human colorectal carcinoma could be a clinically useful tool for determining the stage of malignancy of colorectal carcinomas.

Adenocarcinoma↗
PubMed1999

Characterization of N-acylation of Go alpha purified from bovine retinas.

Heterogeneous N-terminal acylation has been identified in several retinal proteins localized predominantly in the outer segments of the photoreceptor cells, but it is still unclear whether such a unique heteroacylation is determined by a photoreceptor cell-specific factor or not. Here, we characterized the N-terminal modification of bovine retinal Go alpha, which seems to be involved in the neural activities and is not detected in the photoreceptor outer segments. In the proteolytic fragments of immunoaffinity-purified retinal Go alpha, we found a single N-terminal peptide modified with myristate, and concluded that retinal Go alpha is purely myristoylated, just like brain Go alpha. This result indicates that the heteroacylation has a more restricted origin in the retina, and supports the idea that it is a photoreceptor cell-specific modification.

Acylation↗
PubMed1997

Cyst-like lesion of a developing tooth induced by mandibular fracture.

A dentigerous cyst-like formation in the lower canine region caused by mandibular fracture in a 10-year-old boy is reported. His medical history revealed that he had been unconscious for about 2 weeks after traumatic head injuries sustained in a traffic accident, and a complicated mandibular fracture had been left untreated until his dentist diagnosed the lesion. Eleven months after trauma, a dentigerous cyst measuring 20 mm in diameter was found in the fracture area. The lesion was enucleated and the boy's postoperative recovery was uneventful. The mass completely enveloped the developing canine, and epithelial cells proliferated into the connective tissue. However, there was no distinct epithelial lining. Small round cell infiltrations and several vessels with thrombosis were noted in the cyst wall. The cause of cyst formation was considered to be infection of the canine tooth bud and the surrounding soft tissue.

Child↗
PubMed1997

[Combination therapy with 5'-DFUR, MMC and CDDP in patient with far advanced gastric cancer: report of a case].

A 48-year-old man was referred to our hospital for a Borrmann 3 type advanced gastric cancer. Endoscopic biopsy disclosed poorly differentiated adenocarcinoma. Ultrasonography and CT scan revealed left hydronephrosis. Endoscopic retrograde cholangiography detected a stenosis of common bile duct at the hepatic hilum due to lymph nodal metastasis, and laparoscopy revealed peritoneal dissemination. Because the tumor was diagnosed as not for curative resection, the patient was treated by 4 courses of combination therapy with 5'-DFUR, MMC and CDDP. No adverse effect of chemotherapy was observed. As a result, lymph nodal metastasis and peritoneal dissemination were reduced. Curative intent total gastrectomy was performed, together with pancreatico-splenectomy, left hemicolectomy, cholecystectomy, and extended lymph nodal dissection. The patient is well and alive with no sign of recurrence 2 years after operation.

Adenocarcinoma↗
PubMed1996

Calcium-bound recoverin targets rhodopsin kinase to membranes to inhibit rhodopsin phosphorylation.

In rod photoreceptor cells, Ca2+-bound recoverin associates with disk membranes and inhibits light-dependent phosphorylation of rhodopsin. However, the functional significance of Ca2+-induced membrane association of recoverin has not been fully evaluated. We found that Ca2+-bound recoverin forms a complex with rhodopsin kinase preferentially at the membrane surface. Addition of increasing amounts of membranes promoted the membrane association of recoverin, and remarkably suppressed rhodopsin kinase activity. It was concluded that the Ca2+-recoverin-rhodopsin kinase complex is stabilized by membrane association, leading to effective suppression of the kinase activity.

Animals↗
PubMed1995

Role of heterogeneous N-terminal acylation of recoverin in rhodopsin phosphorylation.

Recoverin, a new member of the EF-hand superfamily, plays a critical role in the light/dark adaptation of retinal rods by regulating rhodopsin phosphorylation in a Ca(2+)-dependent manner. Recoverin is composed of four isoforms, each of which is modified at its N terminus by myristate (C14:0) or its structurally related fatty acid (C12:0, C14:2, or C14:1). Although the N-fatty acylation is implicated in protein-membrane and protein-protein interactions, the functional difference among the recoverin isoforms and the significance of the heterogeneous acylation have not been defined. Here we separated the heterogeneous recoverin into three fractions, C14:0-recoverin, C14:1-recoverin, and a mixture of C14:2- and C12:0- (C14:2/C12:0-) recoverin to evaluate the individual properties. Recoverin in every fraction bound Ca2+ as assessed by fluorescence spectroscopy and inhibited the light-dependent rhodopsin phosphorylation in the same range of free Ca2+ concentration (0.3-0.8 microM). However, the magnitude of the inhibition at higher Ca2+ concentration was different among the isoforms and ranked in the same order of the hydrophobicity of the N-fatty acyl groups: C14:0 > C14:1 > C14:2/C12:0. These results indicate that the diverged hydrophobicity of the recoverin N terminus plays an important role in the interaction with the membranes and/or its target protein but not with Ca2+.

Acylation↗
PubMed1994

Genetic polymorphisms of the CST2 locus coding for cystatin SA.

A new genetic polymorphism of cystatin SA has been identified in human submandibular-sublingual saliva by means of basic gel electrophoresis and immunoblotting with anti-cystatin S. Two proteins, SA1 and SA2, are given by two alleles of CST2, viz., CST2*1 and CST*2. Inheritance is controlled by two codominant alleles at an autosomal locus. This hypothesis is supported by studies of 16 families 32 children. Gene frequencies for CST2*1 and CST2*2 are 0.935 and 0.065, respectively (n = 341). Eighteen amino acids determined among 20 N-terminal residues of cystatin SA2 are identical with the sequence encoded by CST2. Three forms of cystatin S (mono-phosphorylated cystatin S, di-phosphorylated cystatin S, and non-phosphorylated cystatin S) are present in the 341 saliva samples tested.

Amino Acid Sequence↗
PubMed1993

Purification and characterization of three MEKA-like proteins in liver: association of a 94 kDa protein with beta gamma subunits of G-proteins.

Retinal 32 kDa MEKA protein (rMEKA) exists in the photoreceptor cells and forms a complex with beta gamma subunit of transducin. Bovine liver contained three MEKA-like proteins (94 kDa, 35 kDa-a, 35 kDa-b) which reacted with a rMEKA antibody. Each protein was purified as a single band on a SDS-PAGE and used for a reconstitution experiment with alpha and beta gamma subunits of cerebral G-proteins (Go/i). The 94 kDa protein inhibited GTP-binding ability of G alpha by forming a complex with beta gamma subunit.

Animals↗