Biomedical subjects

Y Ogata

Publications and source records attributed to Y Ogata.

At least 37 records · Page 2Linked to original sources

PubMed2001

Total mesorectal excision, lateral lymphadenectomy and autonomic nerve preservation for lower rectal cancer: significance in the long-term follow-up study.

We clarify the significance of total mesorectal excision (TME), lateral lymphadenectomy (LLA), and of autonomic nerve preservation (ANP) compared to conventional surgery (CVS), for lower rectal cancer. All 458 patients curatively resected between 1962 and 1997 were retrospectively investigated. In Period I from 1962-1974, when CVS only was performed, in Period II from 1975-1984, TME or TME + LLA was performed, and in Period III from 1985-1997, TME + ANP, TME + ANP + LLA, or TME + LLA was performed. In Dukes A + B disease, there was no significant difference among the three periods, regardless of operation methods. In Dukes C disease, in Period I, CVS (42 patients: pts) had a local recurrence (LR) rate of 45.2% and 5-year disease-free survival (5YDFS) rate of 33.3%. In Period II, TME + LLA (82 pts) had a lower LR rate of 26.8% (p = 0.0628) and higher 5YDFS 51.0% (p < 0.05) vs CVS. In Period III, TME + ANP (12 pts) had LR 25.0% and 5YDFS 55.6%, TME + ANP + LLA (45 pts) had LR 13.3% (p < 0.005, vs CVS) and 5YDFS 56.1% (p < 0.01, vs CVS), and TME + LLA (18 pts) had LR 16.7% (p < 0.05, vs CVS) and 5YDFS 20.8%. Also, CVS had the lowest curability rate 64.8% and the highest mortality rate 7.2%. TME and/or LLA was significant for reducing LR and improving survival in patients with Dukes C lower rectal cancer, compared to CVS. ANP was beneficial with LLA. TME + ANP was suitable for Dukes A or B disease.

Autonomic Nervous System↗

PubMed2001

The usefulness of restorative laparoscopic-assisted total colectomy for ulcerative colitis.

The aim of this study was to evaluate the effectiveness of laparoscopic-assisted total colectomy with ileal J-pouch anal anastomosis in comparison with that of conventional open total colectomy in patients with ulcerative colitis. From 1990 until 1999, 11 patients underwent open total colectomy, while 21 patients had laparoscopic-assisted total colectomy. Patients characteristics, perioperative course, and recovery were compared. Differences between the groups were tested using Student's t-test for independent groups and chi-square tests when appropriate. Nasogastric tube could be removed after POD 1.1 vs. 4.8 (p < 0.05), the mean time to passage of stool was 1.7 (range, 1 to 3) vs. 5.4 (range, 3 to 7) days (p < 0.05), and in the laparoscopic group watery stool was soon made solid after POD 24.3 vs. 87.3 (p < 0.01). There were no significant differences in the mean operating time and mean estimated operating blood loss between two groups. Postoperative morbidity did not differ significantly between the patients treated conventionally (45.5%) and laparoscopically (33.3%). The findings of this study indicate that laparoscopic-assisted total colectomy improved cosmetic results and to be a safe and effective treatment for the elective surgery of ulcerative colitis.

Adult↗

PubMed2001

Significance of cysteine rich transcription factor (CRTF) in the synthesis of tissue inhibitor of metalloproteinases 1 (TIMP-1) in gastrointestinal cancers.

