Biomedical subjects

T Masaki

Publications and source records attributed to T Masaki.

At least 127 records · Page 7Linked to original sources

PubMed1999

Adhesion of cultured bovine aortic endothelial cells to laminin-1 mediated by dystroglycan.

Expression of dystroglycan (DG) by cultured bovine aortic endothelial (BAE) cells was confirmed by cDNA cloning from a BAE cDNA library, Northern blotting of mRNA, Western blotting of membrane proteins, and double immunostaining with antibodies against betaDG and platelet endothelial cell adhesion molecule-1. Immunocytochemical analysis revealed localization of DG in multiple plaques on the basal side of resting cells. This patchy distribution was obscured in migrating cells, in which the most prominent staining was observed in the trailing edge anchoring the cells to the substratum. Biotin-labeled laminin-1 overlay assay of dissociated BAE membrane proteins indicated the interaction of laminin-1 with alphaDG. The laminin alpha5 globular domain fragment expressed in bacteria and labeled with biotin could also bind alphaDG on the membrane blot, and the unlabeled fragment disrupted the binding of biotin-laminin-1 to alphaDG. The interaction of biotin-laminin-1 with alphaDG was inhibited by soluble alphaDG contained in the conditioned medium from DG cDNA-transfected BAE cells and by a series of glycosaminoglycans (heparin, dextran sulfate, and fucoidan). Soluble alphaDG in the conditioned medium inhibited the adhesion of BAE cells to laminin-1-coated dishes, whereas it had no effect on their adhesion to fibronectin. All three glycosaminoglycans that disrupted the biotin-laminin-1 binding to alphaDG inhibited BAE cell adhesion to laminin-1, whereas they failed to inhibit the adhesion to fibronectin. These results indicate a role of DG as a non-integrin laminin receptor involved in vascular endothelial cell adhesion to the extracellular matrix.

Animals↗

PubMed1999

Structure and chromosomal assignment of the human lectin-like oxidized low-density-lipoprotein receptor-1 (LOX-1) gene.

We have reported the cDNA cloning of a modified low-density-lipoprotein (LDL) receptor, designated lectin-like oxidized LDL receptor-1 (LOX-1), which is postulated to be involved in endothelial dysfunction and the pathogenesis of atherosclerosis. Here, we determined the organization of the human LOX-1 gene, including the 5'-regulatory region. The 5'-regulatory region contained several potential cis-regulatory elements, such as GATA-2 binding element, c-ets-1 binding element, 12-O-tetradecanoylphorbol 13-acetate-responsive element and shear-stress-responsive elements, which may mediate the endothelium-specific and inducible expression of LOX-1. The major transcription-initiation site was found to be located 29 nucleotides downstream of the TATA box and 61 nucleotides upstream from the translation-initiation codon. The minor initiation site was found to be 5 bp downstream from the major site. Most of the promoter activity of the LOX-1 gene was ascribed to the region (-150 to -90) containing the GC and CAAT boxes. The coding sequence was divided into 6 exons by 5 introns. The first 3 exons corresponded to the different functional domains of the protein (cytoplasmic, transmembrane and neck domains), and the residual 3 exons encoded the carbohydrate-recognition domain similar to the case of other C-type lectin genes. The LOX-1 gene was a single-copy gene and assigned to the p12.3-p13.2 region of chromosome 12. Since the locus for a familial hypertension has been mapped to the overlapping region, LOX-1 might be the gene responsible for the hypertension.

Base Sequence↗

PubMed1999

Delineation of genomic deletion in cardiomyopathic hamster.

Cardiomyopathic hamster is a representative animal model for autosomal recessive cardiomyopathy. We have previously shown that the transcript of delta-sarcoglycan is missing in the heart of cardiomyopathic hamster due to genomic deletion. Here we define the normal genomic region deleted in cardiomyopathic hamster, which spans about 30 kb interval and includes the two first exons of the delta-sarcoglycan gene. RNA blot analysis using genomic DNA fragments covering the entire deletion as probes failed to detect any transcript other than delta-sarcoglycan in normal hamster heart, suggesting that delta-sarcoglycan is the only transcript defective in the heart of cardiomyopathic hamster.

