Biomedical subjects

Y Kishimoto

Publications and source records attributed to Y Kishimoto.

At least 37 records · Page 2Linked to original sources

PubMed2002

Reduced Fhit expression is associated with mismatch repair deficiency in human advanced colorectal carcinoma.

The Fragile Histidine Triad gene, encompassing the FRA3B fragile site at chromosome 3p14.2, is a candidate tumour suppressor gene involved in multiple tumour types including colorectal carcinomas. Recently, it has been reported that the Fragile Histidine Triad gene may be a target of damage in a fraction of mismatch deficient tumours. To explore this hypothesis, we analysed both Fragile histidine triad and mismatch repair protein (Msh2 and Mlh1) expression using immumohistochemical methods in 52 advanced colorectal carcinomas (19 well-, 17 moderately-, and 16 poorly-differentiated). In addition, we examined whether the Fragile histidine triad and mismatch repair protein expression correlated with p53 expression and clinicopathological findings. Significant loss or reduction of Fragile histidine triad expression was noted in 18 of the 52 (34.6%) advanced colorectal carcinomas: 2 (10.5%) well-differentiated, 3 (17.6%) moderately-differentiated, 13 (81.3%) poorly-differentiated carcinomas, the frequency being significantly higher in the latter than that in the former two (P<0.0001). Loss of mismatch repair protein (mainly, Mlh1) expression was detected in 21 of the 52 (40.4%) colorectal carcinomas. Moreover, reduced Fragile histidine triad expression was significantly associated with absence of mismatch repair protein expression in the advanced colorectal carcinomas (P<0.0001). However, the Fragile histidine triad and mismatch repair protein expression was not significantly associated with p53 expression. These results suggested that reduced Fragile histidine triad expression might be correlated with mismatch repair expression, but not with p53 expression.

Acid Anhydride Hydrolases↗

PubMed2002

Molecular changes in the early stage of colon carcinogenesis in rats treated with azoxymethane.

To elucidate early molecular events related to colon carcinogenesis, we examined alterations in the expression of colon cancer-related genes such as cyclooxygenase (COX)-2, APC and c-Myc, cell proliferation and apoptosis in the background colon mucosa, and K-ras mutation at aberrant crypt foci (ACF) in the colons of azoxymethane (AOM)-treated rats 4 weeks after the first exposure to AOM. About 40 ACF/colon were induced in the colons of rats treated with AOM (Group 1); however, rats not treated with AOM (Group 2) showed no ACF formation in the colon. The level of AgNORs in the colonic mucosa was significantly higher in Group 1 than in Group 2 (P<0.01). The colonic mucosa in Group 1 looked macroscopically and histologically normal, but the proliferative activity of the mucosa of rats treated with AOM was clearly elevated. COX-2 mRNA expression was not detected in normal colonic mucosa in Group 2, but 3 out of 10 rats in Group 1 showed COX-2 mRNA expression in their colons by reverse transcription (RT)-polymerase chain reaction (PCR). There was a tendency toward an increased expression level of COX-2 in the AOM-treated group. The level of APC mRNA expression in Group 1 was significantly lower than that in Group 2 (P<0.01). Moreover, the level of c-Myc mRNA expression in Group 1 was significantly higher than that in Group 2 (P<0.01). An average of 0.034+/-0.006% apoptosis in colonic mucosa was detected in Group 1; the incidence of apoptosis in Group 2 was 0.021+/-0.005%. The difference between Groups 1 and 2 was significant (P<0.01). These results indicate that apoptosis was possibly induced to eliminate cells damaged by AOM administration. Six out of 22 (27%) ACF with 4 or more crypts showed K-ras mutations at codon 12; all mutations were G to A transitions (GGT to GAT). ACF with 1-3 crypts showed no mutations in the K-ras gene. In conclusion, AOM caused an increase in COX-2 and c-Myc mRNA expression, a decrease in APC mRNA expression, induction of apoptosis in normal-appearing colonic mucosa, and a K-ras mutation in ACF with 4 or more crypts. These findings may help to identify key targets in the early steps of colon carcinogenesis, against which drugs that would be broadly effective for chemoprevention of colon cancer could be developed.

Adenomatous Polyposis Coli Protein↗

PubMed2001

hTR repressor-related gene on human chromosome 10p15.1.

