Biomedical subjects

Hideyuki Ishida

Publications and source records attributed to Hideyuki Ishida.

At least 37 records · Page 2Linked to original sources

PubMed2004

Prostacyclin attenuates oxidative damage of myocytes by opening mitochondrial ATP-sensitive K+ channels via the EP3 receptor.

Prostacyclin (PGI2) and the PGE family alleviate myocardial ischemia-reperfusion injury and limit oxidative damage. The cardioprotective effects of PGI2 have been traditionally ascribed to activation of IP receptors. Recent advances in prostanoid research have revealed that PGI2 can bind not only to IP, but also to EP, receptors, suggesting cross talk between PGI2 and PGEs. The mechanism(s) whereby PGI2 protects myocytes from oxidative damage and the specific receptors involved remain unknown. Thus fresh isolated adult rat myocytes were exposed to 200 microM H2O2 with or without carbaprostacyclin (cPGI2), IP-selective agonists, and ONO-AE-248 (an EP3-selective agonist). Cell viability was assessed by trypan blue exclusion after 30 min of H2O2 superfusion. cPGI2 and ONO-AE-248 significantly improved cell survival during H2O2 superfusion; IP-selective agonists did not. The protective effect of cPGI2 and ONO-AE-248 was completely abrogated by pretreatment with 5-hydroxydecanoate or glibenclamide. In the second series of experiments, the mitochondrial ATP-sensitive K+ (K(ATP)) channel opener diazoxide (Dx) reversibly oxidized flavoproteins in control myocytes. Exposure to prostanoid analogs alone had no effect on flavoprotein fluorescence. A second application of Dx in the presence of cPGI2 or ONO-AE-248 significantly increased flavoprotein fluorescence compared with Dx alone, but IP-selective agonists did not. This study demonstrates that PGI2 analogs protect cardiac myocytes from oxidative stress mainly via activation of EP3. The data also indicate that activation of EP3 receptors primes the opening of mitochondrial K(ATP) channels and that this mechanism is essential for EP3-dependent protection.

Adenosine Triphosphate↗

PubMed2004

Ability of anti-glycoprotein IIb/IIIa agents to dissolve platelet thrombi formed on a collagen surface under blood flow conditions.

OBJECTIVES: We examined the lytic effects of anti-glycoprotein (GP) IIb/IIIa agents on platelet thrombi formed on the collagen surface under blood flow conditions. BACKGROUND: Anti-GP IIb/IIIa agents may influence platelet thrombi already formed. METHODS: Blood samples were anticoagulated either by the specific antithrombin Argatroban (100 microM) or by unfractionated heparin (0.1 U/ml). After platelet thrombi were formed on a collagen surface following 6-min perfusion of whole blood obtained from eight adult donors containing fluorescinated platelets at a wall shear rate of 1,500 s(-1), additional blood samples from the same donors either containing or not containing anti-GP IIb/IIIa agents (abciximab, eptifibatide, or tirofiban) were perfused on these thrombi. The three-dimensional structures of the platelet thrombi were continuously observed by laser confocal microscopy equipped with a piezo-electric motor control unit and recorded. RESULTS: The platelet thrombi started to dissolve after perfusion of blood containing the anti-GP IIb/IIIa agents, whereas their growth resumed after subsequent perfusion of control blood. Only a single layer of platelets having heights of 3 +/- 1 microm, 3 +/- 2 microm, and 3 +/- 1 microm, respectively, could be seen after 6-min perfusion of blood containing abciximab, eptifibatide, and tirofiban, whereas the initial height of the platelet thrombi of 8 +/- 2 microm increased to 11 +/- 4 microm after subsequent perfusion of control blood (n = 8). The volume of the platelet thrombi, which was 3,352 +/- 1,045 microm(3) before starting the second perfusion, was reduced to 778 +/- 102 microm(3), 812 +/- 122 microm(3), and 856 +/- 144 microm(3) after 6-min perfusion of blood containing abciximab, eptifibatide, and tirofiban, respectively. CONCLUSIONS: We have shown in this study that anti-GP IIb/IIIa agents possess the ability to dissolve platelet thrombi.