Animals↗

PubMed1999

Characterization of the transmembrane molecular architecture of the dystroglycan complex in schwann cells.

We have demonstrated previously 1) that the dystroglycan complex, but not the sarcoglycan complex, is expressed in peripheral nerve, and 2) that alpha-dystroglycan is an extracellular laminin-2-binding protein anchored to beta-dystroglycan in the Schwann cell membrane. In the present study, we investigated the transmembrane molecular architecture of the dystroglycan complex in Schwann cells. The cytoplasmic domain of beta-dystroglycan was co-localized with Dp116, the Schwann cell-specific isoform of dystrophin, in the abaxonal Schwann cell cytoplasm adjacent to the outer membrane. beta-dystroglycan bound to Dp116 mainly via the 15 C-terminal amino acids of its cytoplasmic domain, but these amino acids were not solely responsible for the interaction of these two proteins. Interestingly, the beta-dystroglycan-precipitating antibody precipitated only a small fraction of alpha-dystroglycan and did not precipitate laminin and Dp116 from the peripheral nerve extracts. Our results indicate 1) that Dp116 is a component of the submembranous cytoskeletal system that anchors the dystroglycan complex in Schwann cells, and 2) that the dystroglycan complex in Schwann cells is fragile compared with that in striated muscle cells. We propose that this fragility may be attributable to the absence of the sarcoglycan complex in Schwann cells.

Animals↗

PubMed1999

The role of endothelin-converting enzyme-1 in the development of alpha1-adrenergic-stimulated hypertrophy in cultured neonatal rat cardiac myocytes.

BACKGROUND: Accumulating evidence suggests that the local synthesis of endothelin-1 (ET-1) plays a role in the development of heart failure in vivo. We investigated the role of endothelin-converting enzyme-1 (ECE-1), which mediates the conversion of big ET-1 to mature ET-1, in the development of alpha1-adrenergic-stimulated hypertrophy in cultured neonatal rat cardiac myocytes. METHODS AND RESULTS: Phenylephrine (PE) induced the expression of ET-1 in rat cardiac myocytes and accelerated the conversion of big ET-1 to ET-1. The ECE-1 mRNA levels were markedly increased 3 hours after PE stimulation (3.6-fold compared with saline stimulation, P<0.005). A specific ECE-1 antagonist, FR901533, inhibited the PE-stimulated increase in protein synthesis rate by 45% (P<0.05). As genetic markers for the hypertrophic response, FR901533 inhibited the PE-stimulated transcriptional activities of the 3.5-kb beta-myosin heavy chain promoter by 79% (P<0.01) but did not affect that of the 3.4-kb atrial natriuretic factor (ANF) promoter. In Bio14.6 Syrian cardiomyopathic hamsters, ventricular ET-1 and ANF mRNA levels did not correlate at 2 different stages. CONCLUSIONS: ET-1-independent pathways may mediate activation of the ANF gene program in ventricular myocytes both in vitro and in vivo. These results also indicate that the conversion of big ET-1 to ET-1 in rat cardiac myocytes is required for the development of alpha1-adrenergic-stimulated hypertrophy and beta-myosin heavy chain gene transcription.

Adrenergic alpha-Agonists↗

PubMed1999

Tumor necrosis factor-alpha regulates in vivo expression of the rat UCP family differentially.