Somatic cells express genes that suppress telomerase activity and these genes may be inactivated in tumour cells. We postulated that cancer cells acquire immortality by activation of telomerase by the loss of such a gene. We have reported recently that a telomerase repressor gene may be located on 10p15.1 by deletion mapping using microcell-mediated chromosome transfer (MMCT), radiated microcell fusion (RMF), fluorescent in situ hybridization (FISH) and STS analysis. To independently confirm this result, we correlated expression of RNA component of telomerase (hTR) as a marker of telomerase expression by in situ hybridization with allelic loss in pulmonary carcinoid tumours. Unlike most malignant tumours, pulmonary carcinoids (which are low-grade malignant tumours) are heterogeneous for telomerase expression. Loss of 5 closely spaced polymorphic markers on 10p15.1, especially D10S1728, were highly correlated with hTR expression. In an additional experiment, 10p15.1 showed higher and more significant correlation than any region of 3p where it has been predicted as another chromosomal location of telomerase repressor with allelic loss of the region. Our findings strongly suggest that 10p15.1 harbours a gene involved in repression of telomerase RNA component in human somatic cells and each putative repressor (on 3p and 10p) may act independently.

Carcinoid Tumor↗

PubMed2001

Age-dependent impairment of delay and trace eyeblink conditioning in mice.

The age effect on classical eyeblink conditioning in unrestrained mice (C57BL/6J strain) was evaluated. Mice were trained at one of three age periods (8, 45-50 or 85-90 weeks). In the delay paradigm, significant learning deficits were evident in the 85-90 week-old group, but no deficits were observed in the behavior of the 45-50 week-old group. On the other hand, in the trace paradigm with a stimulus-free trace interval of 500 ms, significant deficits became apparent at the age of 45-50 weeks. These results indicate that trace eyeblink conditioning is more susceptible to age-related deterioration of memory in mice than delay eyeblink conditioning.

Aging↗

PubMed2001

Impaired delay but normal trace eyeblink conditioning in PLCbeta4 mutant mice.

To elucidate the functional role of phospholipase Cbeta4 (PLCbeta4), which is highly expressed in the Purkinje cells of the rostral cerebellum, cerebellar long-term depression (LTD) and delay and trace eyeblink conditioning were investigated in PLCbeta4-deficient mice. Rostral cerebellar LTD and delay eyeblink conditioning were severely impaired, whereas trace eyeblink conditioning was not. These results indicate that PLCbeta4 is essential for LTD in the rostral cerebellum and delay conditioning, but not trace conditioning. Rostral cerebellar LTD may be required as a neural substrate for delay conditioning, but is not required for trace conditioning.

Afferent Pathways↗

PubMed2001

Phospholipase Cbeta4 and protein kinase Calpha and/or protein kinase CbetaI are involved in the induction of long term depression in cerebellar Purkinje cells.

Activation of the type-1 metabotropic glutamate receptor (mGluR1) signaling pathway in the cerebellum involves activation of phospholipase C (PLC) and protein kinase C (PKC) for the induction of cerebellar long term depression (LTD). The PLC and PKC isoforms that are involved in LTD remain unclear, however. One previous study found no change in LTD in PKCgamma-deficient mice, thus, in the present study, we examined cerebellar LTD in PLCbeta4-deficient mice. Immunohistochemical and Western blot analyses of cerebellum from wild-type mice revealed that PLCbeta1 was expressed weakly and uniformly, PLCbeta2 was not detected, PLCbeta3 was expressed predominantly in caudal cerebellum (lobes 7-10), and PLCbeta4 was expressed uniformly throughout. In PLCbeta4-deficient mice, expression of total PLCbeta, the mGluR1-mediated Ca(2+) response, and LTD induction were greatly reduced in rostral cerebellum (lobes 1-6). Furthermore, we used immunohistochemistry to localize PKCalpha, -betaI, -betaII, and -gamma in mouse cerebellar Purkinje cells during LTD induction. Both PKCalpha and PKCbetaI were found to be translocated to the plasmamembrane under these conditions. Taken together, these results suggest that mGluR1-mediated activation of PLCbeta4 in rostral cerebellar Purkinje cells induced LTD via PKCalpha and/or PKCbetaI.

Animals↗

PubMed2001

Loss of heterozygosity of the mannose 6-phosphate/insulin-like growth factor II receptor and p53 genes in human hepatocellular carcinoma.

Information about M6P/IGF2R and p53 genes in hepatocarcinogenesis is limited and controversial. We tested the loss of heterozygosity (LOH) of M6P/IGF2R and p53 genes in cirrhotic and neoplastic foci in surgically resected livers of 30 patients with hepatocellular carcinoma (HCC). The DNAs extracted from microdissected specimens were used for polymerase-chain-reaction (PCR)-based assay. LOH of the M6P/IGF2R gene in the primary HCCs was detected in 10 of 22 informative cases (45%). In five of these 10 cases (50%), LOH was detected in cirrhotic lesions adjacent to the HCCs. The allelic loss patterns of M6P/IGF2R in liver cirrhosis (LC) were identical to those in the corresponding HCC, suggesting that HCC could develop from one of the cells in which M6P/IGF2R had been lost. Furthermore, LOH of the p53 gene in HCC was detected in 10 (43%) of 23 informative cases, and p53 loss in cirrhotic foci adjacent to HCC was shown in one of the 10 cases (10%). The pattern of allelic loss of the p53 gene in the cirrhotic foci was identical with that in the corresponding tumor. The LOH of the M6P/IGF2R and p53 genes occurred independently in HCCs. LOH of the M6P/IGF2R locus was a relatively frequent and possibly early event in hepatocarcinogenesis, and LOH of the M6P/IGF2R gene and LOH of the p53 gene occurred independently.