Abciximab↗

PubMed2004

Ki-67 and CEA expression as prognostic markers in Dukes' C colorectal cancer.

This study investigated the relationship between clinicopathological or immunohistochemical factors and postoperative prognosis for Dukes' C colorectal cancer. Short-term survivors died from cancer within 2 years of surgery, whereas long-term survivors were disease-free for over 10 years. The groups differed in Ki-67 antigen and CEA expression in colon cancer, and CEA expression in rectal cancer that was limited to the metastatic lymph nodes. The immunohistochemical scores were higher in short-term survivors. Our data suggest that the characteristics of metastatic lymph nodes are important as a predictor of the aggressiveness of tumor behavior and that the expression of Ki-67 antigen or CEA there may be a useful indicators of patients' survival in Dukes' C colorectal cancer.

Aged↗

PubMed2004

Anorectal agenesis with a rectourethral fistula diagnosed in an adult: report of a case.

We report an unusual case of anorectal agenesis with a rectourethral fistula diagnosed in a 48-year-old man. The patient presented after noticing hematuria, although he had been aware of urinary leakage from his colostomy with occasional fecal urine for about 4 years. He had had a double-barrel colostomy created soon after birth for an imperforate anus, with revision at the age of 4 years to correct a prolapse of the stoma, but his malformation had never been repaired. We performed a physical examination, which did not reveal a perineal fistula, but urethrocystography demonstrated high anorectal agenesis with a rectourethral fistula. Thus, we resected the rectourethral fistula and created an end-colostomy. The patient had an uneventful postoperative course, and was discharged in good health on postoperative day 19. To our knowledge, this is the oldest patient to be diagnosed with anorectal agenesis and undergo resection of a rectourethral fistula.

Anus, Imperforate↗

PubMed2004

Direct nitric oxide release from nipradilol in human coronary arterial smooth muscle cells observed with fluorescent NO probe and NO-electrode.

BACKGROUND:: Nipradilol (3,4-dihydro-8-[2-hydroxy-3-isopropyl-amino]propoxy-3-nitroxy-2-H-1-benzopyran), a potent non-selective beta-adrenoceptor antagonist, has been shown to increase NO production. The mechanisms are up-regulation of nitric oxide synthase (NOS) and direct release of NO from nipradilol. The process of direct NO release from nipradilol requires a reductase, such as glutathione S-transferase (GST) in some cells but non-enzymatic NO release was reported in pig coronary arteries. Direct NO release from nipradilol in human coronary arteries has not been examined yet, though this information is of importance. PURPOSE:: To demonstrate direct NO release from nipradilol in human coronary arterial smooth muscle cells (HCASMC) by using a fluorescent NO probe (DAF-2) and an NO-electrode. METHODS AND RESULTS:: HCASMC were loaded with DAF-2 and images of fluorescence (515nm) were obtained under excitation at 488nm through an intensified CCD with an inverted phase-contrast microscope. Concomitantly, NO was measured using an NO-electrode (0.2mm o.d.; 501, Inter Medical Co. Ltd., Nagoya, Japan) after addition of various concentrations of nipradilol (1, 5 or 10microM) with or without ethacrynic acid (GST inhibitor). The cells showed no fluorescence at baseline, but intense fluorescence appeared at 30min after addition of 10microM nipradilol. The intensities of fluorescence at 30min in the control, nipradilol and nipradilol with ethacrynic acid groups were 98 +/- 6, 163 +/- 10 and 128 +/- 6% of the baseline level, respectively. Ethacrynic acid itself did not affect the fluorescence. Continuous measurements of NO by the electrode showed the NO generation peaked at about 30min, remained at the same level till about 45min and then gradually declined. Nipradilol did not produce NO at all in the absence of cells. The dose-dependency study of NO release from nipradilol showed 45 +/- 12, 72 +/- 24 and 157 +/- 23nM, respectively, at 1, 5 and 10microM nipradilol. All experiments were performed under conditions where endogenous formation of NO was inhibited by an NOS inhibitor (10(-4)M N(G)-monomethyl-l-arginine (l-NMMA)). CONCLUSION:: Nipradilol can release NO in the presence of human coronary arterial smooth muscle cells and the denitration reaction catalyzed by a reductase such as glutathione S-transferase contributes substantially to NO release from nipradilol.