A family of uncoupling proteins (UCPs), free fatty acid anion transporters, plays a crucial role in energy homeostatic thermoregulation. Tumor necrosis factor-alpha (TNF-alpha), a member of the cytokine family, is well known as an endogenous pyrogen. To evaluate the interaction of TNF-alpha with UCPs in thermogenesis, effects of TNF-alpha on rat UCP gene expression were examined in intrascapular brown adipose tissue (BAT), epididymal white adipose tissue (WAT) and soleus muscle (Muscle). Administration of TNF-alpha elevated rectal temperature by 0.7 degree C as well as serum leptin which peaked at 6 h, compared with saline controls. BAT UCP1 mRNA expression was increased by 1.2-fold at 6 h after the TNF-alpha treatment and decreased by 0.8-fold at 16 h after the treatment. In contrast to UCP1 expression in BAT, UCP2 mRNA expressions in BAT, WAT, and Muscle was increased to reach maximum levels of 1.3-, 1.6- and 1.8-fold, respectively, at 16 h after the treatment. UCP3 mRNA in Muscle, but not in BAT or WAT, was exclusively up-regulated by 1.7-fold at 16 h after the treatment. These results indicate that TNF-alpha up-regulates UCP gene expression differentially and tissue dependently, and add novel insights into thermogenesis under conditions of malignancy and inflammation.

Adipose Tissue↗

PubMed1999

T cell recognition of hypervariable region-1 from hepatitis C virus envelope protein with multiple class II MHC molecules in mice and humans: preferential help for induction of antibodies to the hypervariable region.

Hypervariable region-1 (HVR1) from the hepatitis C virus (HCV) envelope protein is thought to be a target for neutralizing Abs. To explore HVR1 recognition by helper T cells, and their role in Ab responses, we attempted to generate helper T cells specific for HVR1 in mice of three MHC types, and with PBMC from HCV-infected HLA-diverse humans. In both species, HVR1 was presented by >1 class II MHC molecule to CD4+ helper T cells and showed surprising interisolate cross-reactivity. The epitope for two DR4+ patients was mapped to a more conserved C-terminal sequence containing a DR4 binding motif, possibly accounting for cross-reactivity. Strikingly, Abs to patients' own HVR1 sequences were found only in patients with T cell responses to HVR1, even though all had Abs to envelope protein, suggesting that induction of Abs to HVR1 depends on helper T cells specific for a sequence proximal to the Ab epitope. Thus, helper T cells specific for HVR1 may be functionally important in inducing neutralizing Abs to HCV. These results may be the first example of "T-B reciprocity," in which proximity of a helper T cell epitope determines Ab epitope specificity, in a human disease setting.

Adult↗

PubMed1999

Familial paroxysmal dystonic choreoathetosis: clinical findings in a large Japanese family and genetic linkage to 2q.

BACKGROUND: Paroxysmal dystonic choreoathetosis (PDC) is a rare familial movement disorder that has been mapped to chromosome 2q31-36. OBJECTIVE: To study the first Japanese family with PDC clinically and genetically. PATIENTS AND METHODS: We studied a large Japanese family in which at least 17 members in 6 generations have been affected by PDC. We interviewed and examined 26 family members, 8 of whom revealed choreoathetosis-like and dystonialike involuntary movement and 1 of whom revealed no involuntary movement but only muscle stiffness such as the aura of paroxysmal dystonic choreoathetosis (PDC). Genetic linkage studies of this family were carried out with polymorphic DNA markers. RESULTS: The attacks of involuntary movement or muscle stiffness were precipitated by ovulation, menstruation, emotional stress, or caffeine or alcohol ingestion. Magnetic resonance imaging of the brain revealed no abnormalities. Clonazepam therapy was effective for reducing the attacks, and ingestion of garlic was believed by patients to be effective for softening the attacks. An affected woman with only muscle stiffness showed remission after hysterectomy for hysteromyoma. This woman also had the disease haplotype and transferred it to her typical PDC-affected daughter. Maximal pairwise logarithm of odds scores exceeding 2.00 were obtained at D2S2250, D2S1242, D2S377, D2S2148, and D2S126. The PDC gene was demonstrated by linkage analyses to be located in a 15.3-centimorgan interval lying between D2S371 and D2S339 based on pairwise and multipoint logarithm of odds scores and obligate recombination events in affected individuals. CONCLUSIONS: Linkage of PDC to chromosome 2q32-36 was confirmed in a Japanese family. The clinical characterizations of this family with PDC include that ovulation seems also to be a precipitating factor of the attacks and that hysterectomy seems to be effective for softening the attacks. Although low-dose clonazepam treatment was most effective, garlic use was believed by affected members to be effective for softening the attacks. Furthermore, based on the results of clinical and genetic analyses, we suggest that muscle stiffness without involuntary movement may represent a forme fruste of PDC.