Journal Article↗

PubMed2001

Comparison of the kinetic disposition of and serum gastrin change by lansoprazole versus rabeprazole during an 8-day dosing scheme in relation to CYP2C19 polymorphism.

BACKGROUND: Little is known about differences in the disposition kinetics and pharmacological effects on gastrin levels between lansoprazole and rabeprazole given in a repeated dosing scheme with respect to the polymorphic CYP2C19. AIM: To provide preliminary information that should be considered when prescribing proton-pump inhibitors (PPIs) for the treatment of acid-related diseases with reference to the CYP2C/9 genotypic status. METHODS: Helicobacter pylori-negative healthy volunteers were divided into the following three groups (n = 5 each) on the basis of genotyping for CYP2C19: homozygous (hmEMs) and heterozygous extensive metabolizers (htEMs), and poor metabolizers (PMs). All received once-daily 30-mg doses of lansoprazole or 10-mg doses of rabeprazole during an 8-day course in a crossover manner. RESULTS: The relative values for the area under the serum concentration-time curve (AUC) of lansoprazole and rabeprazole in the hmEMs, htEMs, and PMs after the final doses were 1:1.7:3.9 and 1:1.7:3.8, respectively. The relative AUCs of gastrin in the hmEMs, htEMs, and PMs were 1.6:2.6:3.1 for lansoprazole and 1.6:2.6:2.9 for rabeprazole, respectively. CONCLUSION: The disposition kinetic behavior of the two PPIs is co-segregated with CYP2C19. The magnitude of CYP2C19-dependent drug availability in the systemic circulation and resulting gastrin response appears to be fairly similar between the two drugs within the same CYP2C19 genotypic groups after a multiple-dosing regimen.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed2001

Multicenter prospective study of interferon-alpha versus bone marrow transplantation for newly diagnosed patients with chronic myelogenous leukemia: a preliminary analysis.

Interferon-alpha (IFN-alpha) therapy was compared with bone marrow transplantation (BMT) in patients with chronic myelogenous leukemia (CML) in a multicenter, prospective study. Of 254 evaluable patients, 175 received IFN-alpha and 79 received allogeneic BMT, 50 of whom received transplants from human leukocyte antigen (HLA)-identical related donors and 29 from HLA-matched unrelated donors. Complete hematologic response was achieved by 148 patients (89%) in the IFN-alpha group and 53 (78%) in the BMT group. In the IFN-alpha group, a complete cytogenetic response was induced in 25 patients (15%), a partial cytogenetic response in 37 (23%), and a minor cytogenetic response in 41 (25%). At a median follow-up of 38 months, in the IFN-alpha group the predicted 5-year survival rate was 79%, and the predicted 5-year rate of remaining in chronic phase was 66%. In the BMT group the predicted 5-year survival rate was 72% for related-donor BMT and 67% for unrelated-donor BMT. Among low Sokal-risk patients, 5-year survival did not differ between IFN-alpha therapy and BMT, irrespective of age. In higher Sokal-risk patients, survival for related-donor BMT and unrelated-donor BMT tended to be better than that with IFN-alpha therapy in younger patients. On the other hand, in older patients, survival in the BMT group, especially for those receiving unrelated-donor BMT, appeared to be inferior to that in the IFN-alpha group. Unrelated-donor BMT can be recommended for high-risk younger patients. However, for older patients, it should be performed after careful consideration of prognostic factors such as age, Sokal score, and response to IFN-alpha.

Adolescent↗

PubMed2001

Influence of angiotensin II type 1 receptor polymorphism on hypertension in patients with hypercholesterolemia.