Journal Article↗

PubMed2004

Direct inhibition by a statin of TNFalpha-induced leukocyte recruitment in rat pial venules - in vivo confocal microscopic study.

3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to block leukocyte-endothelial interaction independently of their cholesterol-lowering properties. The effects of statins are generally attributed to a decrease in mevalonate caused by inhibition of HMG-CoA reductase, which results in an increase of nitric oxide (NO). However, a recent in vitro study demonstrated a novel effect which depended on the lipophilicity of statin and appeared to be unrelated to HMG-CoA reductase inhibition. The purpose of this study is to investigate whether the proposed mechanism actually operates in vivo. We examined the effects of simvastatin (lipophilic) and pravastatin (hydrophilic) on leukocyte behavior in a tumor necrosis factor alpha (TNFalpha)-induced leukocyte recruitment model. Leukocyte adhesion and rolling were examined in pial venules of rat brain by using confocal laser scanning microscopy after labeling leukocytes with rhodamine 6G. Experiments were conducted 4h after TNFalpha injection (0.5microg) in six groups: control, TNFalpha alone, TNFalpha + vehicle of simvastatin, TNFalpha + simvastatin (20mg/kg, 2ml/kg), TNFalpha + vehicle of pravastatin, and TNFalpha + pravastatin (40mg/kg, 2ml/kg). Statins and vehicles were injected subcutaneously for 3 days. TNFalpha caused a marked increase in rolling and adhered leukocytes. The number of adhered leukocytes in the simvastatin group was significantly less than in the vehicle group (276 +/- 38 cells/mm(2) versus 1155 +/- 89 cells/mm(2), P < 0.01), whereas pravastatin had little effect. Both simvastatin and pravastatin showed a tendency to decrease the number of rolling leukocytes, but there were no significant differences among TNFalpha-treated groups. Up-regulation of endothelial nitric oxide synthase (eNOS) mRNA or increased expression of P-selectin or intercellular adhesion molecule-1 (ICAM-1) was not observed, and therefore cannot account for the simvastatin-induced reduction of adhered leukocytes. Markedly different effect on leukocyte adhesion between simvastatin and pravastatin under comparable level of HMG-CoA reductase inhibitor was demonstrated in in vivo as was shown in in vitro study.

Journal Article↗

PubMed2004

[The research method for investigating the role of the mitochondrial permeability transition pore in cell death].

Mitochondria play a key role in the regulation of cell death, necrosis, and apoptosis. It is well known that the opening of the mitochondrial permeability transition pore (PTP) induces the cytochrome C release and results in apoptosis. Also, it has been reported that the inhibition of PTP by cyclosporin A prevents the ischemia/reperfusion-induced necrosis. Thus, the opening of mitochondrial PTP may be a central coordinating event of apoptotic and necrotic cell death. However, the relationship between PTP opening and both modes of cell death remains elusive. In this paper, we report the recent state of our research method and the role of mitochondrial PTP in cardiac cell death.

Apoptosis↗

PubMed2004

[Tumoral dihydropyrimidine dehydrogenase expression and efficacy of 5-fluorouracil plus leucovorin plus UFT therapy in patients with colorectal cancer].