We previously reported that a novel promoter enhancer element "human tissue inhibitors of metalloproteinases 1 (TIMP-1) enhancer" (HTE) and a novel transacting protein "cysteine rich transcription factor" (CRTF) induced TIMP-1 synthesis in prostate cancer cells 2xN.I.PC-3. In the present study, to clarify the significance of CRTF in gastrointestinal cancers we measured the binding activity of CRTF to HTE using an electrophoretic mobility shift assay (EMSA), and the TIMP-1 concentration by ELISA after various stimulation of six cancer cell lines (KE-3, TE-9, MKN-28, MKN-45, KM12SM, SW620). In three cell lines (KE-3, MKN-45, SW620), both the binding activity of CRTF and TIMP-1 concentration significantly increased after IL-10 stimulation. Fetal bovine serum (FBS) did not affect the binding activity of CRTF, whereas FBS induced TIMP-1 synthesis in all cell lines. In KE-3 esophageal cancer cells and SW620 colon cancer cells, both the binding activity of CRTF and TIMP-1 concentration increased in the presence of a conditioned medium (CM) of fibroblasts which was isolated from human colon cancer tissues, but did not increase in MKN-45 cells. Moreover, in the fibroblasts, both the binding activity of CRTF and the TIMP-1 concentration increased in the presence of CM from KM12SM, SW620, and TE-9 cancer cell lines. These results suggested that IL-I0, and unknown factors in addition to IL-10, induced TIMP-1 synthesis via an increase in the binding activity of CRTF in gastrointestinal cancers, and that interaction between cancer cells and fibroblasts may play an important role in TIMP-1 synthesis through a signal transduction pathway consisting of CRTF phosphorylation and HTE activation.

Cells, Cultured↗

PubMed2001

[Relationship between the anti-metastatic effect of UFT and in vitro chemosensitivity to 5-FU in metastatic tumors from orthotopic implanted colon cancer in nude rats].

We have investigated the correlation between the in vitro chemosensitivity to 5-FU, measured using the collagen gel droplet embedded culture drug sensitivity test (CD-DST), and the anti-tumor effect of UFT, a prodrug of 5-FU, in metastatic tumors from orthotopic implanted colon cancer in nude rats. Human colon cancer cells (KM12SM) were injected into the cecal wall of the nude rats. Five weeks later, the implanted cecal tumors were removed. Oral UFT (a daily dose of 30 mg/kg) was administered postoperatively for four weeks. After the UFT administration period, the lung and lymph nodes were analyzed macroscopically and microscopically. In vitro chemosensitivity to 5-FU in the lung and lymph node metastases was tested using CD-DST, and the enzymatic activities of thymidine synthetase (TS) and dihydropyrimidine dehydrogenase (DPD) in the lung and lymph node metastases were measured. A daily administration of UFT produced an inhibitory effect on lung metastasis compared with the control group. However, there was no difference in the frequency of lymph node metastasis. The inhibition rate produced by 5-FU in CD-DST was significantly higher for lung metastases than for lymph node metastases. There was no difference in the TS and DPD activities between the metastatic tumoral tissues. These results suggest that the organ specificity of the anti-tumor effects of UFT on colon metastases may be determined by CD-DST of 5-FU for individual tumors. The TS and DPD activity in the tumoral tissues may not affect the organ specificity of the anti-tumor effect of UFT on colon metastases.

Animals↗

PubMed2001

[Cellular immunotherapy for local recurrence of rectal cancer after surgery by activated lymphocyte administration--a case report].

UNLABELLED: Intrapelvic recurrence of the rectal cancer after surgery is a challenging status. We report here a case of intrapelvic tumor due to the recurrence of rectal cancer postoperatively treated by adoptive cellular immunotherapy. CASE REPORT: A 57-year-old Japanese man with an intrapelvic tumor showing bone destruction due to the recurrence of rectal cancer after abdomino-peritoneal resection was diagnosed by CT scan. He consented to simultaneous adaptive cellular immunotherapy for local recurrent lesions by administration of the activated lymphocytes. The tumor sample used for the activation of PBMC was obtained by operation. Tumor cells were prepared by mincing and enzymatic digestion of the tumor sample, and they were irradiated with a dosage of 50 Gy. Peripheral blood samples were collected from the same patient. PBMC for about 2 weeks to prepare cells for treatment were obtained from the blood sample. One million PBMC were incubated in 2 ml of the culture medium containing 10(5) irradiated autologous tumor cells and 100 IU/ml recombinant IL-2. The activated PBMCs, as autologous cancer specific killer T cells, were administered by direct regional injection (from 2 million to 8 x 10(7) cells). These injections were given repeatedly about once a week at 2-week intervals for three months. The surface phenotypes of activated PBMC or PBMC were tested by two color immunostaining technique with anti-CD3, -CD4, -CD8 and also anti-CD16, -CD25 or -CD56. Natural killer cell activity was also investigated. The clinical outcome was evaluated by CT scan and serum CEA levels. In the cultured activated PBMCs, NK cell activity was 40%, both CD3 and CD4 positive cells was 30%, and both CD3 and CD8 positive cells was 48%. There were far more CD8 cells than CD4 cells. In the PBMC, NK cell activity had increased, both CD3 and CD4 positive cells had decreased and both CD3 and CD8 positive cells had increased. There were then predominantly more CD8 cells than CD4 cells by repeated administration of the cultured activated PBMCs. The only adverse effect was grade 2 fever. Serum CEA levels fell from 293.7 ng/ml to 160 ng/ml, but the tumor size on the CT scan was slightly increased except for the directly administered region. We have been observing him as an outpatient.