Athetosis↗

PubMed1999

Reduced C-terminal Src kinase (Csk) activities in hepatocellular carcinoma.

The proto-oncogene product pp60(c-src) is the cellular homologue of the Rous sarcoma transforming gene, and it is a non-receptor-linked and membrane-associated tyrosine kinase. There is a close correlation between elevated pp60(c-src) activity and cell transformation. We have recently reported that pp60(c-src) was activated in hepatocellular carcinoma (HCC) of human and Long-Evans cinnamon (LEC) rats. However, the mechanisms involved in this process remain unknown. C-terminal Src kinase (Csk) is a novel cytoplasmic protein tyrosine kinase that inactivates the members of the Src family protein tyrosine kinase in vitro. We investigated the role of Csk in hepatocarcinogenesis by analyzing the location, amount of Csk, and its kinase activity levels in nontumorous cirrhotic and tumorous sections of HCC of patients and an animal model of LEC rats. Csk tyrosine kinase activity was significantly reduced in tumorous tissues compared with nontumorous sections of patients as well as LEC rats. A single immunoreactive band at 50 kd was detected with Csk antibody in normal liver (NL), chronic hepatitis (CH), and nontumorous cirrhotic (NTC) segments of HCC of patients and LEC rats. In human tumorous tissues, Western blot revealed a 53-kd immunoreactive band, which was slightly larger than the usual 50-kd band of Csk. These results suggest that the reduced activity of tyrosine kinase of Csk may play an important role in the malignant transformation of hepatocytes in human and LEC rat, and the appearance of 53-kd Csk-related protein may be closely involved in the progression of cirrhosis to HCC in humans, and that 50-kd Csk may act as an antioncogene through the negative regulation of pp60(c-src) in the development of human HCC.

Aged↗

PubMed1999

YMDD motif in hepatitis B virus DNA polymerase influences on replication and lamivudine resistance: A study by in vitro full-length viral DNA transfection.

Recently, lamivudine used to treat patients with hepatitis B virus (HBV) infection was revealed to have potent antiviral activity. However, HBV resistance to lamivudine has been reported and shown to have amino acid substitutions in the methionine residue of the conserved tyrosine (Y), methionine (M), aspartate (D), aspartate (D) motif of RNA-dependent DNA polymerase. To explore the consequences of substitutions in this motif (YMDD), we made 7 variants by substituting the methionine of the YMDD motif with isoleucine (I), valine (V), alanine (A), leucine (L), lysine (K), arginine (R), and threonine (T). Replication ability of these variants was evaluated by transfection into human hepatoma cells. Sensitivity to lamivudine was tested for replication-competent variants. Four variants with hydrophobic substitutions (I, V, A, and L) remained replication-competent, whereas 3 others with hydrophilic substitutions (K, R, and T) exhibited impaired replication. Of the 4 replication-competent variants, 2 (I and V) were resistant, and 2 (A and L) were sensitive to lamivudine. Because the polymerase and the surface gene overlap, the introduction of these mutations affected the secretion of hepatitis B surface antigen (HBsAg), namely 4 variants (I, V, L, and R) secreted HBsAg, whereas 3 variants (A, K, and T) did not. Our study elucidated that only one amino acid substitution in the YMDD motif was sufficient to cause lamivudine resistance in vitro. As a result of replication competence and lamivudine sensitivity, only viruses having YIDD or YVDD sequences may appear during treatment with lamivudine. This in vitro system could be used to study HBV mutations, replication competence, and their susceptibility to antivirals.