The purpose of this study was to examine the relation between tumoral expression of dihydropyrimidine dehydrogenase (DPD), the rate limiting enzyme of the degradation pathway 5-fluorouracil (5-FU), and the efficacy of 5-FU based chemotherapy for colorectal cancer. Twenty-eight colorectal cancer patients who had underwent noncurative resection (n = 16) or had developed recurrence (n = 12) were enrolled. All patients were given 5-FU plus leucovorin intravenously and UFT (1 M Tegafur, 4 M Uracil) perorally. The expression levels of the DPD in the primary lesions were determined by the enzyme-linked immunosorbent assay. Group A (n = 10) consisted of one patient with complete response, 4 with partial response, and 5 with no change (time to disease progression (TTP) > = 90 days). Group B (n = 18) consisted of 14 patients with progressive disease and 4 with NC (time to progression, < 90 days). The tumoral DPD levels did not differ between the groups (p = 0.58). There were no effective cases (n = 6) whose tumoral DPD levels were equal to or more than 83.2 U/mg protein (high DPD expression). There were marked overlaps in the DPD levels between the two groups whose DPD levels were less than 83.0 U/mg protein (moderate or low expression). These results suggest that high expression of tumoral DPD would be predictive to failure of fluoropyrimidine-based treatment. However, it is unlikely to set the optimal cutoff value for predicting the efficacy of this type of chemotherapy.

Adult↗

PubMed2004

Application of RT-PCR to clinical diagnosis of micrometastasis of colorectal cancer: A translational research study.

We previously reported in a retrospective study that CEA-based RT-PCR was useful for predicting the prognosis of patients with node-negative colorectal cancer. RT-PCR is well established for laboratory use, but many issues remain to be resolved prior to its clinical application. In addition to the false positive rate of RT-PCR, we addressed several issues, including the timing of lymph node sampling, stability of RNA after surgery, and reproducibility of results. After appropriate modification, including development of a tissue sampling kit, a multi-institutional clinical study was commenced prospectively from November 2001, and 100 patients were enrolled for examination of micrometastasis. RNA was stable in lymph nodes for up to 3 h after surgical resection. This range of sampling time was acceptable to the surgeons. RNA was well preserved in RNA later at -20 degrees C for 3 weeks. Dilutions of MKN45 and LoVo cells served as positive controls for conventional PCR since these controls were found to be highly stable and ensured reproducibility. Moreover, simultaneous use of quantitative PCR (Light Cycler) ensured double confirmation of the results. Our clinical study showed that the quality of RNA was excellent or good in most samples (98 of 100; 98%). Twenty-four of 98 (24.5%) cases were judged to be micrometastasis-positive. In conclusion, the current translational research study established a clinically feasible RT-PCR system for micrometastasis. Our system could potentially be useful as a clinical tool.

Colorectal Neoplasms↗

PubMed2004

[Two cases of resection of synchronous bilobar multiple liver metastases from colorectal cancer after hepatic arterial infusion chemotherapy].

We report 2 cases of synchronous bilobar multiple liver metastases from colorectal cancer which are hepatectomised following a hepatic arterial infusion chemotherapy. Both cases were considered unresectable metastases before chemotherapy. Case 1: A 55-year-old male, with rectal cancer and multiple hepatic metastases, was performed a low anterior resection. Hepatic arterial infusion chemotherapy (5-FU 1 g/m2 5h qw) and systemic chemotherapy (5-FU/LV) were administered. Twelve months after the first surgery, hepatectomy was performed. Case 2: Right hemicolectomy was performed on a 66-year-old male, with cancer of the transverse colon and multiple hepatic metastases. Hepatic arterial infusion chemotherapy was administered 38 times. Thirteen months after the first surgery, hepatectomy and MCT were performed. Even among the cases of unresectable hepatic metastases from colorectal cancer, there are some in which resection is possible followed by hepatic arterial infusion chemotherapy. Re-evaluation for hepatectomy is needed for the cases where hepatic arterial infusion chemotherapy is administered.

Aged↗

PubMed2004

[Usefulness of F-18-fluorodeoxyglucose positron emission tomography for evaluating the efficacy of transient hepatic arterial chemoembolization for liver metastases of rectal cancer--a case report].