Humans↗

PubMed2001

[A case of lung metastasis from colon cancer treated successfully with combined chemotherapy of CPT-11 and 5'-DFUR].

The patient was a 52-year-old woman who had sigmoid colon cancer with liver metastasis and multiple lung metastases. Resection of curability B was performed, and alternating adjuvant chemotherapy consisting of hepatic artery injection of 5-FU and systemic administration of CPT-11 was performed. Lung recurrence was found and no antitumor effect of chemotherapy was observed, so the CPT-11 which had been administered every other week was given every week in a dose of 60 mg/body, half of the original dose. Moreover, 5'-DFUR was administered in a dose of 800 mg/day every day. As a result, lung metastasis tumors were reduced markedly. Adverse events such as nausea, vomiting and depilation were mitigated, and no other toxicity was observed. The patient could thus be treated extremely safely in the outpatient clinic. This was considered to be a valuable case suggestive of the significance of combination chemotherapy of CPT-11 and 5'-DFUR and the importance of appropriate administration of CPT-11.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2001

[Relationship between prothrombin time international normalized ratio and thrombo test (%)].

OBJECTIVES: The optimal therapeutic range for laboratory evaluation of oral anticoagulant therapy is now defined by the prothrombin time international normalized ratio (PT-INR). However, the thrombo test (TT), an alternative method to measure intensity of anticoagulation, is also currently used throughout Japan. The relationship between PT-INR and TT (%) has yet to be clarified. This study investigated the relationship between PT-INR and TT (%). METHODS: The PT-INR and TT (%) were simultaneously measured of 505 consecutive samples from patients treated with warfarin in our hospital. Fourteen functions were used for regression analyses: a fractional function (Y = a/X + b), a square root function (Y = aX0.5 + b), a natural logarithmic function (Y = a.lnX + b), a power series function (Y = aXb), a quotient function (Y = abX), and polynomial functions [Y = anXn + an - 1Xn - 1 +......+ a1X1 + b, (1 < or = n < or = 9)]. The results were confirmed by the same methods in 383 samples and 296 samples from another two laboratories. RESULTS: The power series function showed the most significant (p < 0.0001) and highest adjusted R2 (0.858) correlation, with a regression formula of TT (%) = e4.48 (PT-INR)-2.09 in our laboratory. Using the same analyses, the power series function also showed the most significant and highest adjusted R2 in samples from the other two laboratories. CONCLUSIONS: This study showed that a power series function is the most appropriate for expressing the relationship between PT-INR and TT (%) among the 14 functions. The function between PT-INR and TT (%) is mainly derived from the relationship between TT (%) and TT (sec). Both internal validity and external validity confirmed the relationship between PT-INR and TT (%).

Aged↗

PubMed2000

Identification of a novel response element in the rat bone sialoprotein (BSP) gene promoter that mediates constitutive and fibroblast growth factor 2-induced expression of BSP.