Amino Acid Sequence↗

PubMed1999

Small hyperechoic nodules in chronic liver diseases include hepatocellular carcinomas with low cyclin D1 and Ki-67 expression.

In spite of the importance of periodic screening for hepatocellular carcinoma (HCC) by ultrasonography (US) in patients with underlying liver disease, the clinicopathological characteristics of hyperechoic nodules have not been clearly evaluated. The aim of this study was to characterize the pathological and proliferating features of small hyperechoic nodules. Tissue specimens of 55 hyperechoic and 107 hypoechoic nodules less than 20 mm in diameter in patients with chronic liver disease were obtained by echo-guided needle biopsy and examined histopathologically. Of these, 42 (76%) hyperechoic and 56 (52%) hypoechoic nodules were diagnosed as HCC, and 82% of hyperechoic HCCs contained fatty change and/or clear cell change. In addition, immunohistochemical staining using cyclin D1, p53, and Ki-67 was examined. A high-level expression of cyclin D1 was found in only 5% of hyperechoic HCCs, in contrast to 38% of hypoechoic HCCs (P <.02). The labeling index of Ki-67 in hyperechoic HCCs was lower than in hypoechoic HCCs (4.2% vs. 8.9%; P <.003). However, there was no difference on p53 staining between them. Retrospective follow-up study revealed that hyperechoic nodules showed slow growth (doubling time, median: 1,403 days) initially, and came to show rapid growth (doubling time, median: 56 days). From these results, small hyperechoic nodules in chronic liver diseases are worth notice as candidates for well-differentiated HCC with low cyclin D1 and Ki-67 expression.

Adult↗

PubMed1999

Induction of lectin-like oxidized LDL receptor by oxidized LDL and lysophosphatidylcholine in cultured endothelial cells.

A functional change in the endothelium induced by oxidized low density lipoprotein (OxLDL) and its lipid-constituent, lysophosphatidylcholine (LPC), has been implicated in atherogenesis. Recently, we have cloned lectin-like OxLDL receptor (LOX-1) from bovine aortic endothelial cells (BAE). It is the major binding protein for OxLDL on the surface of BAE and is expressed in atheromatous intima of the human carotid artery as well as in intima of normal bovine aorta. In the present study, we found that OxLDL induced the expression of LOX-1 in BAE. OxLDL upregulated the level of mRNA and protein for LOX-1 in a dose- and time-dependent manner. This induction was blocked by anti-LOX-1 antibody. OxLDL also increased the activity for taking up OxLDL in BAE. Similarly, a major constituent of OxLDL, lysophosphatidylcholine (LPC), induced expression of LOX-1 in mRNA, protein and activity level, suggesting the OxLDL induced expression of LOX-1, at least in part, mediated by LPC. Since LPC did not significantly change the half-life of LOX-1 mRNA, the upregulation seemed to occur at the transcriptional level. These results suggest that LOX-1 is upregulated by the uptake of OxLDL through LOX-1 in atheromatous tissues in vivo, which would further enhance the uptake and endothelial activation and dysfunction.

Animals↗

PubMed1999

Sigmoid colon cancer associated with primary hyperparathyroidism: report of a case.

We present herein a case of sigmoid colon cancer associated with primary hyperparathyroidism (PHP). PHP is known to be associated with malignancy, and decreased intracolonic calcium (Ca) resulting from increased vitamin D (VD) levels may play a role in colorectal carcinogenesis. PHP was diagnosed in this patient by preoperative screening blood chemistry examination. The blood level of intact parathyroid hormone (PTH) was elevated and a parathyroid gland scintigram demonstrated abnormal uptake near the right lower lobe of the thyroid. There was no evidence of bone metastasis, and a sigmoid colectomy was performed with curative intent. The patient had an uneventful postoperative course without a critical elevation of the serum Ca level. This case report suggests that a relationship exists between PHP and colon cancer, and the possible mechanisms of this association are presented in our discussion.