It is pointed out that there can be a discrepancy between the effect diagnosed by radiographic imaging and that by histological examination, when we treat patients with liver metastases of colorectal cancer by a transient hepatic arterial chemoembolization. We report a case of liver metastases of rectal cancer in which F-18-fluorodeoxyglucose positron emission tomography (FDG-PET) was useful for evaluating the therapeutic efficacy for transient hepatic arterial chemoembolization. A 58-year-old man with synchronous liver metastases (H2) of rectal cancer underwent a low anterior resection, a partial hepatectomy, cholecystectomy, and ligation of the gastroduodenal artery. After these operations, the patient received 6 hepatic arterial injections with degradable starch microspheres (300-600 mg), adriamycin (30 mg), and mitomycin C (10 mg) for the remaining metastatic lesion (S7). Although abdominal CT scan revealed a partial response, FDG-PET did not show any abnormal deposits. Hepatic posterior segmentectomy was performed 7 months after the first operation. Histological examination did not show any viable tumor cells in the resected specimen.

Chemoembolization, Therapeutic↗

PubMed2004

[Histological examination of the effect of hepatic arterial infusion of degradable starch microspheres mixed with adriamycin and mitomycin C for liver metastases of colorectal cancer--second report].

We histologically examined the effect of hepatic arterial infusion of degradable starch microspheres mixed with adriamycin and mitomycin C (DSM therapy) for liver metastases of colorectal cancer. The subjects were 15 liver metastatic lesions from 9 patients with colorectal cancer who underwent potentially curative hepatectomy after DSM therapy. Ages were ranged from 36 to 71 years old (mean, 57). The ratio of male to female was 4 to 5. Six patients had synchronous lesion(s). A single injection dosage of the DSM therapy was comprised of 300-600 mg degradable starch microspheres, 30 mg ADM, and 10 mg MMC. Three lesions from the two patients who were given a single DSM therapy did not show any radiographical changes. In addition, histological examination of these lesions demonstrated a grade 1 effect. The radiographical effect of the 12 lesions from the 7 patients, who were given the DSM therapy at least three times, showed SD in 4 lesions, PR in 6 lesions, and PD in two lesions. Histological examination of these lesions demonstrated Grade 2 in 4 lesions and Grade 3 in 5 lesions. In conclusion, it was histologically confirmed that a repeated DSM therapy could cause satisfactory effects beyond expectations by radiographic imaging in patients with liver metastases of colorectal cancer.

Adult↗

PubMed2004

[Efficacy of hepatic arterial infusion of adriamycin and mitomycin C mixed with degradable starch microspheres for liver metastasis of colorectal cancer--correlation with the mRNA expression of DNA topoisomerase-IIalpha and glutathione-S transferase-pi in primary lesions].

DNA topoisomerase-IIalpha (topo-IIalpha) is a target enzyme of adriamycin (ADM). Glutathione-S-transferase-pi is known to be correlated with the resistance of various anticancer drugs including mitomycin C (MMC) and ADM. Expression levels of topo-IIalpha and GST-pi mRNA of primary colorectal lesions were semi-quantitatively determined by the RT-PCR method in 22 patients with colorectal cancer, who underwent hepatic arterial infusion of ADM and MMC mixed with degradable starch microspheres for synchronous (n=17) or metachronous (n=5) liver metastasis. Expression of topo-IIalpha mRNA/beta-actin mRNA was 0.872+/-0.564 (mean+/-SD) in responders (PR, n=10) and 0.369+/-0.133 in non-responders (SD+PD, n=12) (p=0.047). The relative expression of GST-pi was 0.638+/-0.593 in responders and 1.014+/-0.682 in non-responders (p=0.22). These results suggest that determining the mRNA expression of topo-IIalpha is useful for predicting the efficacy for this regimen, whereas determining the mRNA expression of GST-pi is not.

Adult↗

PubMed2003

Nicorandil attenuates the mitochondrial Ca2+ overload with accompanying depolarization of the mitochondrial membrane in the heart.