Bone sialoprotein (BSP) is a sulfated and phosphorylated glycoprotein, found almost exclusively in mineralized connective tissues, that may function in the nucleation of hydroxyapatite crystals. We have found that expression of BSP in osteoblastic ROS 17/2.8 cells is stimulated by fibroblast growth factor 2 (FGF2), a potent mitogen for mesenchymal cells. Stimulation of BSP mRNA with 10 ng/ml FGF2 was first evident at 3 h ( approximately 2.6-fold) and reached maximal levels at 6 h ( approximately 4-fold). From transient transfection assays, a FGF response element (FRE) was identified (nucleotides -92 to -85, "GGTGAGAA") as a target of transcriptional activation by FGF2. Ligation of two copies of the FRE 5' to an SV40 promoter was sufficient to confer FGF-responsive transcription. A sequence-specific protein-DNA complex, formed with a double-stranded oligonucleotide encompassing the FRE and nuclear extracts from ROS 17/2.8 cells, but not from fibroblasts, was increased following FGF2 stimulation. Several point mutations within the critical FRE sequence abrogated the formation of this complex and suppressed both basal and FGF2-mediated promoter activity. These studies, therefore, have identified a novel FRE in the proximal promoter of the BSP gene that mediates both constitutive and FGF2-induced BSP transcription.

Base Sequence↗

PubMed2000

Bradykinin potentiates prostaglandin E(2) release in the human gingival fibroblasts pretreated with interleukin-1beta via Ca(2+) mobilization.

Interleukin-1beta, a proinflammatory cytokine, causes a slow increase in prostaglandin E(2) release. On the other hand, bradykinin, a chemical mediator for inflammation, induces a rapid prostaglandin E(2) release. Simultaneous stimulation with interleukin-1beta (200 pg/ml) and bradykinin (1 microM) evoked a moderately synergistic increase in prostaglandin E(2) release in human gingival fibroblasts. However, in the human gingival fibroblasts pretreated with interleukin-1beta, bradykinin drastically enhanced prostaglandin E(2) release. NS-398, a specific inhibitor of cyclooxygenase-2, inhibited not only interleukin-1beta-induced prostaglandin E(2) release but also bradykinin-induced prostaglandin E(2) release in the human gingival fibroblasts pretreated with interleukin-1beta. Transcriptional and translational inhibitors such as actinomycin D, cycloheximide, and dexamethasone also suppressed the interleukin-1beta-induced prostaglandin E(2) release and the bradykinin-induced prostaglandin E(2) release in interleukin-1beta-pretreated human gingival fibroblasts. In the fibroblasts pretreated with interleukin-1beta, Ca(2+)-mobilizing reagents such as ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on prostaglandin E(2) release. These results suggest that interleukin-1beta- and bradykinin-induced prostaglandin E(2) release is dependent on cyclooxygenase-2 and the potentiated effect of bradykinin in the human gingival fibroblasts primed with interleukin-1beta is caused by Ca(2+) mobilization.

Bradykinin↗

PubMed2000

Significance of coexpression of urokinase-type plasminogen activator, and matrix metalloproteinase 3 (stromelysin) and 9 (gelatinase B) in colorectal carcinoma.

Our previous study showed that proMMP-9 was activated by MMP-3 directly, and that proMMP-3 was activated by plasmin. It was postulated that the proMMP-9 activation mechanism through the protease-protease cascade existed even in vivo. The purpose of the present study was to clarify the clinical significance of the combined expression of MMP-9, MMP-3, and urokinase-type plasminogen activator (uPA) in colorectal cancer, and the role of MMP-3 or uPA expression as an activator for MMP-9. The expression of both MMP-9 and uPA was found to be correlated with liver metastasis, and with survival rate. The coexpression of MMP-9 and uPA by tumor cells was also significantly correlated with postoperative hepatic recurrence and survival rate. MMP-9 tended to be coexpressed with uPA, and was consistently associated with MMP-3 localized at the tumor-invasive front with inflammatory cells such as monocyte-macrophages. In gelatin zymography, the MMP-9 active form tended to be identified in the tumors that coexpressed both MMP-9 and uPA. We concluded that coexpression of MMP-9 and uPA in tumor tissues might be a useful predictive factor for postoperative survival and hepatic metastasis. The following activation mechanism for proteinase might occur: uPA coexpressed with MMP-9 activated plasminogen, and plasmin activated proMMP-3, which was secreted depending upon inflammatory infiltration, and then MMP-3 activated proMMP-9, resulting in colorectal cancer progression and metastasis.