Adenocarcinoma↗

PubMed1999

The occurrence of an abdominal wall abscess 11 years after appendectomy: report of a case.

Most complications after appendectomy occur within 10 days; however, we report herein the unusual case of a patient in whom a wound abscess was detected more than 10 years after an appendectomy. A 26-year-old woman presented to our hospital with nausea and vomiting, pain, and a mass in the right lower abdominal wall. She had undergone an appendectomy 11 years previously. Physical examination revealed a tender mass, 5 cm in diameter, under the appendectomy scar. An abdominal ultrasonography demonstrated a low-echoic mass lesion measuring 9.0 x 5.0 x 2.0 cm. Incision of the connective tissue revealed about 3 ml of cream-colored and odorless fluid in the abscess cavity. Fistulography revealed an abscess cavity not communicating with the bowel lumen. Floss was discovered in the connective tissue and removed. Debridement of the abscess wall was performed and a piece of the wall was sent for histologic examination. Pathological examination revealed panniculitis of the subcutaneous tissue, and panniculitis with granulation and granuloma of the abscess wall. This case report demonstrates that a preoperative diagnosis should be based not on one finding, but on all findings collected, inclusively.

Abdominal Abscess↗

PubMed1999

Pharmacological characterization of receptor-mediated Ca2+ entry in endothelin-1-induced catecholamine release from cultured bovine adrenal chromaffin cells.

To clarify the mechanism for the endothelin-1 (ET-1)-induced release of catecholamines from the adrenal gland, we examined the effects of removal of extracellular Ca2+, blockers of L-, N-, P- and Q-types of voltage-operated Ca2+ channels (VOCC) such as nifedipine (L-type), omega-conotoxin GVIA (N-type), omega-agatoxin IVA (P-type) and omega-conotoxin MVIIC (Q-type) and blockers of voltage-independent Ca2+ entry channel such as SK&F 96365 and LOE 908 on release of catecholamines, the cytosolic free Ca2+ concentration ([Ca2+]i), and 45Ca2+ uptake in cultured bovine adrenal chromaffin cells. ET-1 but not ET-3 induced increases in release of catecholamines, [Ca2+]i, and 45Ca2+ uptake. The responses to ET-1 were abolished by the antagonist for ET(A) receptors, BQ-123, but not by the antagonist for ET(B) receptors, BQ-788, and they were abolished by removal of extracellular Ca2+. The increases were only partially inhibited (to about 65% of control) by nifedipine but unaffected by any of the omega-toxins. The nifedipine-resistant increase was inhibited by SK&F 96365 (to about 40%) and abolished by LOE 908 alone. These results indicate that ET-1 augments the release of catecholamines from adrenal chromaffin cells through ET(A) receptors, by activating two types of Ca2+ entry channels in addition to L-type VOCC: one (nonselective cation channel-1; NSCC-1) is sensitive to LOE 908 but resistant to SK&F 96365, whereas the other (NSCC-2) is sensitive to both LOE 908 and SK&F 96365.

Acetamides↗

PubMed1999

Rapid growth of residual colonic tumor after incomplete mucosal resection.