The anti-anginal drug nicorandil has been demonstrated to protect the myocardium against ischemic injury in both experimental and clinical studies. Although nicorandil seems to protect the myocardium via activation of mitochondrial ATP-sensitive K+ (mitoKATP) channels, the mechanisms underlying its cardioprotection have remained elusive. We therefore examined whether nicorandil depolarizes the mitochondrial membrane and attenuates the mitochondrial Ca2+ overload. With the use of a Nipkow confocal system, the mitochondrial Ca2+ concentration ([Ca2+]m) and the mitochondrial membrane potential (DeltaPsim) in rat ventricular myocytes were measured by loading cells with rhod-2 and JC-1 respectively. The number of cell hypercontractures resulting from mitochondrial Ca2+ overload was counted. Exposing cells to ouabain (1 mM) evoked mitochondrial Ca2+ overload and increased the intensity of rhod-2 fluorescence to 180+/-15% of baseline ( p<0.001). Nicorandil (100 microM) significantly attenuated the ouabain-induced mitochondrial Ca2+ overload (129+/-4% of baseline; p<0.001 vs. ouabain). Nicorandil decreased the DeltaPsim during application of ouabain, thereby reducing the intensity of JC-1 fluorescence to 89+/-2% of baseline ( p<0.05). Exposure of myocytes to ouabain eventually resulted in cell hypercontracture (51+/-2%). This ouabain-induced cell hypercontracture was blunted by application of nicorandil (37+/-2%, p<0.05 vs. ouabain). Moreover, these effects of nicorandil were abolished by 5-hydroxydecanoate (500 microM), a putative mitoKATP channel blocker, and by glibenclamide (10 microM), a nonselective KATP channel blocker. Our results suggest that nicorandil attenuates the matrix Ca2+ overload with accompanying depolarization of the mitochondrial membrane. Such effect might potentially be attributed to the mechanism of cardioprotection afforded by nicorandil.

Adenosine Triphosphate↗

PubMed2003

Saxitoxin blocks L-type ICa.

Saxitoxin (STX) and tetrodotoxin (TTX) are frequently used to selectively block sodium channels. In this study, we provide evidence that commercial STX also inhibits L-type Ca2+ currents (I(Ca,L)) in adult mouse ventricular myocytes (VMs) and tsA-201 cells that were transiently cotransfected with three calcium channel subunits. We measured inhibition of sodium currents (INa) in mouse VMs, of I(Ca,L) in mouse VM and tsA-201 cells, and intracellular calcium concentration ([Ca2+]i) transients in single mouse VMs. STX or TTX was abruptly applied before the test voltage pulse using a rapid solution switcher device. STX (10 microM; Calbiochem) and TTX (60 microM; Sigma-Aldrich) completely blocked INa in mouse VMs. However, STX at 10 microM also reduced I(Ca,L) in mouse VM by 39% (P < 0.0001; n = 14), whereas TTX at 60 microM had no effect on I(Ca,L). STX (10 microM; Calbiochem) reduced the amplitude of the [Ca2+]i transients in mouse VMs by 36% (P < 0.0001; n = 10). In contrast, TTX (60 microM; Sigma-Aldrich) only reduced the amplitude of the [Ca2+]i transients by 9% (P = 0.003; n = 5). STX (10 microM) obtained from Sigma-Aldrich showed a similar inhibitory effect on I(Ca,L) (33%) (P < 0.0001; n = 5) in mouse VMs. STX (Calbiochem) inhibited the calcium currents of tsA-201 cells in a dose-dependent manner. This inhibition was voltage-independent. The current-voltage relationship of calcium currents in tsA-201 cells was not altered by STX. These results indicate that STX partially blocks L-type Ca2+ channels and thus provide further evidence that its effects are not specific for Na+ channels.

Animals↗

PubMed2003

Fulminant amoebic colitis with perforation successfully treated by staged surgery: a case report.