Carcinoma↗

PubMed2000

Expression of the SART1 tumor-rejection antigens in colorectal cancers.

PURPOSE: Colorectal cancer is one of the major causes of cancer death in the world, including in the United States and Japan. We recently identified the tumor-rejection antigen gene SART1, which encodes both the SART1(259) antigen expressed in the cytosol of epithelial cancers and the SART1(800) antigen expressed in the nucleus of the majority of proliferating cells. This study investigated the expression of these tumor antigens to explore a potential molecule for specific immunotherapy of colorectal cancer patients. METHODS: SART1 antigens were investigated by Western blotting in six colorectal cancer cell lines and in 33 colorectal cancer tissues. The cancer cell lines were tested for their ability to stimulate interferon-gamma production by the human-leukocyte-antigen-A24-restricted and SART1-specific cytotoxic T lymphocytes and were also tested for their susceptibility to the lysis by the cytotoxic T lymphocytes. RESULTS: The SART1(259) antigen was detected in the cytosol of four of six cancer cell lines, 13 of 33 (39 percent) cancer tissues, and 0 of 20 nontumorous colorectal tissues. The SART1(800) antigen was expressed in the nucleus of all the colorectal cancer cell lines, 18 of 33 (55 percent) cancer tissues, and 0 of 20 nontumorous tissues. The human-lymphocyte-antigen-A24-restricted and SART1-specific cytotoxic T lymphocytes killed the human-lymphocyte-antigen-A24+ SART1(259+) cancer cells. CONCLUSIONS: The SART1(259) antigen could be an appropriate target molecule for specific immunotherapy of approximately 40 percent of the human-lymphocyte-antigen-A24+ patients with colorectal cancer.

Adenocarcinoma↗

PubMed2000

Parathyroid hormone regulation of bone sialoprotein (BSP) gene transcription is mediated through a pituitary-specific transcription factor-1 (Pit-1) motif in the rat BSP gene promoter.

Bone sialoprotein (BSP) is a mineralized tissue-specific protein expressed by differentiated osteoblasts that appears to function in the initial mineralization of bone. Parathyroid hormone (PTH), which regulates serum calcium through its actions on bone cells, increases the expression of BSP in the rat osteosarcoma cell line (ROS 17/2.8). At 10(-8) M PTH (human 1-34 PTH), stimulation of BSP mRNA was first evident at 3 h ( approximately 3.8-fold), reached maximal levels at 6 h ( approximately 4.7-fold), and declined slowly thereafter. The effects of PTH, which were abrogated by cycloheximide (28 microg/ml), did not alter the stability of the BSP mRNA. The increased transcription was mimicked by both forskolin (10(-6) M) and isoproterenol (10(-7) M), and was also increased by 3-isobutyl-1-methylxanthine (IBMX; 10(-5) M), while the transcriptional activity induced by PTH was inhibited by the protein kinase A inhibitor, H89 (5x10(-6) M). From transient transfection assays using various BSP promoter-luciferase constructs, a pituitary-specific transcription factor-1 (Pit-1) regulatory element (nts -111 to -105) was identified as the target of transcriptional activation by PTH. Thus, transcriptional activity of constructs including the Pit-1 was enhanced approximately 4.7-fold by 10(-8) M PTH while 5'-ligation of the Pit-1 element conferred PTH regulation in an SV40 promoter construct. Binding of a nuclear protein, recognized by anti-Pit-1 antibodies, to a radiolabelled Pit-1-BSP probe was decreased in nuclear extracts prepared from PTH, forskolin and isoproterenol-stimulated ROS 17/2.8 cells. Moreover, co-transfection of ROS cells with a double-stranded Pit-1 oligonucleotide also increased luciferase activity. Collectively, these results indicate that PTH acts through a protein kinase A pathway involving cAMP to stimulate BSP transcription by blocking the action of a Pit-1-related nuclear protein that suppresses BSP transcription by binding a cognate element in the BSP promoter. Thus, we have identified a novel Pit-1 suppressor element in the rat BSP gene promoter that is the target of PTH-stimulated transcription of the BSP gene.