We report an 89-year-old man with colon cancer that developed rapidly after an incomplete endoscopic mucosal resection (EMR), and discuss the adverse effect of this maneuver on the tumor biology. A sessile polyp, 15 mm in size, was detected at the hepatic flexure. EMR was performed immediately. Histological examination showed well differentiated adenocarcinoma with an adenomatous component invading the submucosal layer. There was vascular invasion (positive on elastica van Gieson staining) and the surgical margin was positive for cancer. A right hemicolectomy was performed. The surgical specimen showed the residual tumor, 22 mm in diameter. The relevant histopathological findings of the surgical specimen were: well differentiated adenocarcinoma, with partly mucinous carcinoma and a tubular adenomatous component, depth muscularis propria (mp), lymph node (LN) (0/9). Most of the submucosally invasive cancer was resected by the initial EMR, but the small residual tumor showed rapid growth within only 3 months after the EMR. It was assumed that the residual tumor cells had acquired more malignant characteristics after EMR. In regard to EMR we propose that: (1) except for patients who are at high risk for a major operation, EMR should be avoided for carcinoma with massive submucosal invasion, (2) colonic resection should be performed immediately when histology shows a positive surgical margin for carcinoma, and (3) patients operated after an incomplete EMR should be watched very carefully for the detection of recurrence.

Adenocarcinoma↗

PubMed1999

Severe complications of ulcerative colitis after high-dose prednisolone and azathioprine treatment.

We report a rare case of ulcerative colitis (UC) associated with methicillin-resistant Staphylococcus aureus (MRSA) and Pseudomonas aeruginosa infections in multiple organs, and with compressive fracture from osteoporosis after the administration of high-dose prednisolone and azathioprine. A 25-year-old man had been treated with high-dose prednisolone for UC. He suddenly experienced severe lumbago, which prevented him from walking. Plain X-ray demonstrated compressive fractures of the thoracic and the lumbar vertebrae, which were thought to be due to osteoporosis as a side effect of the high-dose prednisolone. At this admission, in another hospital, he also had a bloody discharge from the rectum, and azathioprine was started; however, the patient's condition still did not show any improvement. The total doses of azathioprine and prednisolone he had received were 3150 mg and more than 15,000 mg, respectively. Considering the presence of the serious complications, surgical intervention was the treatment selected. Culture study revealed MRSA in the feces and nasal cavity, and P. aeruginosa in the feces and urine. Vancomycin hydrochloride and gentamicin were administered, and were effective, with a subsequent negative culture study. Subtotal colectomy with mucus fistula was performed. After the operation, culture studies remained negative. Major steroid side effects such as bone fracture and osteoporosis should be considered as an indication for surgery in UC patients. MRSA and P. aeruginosa are a menace, especially for UC immunosuppressed patients on steroid or immunosuppressive therapy. When these bacteria are detected, there should be prompt and adequate antimicrobial therapy against the organisms and the immunosuppressive therapy should be immediately discontinued. We conclude that surgical therapy should be considered in the earlier stage for patients with intractable UC, rather than continuing long-term administration of steroid or azathioprine, which may lead to serious complications.

Adult↗

PubMed1999

Gasless laparoscopically assisted colonic surgery.

BACKGROUND: Laparoscopic technique has been applied to a variety of colonic and rectal operations, generally using carbon dioxide insufflation (CDI). However, CDI is inevitably associated with cardiopulmonary loading and can cause complications. The objective of this study was to determine the feasibility of gasless laparoscopic colonic surgery. METHODS: The abdominal wall was lifted up using an originally designed retractor. A small incision, 3 to 5 cm in length, was made at the start of the operation. The surgeon operated through this incision using both conventional and laparoscopic instruments. RESULTS: Operations were undertaken in 67 patients. In 6 patients (9%), conversion to open surgery was necessitated. In the remaining 61 patients, operations were completed with gasless laparoscopically assisted technique. Four reoperations (7%) were performed because of postoperative bleeding, anastomotic rotation, anastomotic stricture, and transmesenteric hernia. Fifty-three patients with colonic cancer were operated on with potentially curative intent. Of these, 1 (2%) developed hepatic recurrence during the mean follow-up period of 23.8 months. There was no port site recurrence. CONCLUSIONS: Gasless laparoscopic colonic surgery is technically feasible. CDI is not necessary to perform minimal access surgery.

Carbon Dioxide↗