Radical surgery for fulminant amoebic colitis leads to extremely high mortality; however, resective surgery is mandatory if a patient develops massive fecal peritonitis. We herein report an extremely rare case of fulminant amoebic colitis with multiple perforations, which was successfully treated by staged surgical procedures. A 48-year-old man who had been treated with predonisolone under a diagnosis of ulcerative colitis was admitted. Biopsy specimens from the colonic mucosa revealed Entamoeba histolytica. On the day of diagnosis, he developed severe abdominal pain and underwent emergency laparoptomy, showing total colonic gangrene with multiple perforations associated with massive fecal peritonitis. Subtotal colectomy, mucous fistula of the rectosigmoid, and ileostomy were performed. He recovered well although disseminated intravascular coagulopathy developed postoperatively. As the middle and upper part of rectum was found to be severely stenotic 4 months after surgery, we performed proctectomy, ileal pouch anal canal anastomosis, and diverting ileostomy, which was reversed 6 months later. The patient has been well with satisfactory anal function 37 months after the initial surgery. This case suggests that (1). early and accurate diagnosis of amoebiasis is important to avoid surgical intervention, and (2). staged surgery including total colectomy should be considered as one of the treatment choices even in patients with total necrotizing amoebic colitis.

Colectomy↗

PubMed2003

Serum levels of tissue inhibitor of metalloproteinases-1 (TIMP-1) in colorectal cancer patients.

PURPOSE: Expression of tissue inhibitor of metalloproteinases (TIMP)-1 in colorectal cancer tissue is known to be related to disease progression; however, the clinical significance of measuring the blood level of TIMP-1, which we evaluate herein, has not yet been clarified. METHODS: The serum level of TIMP-1 was measured by a one-step enzyme immunoassay in 123 patients who underwent resection of primary colorectal cancer. RESULTS: An elevated level of serum TIMP-1 was associated with advanced Dukes' stage ( P = 0.03), greater diameter of the primary tumor ( P = 0.03), more lymph node metastasis ( P = 0.04), and liver metastasis ( P < 0.001). There was a weakly positive correlation between the serum carcinoembryonic antigen (CEA) level and the serum TIMP-1 level. In patients who underwent potentially curative resection, the disease-free survival was not different between those with a high TIMP-1 level (>=203.5 ng/ml, n = 32) and those with a low TIMP-1 level (<203.5 ng/ml, n = 66, P = 0.62). In patients with Dukes' stage D cancer who underwent noncurative resection, the survival times were not different between those with a high TIMP-1 level ( n = 13) and those with a low TIMP-1 level ( n = 10, P = 0.20). CONCLUSIONS: Elevated levels of serum TIMP-1 reflect the extent of colorectal cancer, without a close correlation with the serum CEA level. These findings suggest that measuring the serum TIMP-1 level would not help to predict the prognosis of patients with colorectal cancer.

Aged↗

PubMed2003

Muscle strength and walking ability after laparoscopic hernioplasty versus conventional repair.

PURPOSE: We examined muscle strength and walking ability after hernia repair to compare the effects of laparoscopic hernioplasty and conventional repair. METHODS: Twenty-seven patients with primary inguinal hernias were randomly divided into two groups according to the surgical procedure: 15 patients were treated with laparoscopic hernioplasty and 12 with conventional repair. Two types of muscle testing around the inguinal region, one by manual examination and one using a musculator, were done preoperatively and 1 week postoperatively. Walking exercise tests were performed at the same time as muscle testing. RESULTS: Manual examination showed that the postoperative muscle strength of the iliopsoas muscle was decreased in six patients from the conventional repair group, but not in any of those from the laparoscopic hernioplasty group. The musculator showed decreased strength of the iliopsoas muscle after conventional repair, but not after laparoscopic hernioplasty. The walking exercise test showed that conventional hernia repair influenced walking. CONCLUSION: A decline in muscle strength of the iliopsoas muscle and walking ability was evident after conventional repair, but not after laparoscopic hernioplasty. Thus, laparoscopic hernioplasty is superior to conventional repair from the perspective of muscle testing and walking ability.

Adult↗