Amino Acid Motifs↗

PubMed2000

Activation of NFkappaB is necessary for IL-1beta-induced cyclooxygenase-2 (COX-2) expression in human gingival fibroblasts.

The immediate-early cyclooxygenase-2 (COX-2) gene encodes an inducible prostaglandin synthase enzyme which is implicated in inflammatory and proliferative diseases. COX-2 is highly induced during cell activation by various factors, including mitogens, hormones and cytokines. Since pro-inflammatory cytokine IL-1beta has been shown to induce prostaglandin E2 (PGE2) release in human gingival fibroblasts (HGF), here we analyzed the effect of IL-1beta on the expression of COX-2 and the activation of NFkappaB in HGF. Northern hybridization analysis revealed that IL-1beta (200 pg/ml) increased the expression of COX-2 mRNA in HGF. The effect of IL-1beta was abrogated by herbimycin A, a protein tyrosine kinase inhibitor, and enhanced by orthovanadate, a protein tyrosine phosphatase inhibitor. IL-1beta-induced PGE2 release was blocked by the tyrosine kinase inhibitor and increased by the tyrosine phosphatase inhibitor. The results of transient transfection assays using chimeric constructs of the human COX-2 promoter (nt -1432 approximately +59) ligated to a luciferase reporter gene indicated that IL-1beta stimulated the transcriptional activity approximately 1.5-fold. Gel mobility shift assays with a radiolabelled COX-2-NFkappaB oligonucleotide (nts-223 to-214) revealed an increase in the binding of nuclear proteins from IL-1beta-stimulated HGF. This increase of DNA-protein complex formation induced by IL-1beta was blocked by herbimycin A and another tyrosine kinase inhibitor, genistein. These results suggest that NFkappaB is an important transcription factor for IL-1beta-induced COX-2 gene expression, and is involved in inducing COX-2 gene transcription through tyrosine phosphorylation in HGF.

Animals↗

PubMed2000

Hydrothermal circulation of seawater through hot vents and contribution of interface chemistry to prebiotic synthesis.

Synthesizing oligopeptides from glycine and alanine in a flow reactor, which stimulates constant hydrothermal circulation of seawater through hot vents on the primitive Earth, demonstrated that an exponential growth of the products is possible. The initial rapid growth of the product is a consequence of using the products formed in one cycle as the starting materials for the cycle of synthesis.

Alanine↗

PubMed2000

Role of leukocyte adhesion molecules in monocyte/ macrophage infiltration in weanling rats with unilateral ureteral obstruction.

BACKGROUND: Unilateral ureteral obstruction (UUO) of rats is a well-established model for studying obstructive nephropathy. Meanwhile, pathophysiology of pediatric obstructive nephropathy is not well understood. In this report, we studied monocyte/macrophage infiltration and expression of intercellular adhesion molecule 1 (ICAM-1) and macrophage antigen 1 (Mac-1) in weanling rats with UUO. METHODS: Three-week-old male Sprague-Dawley rats underwent left unilateral ureteral ligation. Both obstructed kidneys (OBK) and contralateral kidneys (CLK) were harvested at 3, 6, 12, 24, 72 and 120 h after surgery. Monocyte/macrophage infiltration and expression of ICAM-1 and Mac-1 were evaluated immunohistochemically, and results were compared with those of sham-operated control rats (SOK). RESULTS: Monocyte/macrophage infiltration was observed in the interstitium and perivascular region in the cortex of OBK within 6 h. The CLK and SOK showed slight monocyte/macrophage infiltration. Expression of ICAM-1 was markedly observed in the periarterial and peritubular interstitium and in renal cortical peritubular capillaries 12 h after obstruction. In CLK and SOK, ICAM-1 was slightly expressed in the endothelium of microvessels and parietal linings of Bowman's capsule. Expression of Mac-1 was detected mainly in cells infiltrating the perivascular interstitium in OBK. In CLK and SOK, few Mac-1-positive cells were observed. CONCLUSIONS: Adhesion molecules, ICAM-1 and Mac-1, are expected to recruit monocyte/macrophage infiltration into OBK of weanling rats with UUO.

Animals↗

PubMed2000

CALNUC (nucleobindin) is localized in the Golgi apparatus in insect cells.

A mouse monoclonal antibody 12B1 was raised against Golgi fractions from Sf21 insect cells and selected as Golgi-specific by immunostaining of the cells. The antigen was purified from the cells by immunoaffinity chromatography with the monoclonal antibody, and its N-terminal and internal amino acid sequences were determined. Based on the partial amino acid sequences, cDNA encoding the antigen protein was cloned and sequenced. The amino acid sequence deduced from the cDNA nucleotide sequence showed a homology to those of CALNUC family proteins, CALNUC (or nucleobindin, a calcium-binding Golgi protein with DNA-binding activity) and protein NEFA (a cell surface protein with DNA-binding, EF-hand, and acidic domains). The insect protein had two EF-hand loops at the same sites as the mammalian CALNUC family proteins, but had no leucine zipper which the mammalian homologues commonly have. An electron microscopic immunoperoxidase study demonstrated that the insect protein was localized in the cis-Golgi cisternae and cis-Golgi networks. Since this localization is identical to that of mammalian CALNUC, the insect protein was considered to be a homologue of CALNUC rather than that of NEFA. Assays involving proteinase K digestion, sodium carbonate extraction and Triton X-114 extraction revealed that the insect CALNUC-like protein was a soluble protein tightly associated with the luminal surface of Golgi membranes as reported for mammalian CALNUC. The insect protein was also shown to have calcium-binding activity as does mammalian CALNUC. These data verify that the insect protein is CALNUC. The existence of CALNUC in insect cells suggests that CALNUC is an essential calcium-binding Golgi protein in a wide range of the animal kingdom. A phylogenetic tree analysis, however, suggested that NEFA was derived from CALNUC long after the segregation of a mammalian ancestor from an insect ancestor.

Acetylglucosaminidase↗

PubMed2000

Chronic unilateral ureteral obstruction represented as renin-dependent hypertension.

A 50-year-old woman developed renin-dependent hypertension immediately after accidental unilateral ureteral ligation during hysterectomy, and the hypertension lasted for 5 months. Surgical release of the obstruction was carried out 157 days after the ligation. Then, her blood pressure was normalized. However, the obstructed kidney showed intensive tubulointerstitial fibrosis and functional recovery was not obtained. This case suggests that the renin-angiotensin system may be upregulated in human kidney during unilateral ureteral obstruction for a long duration.

Atrophy↗

PubMed2000

Expression of MTA1, a metastasis-associated gene with histone deacetylase activity in pancreatic cancer.

MTA1 has been identified as a metastasis-promoting gene, and its gene expression is correlated with serosal invasion and lymph node metastasis in the gastrointestinal and esophageal cancers. We examined MTA1 mRNA expression levels in 13 cell lines and 23 tumor tissues of pancreatic cancer by quantitative reverse transcription polymerase chain reaction. MTA1 mRNA expression was found in all the cell lines, however its levels were not correlated with the metastatic pontential of each cell line representing hematogenous distant metastasis. In the pancreatic cancer tissues, the overexpression of MTA1 mRNA (tumor/normal ratio >/=1) was observed in 12 out of 23. Pancreatic cancer tissues overexpressing MTA1 mRNA (T/N ratio >/=1) tended to have higher incidence of lymph node metastasis. These results together with previous findings in the gastrointestinal and esophageal cancers suggest that MTA1 might be involved in the progression, particularly in lymph node metastasis of pancreatic cancer.

Carcinoma↗