Essential hypertension results from the combined influence of environmental and genetic factors. The relationship between angiotensin II type 1 receptor (AT(1)) A-C(1166) polymorphism and essential hypertension is controversial. Because it is accepted that high concentration of serum cholesterol is one of risk factors of atherosclerosis, we investigated the influence of the AT(1) A-C(1166) polymorphism on hypertension in patients with hypercholesterolemia. A total of 131 hypertensive, 97 borderline, and 175 normotensive subjects were enrolled in this study. We selected hypercholesterolemic subjects on the condition that their serum concentration of total cholesterol was >220 mg/dl, and obtained 55 hypertensive, 24 borderline, and 52 normotensive subjects with hypercholesterolemia. There were no significant differences in the genotype nor allele frequency between hypertensive and normotensive subjects in the overall population. However, the presence of the C allele of the AT(1) gene has a tendency to increase the value of systolic blood pressure not only in subjects with hypercholesterolemia but also in the overall population. Furthermore, we found a significant relationship between the AT(1) polymorphism and hypertension in subjects with hypercholesterolemia; i.e., the frequency of the C allele of the AT(1) gene was significantly higher in hypertensives than in normotensives (P<0.005). These results suggested that high concentration of total cholesterol was an important risk factor to the occurrence of essential hypertension for patients who carried the C allele of the AT(1) gene.

Aged↗

PubMed2001

Effects of the noncompetitive NMDA receptor antagonist MK-801 on classical eyeblink conditioning in mice.

N-methyl-D-aspartate (NMDA) receptors are involved in synaptic plasticity and play a critical role in learning and memory. We investigated the effects of the noncompetitive NMDA receptor antagonist (+)MK-801 on classical eyeblink conditioning of mice, using various interstimulus intervals between the conditioned stimulus (CS) and unconditioned stimulus (US). A tone was used for the CS and a periorbital shock was used for the US. In the delay paradigm, in which the US coterminated with the CS or started immediately after CS offset, the effect of (+)MK-801 (0.1mg/kg, i.p.) was a slight impairment in the acquisition of the conditioned response (CR). During subsequent CS-alone trials, the responses of (+)MK-801-injected mice were extinguished as easily as those of saline-injected mice. In the trace paradigm, (+)MK-801 impaired acquisition of the CR with a trace interval of 250 ms more than it did with a trace interval of 100 ms, and more than in the delay paradigm. (+)MK-801 injected after acquisition of 250-ms trace conditioning did not impair expression or extinction of the CR. These results suggest that NMDA receptors are involved in acquisition of the CR during longer trace interval conditioning more than during shorter trace interval conditioning or delay conditioning, and that their contribution to extinction is much smaller than their contribution to acquisition in mouse eyeblink conditioning.

Animals↗

PubMed2001

Interferon alpha inhibits intrahepatic recurrence in hepatocellular carcinoma with chronic hepatitis C: a pilot study.

The aim of the present study is to evaluate whether interferon alpha (IFNalpha) therapy can inhibit intrahepatic recurrence after the curative treatment of small HCC with underlying chronic hepatitis C. Forty patients were enrolled in this study. They had solitary, small HCC</=3 cm in diameter, underlying chronic hepatitis C, and were </=70 years old. Of the patients, 18 were treated with IFNalpha for 6 months after the treatment of HCC, and 22 patients who did not receive IFNalpha therapy were used as controls. Six (33%) patients in the IFN group showed sustained response. The incidence of local recurrence was not different in the IFN and non-IFN groups (6 vs. 9%). The cumulative incidences of distant recurrence in the non-IFN and IFN groups were 9 and 6% at 1 year, 27 and 11% at 2 years, 63 and 18% at 3 years, 76 and 28% at 4 years, and 82 and 28% at 5 years; they were significantly different (P<0.01). Six (27%) patients in the non-IFN group died from the progression of HCC, but all IFN-treated patients were alive (P<0.05). The pilot study demonstrates that IFNalpha therapy after the curative treatment of small HCC can inhibit intrahepatic recurrence in the remnant liver and improve the prognosis of hepatitis C virus-related HCC.

Journal Article↗

PubMed2001

Long-trace interval eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit epsilon 1.

To elucidate the role of the N-methyl-D-aspartate (NMDA) -type glutamate receptor subunit epsilon 1 (GluR epsilon 1) in classical eyeblink conditioning, delay and trace eyeblink conditioning were investigated in GluR epsilon 1-null mutant mice. In delay conditioning and short-trace interval conditioning with a trace interval of 250 ms, GluR epsilon 1 mutant mice attained a normal level of the conditioned response (CR), although acquisition was a little slower than in wild-type mice. In contrast, GluR epsilon 1 mutant mice exhibited severe impairment of the attained level of the CR and disturbed temporal pattern of CR expression in trace conditioning with a longer trace interval of 500 ms. These findings indicate that GluR epsilon 1 is essential for long-trace interval eyeblink conditioning. The impairments of the associative learning with a long temporal separation between the conditioned and unconditioned stimuli observed in the GluR epsilon 1 mutant mice could be attributed to an impairment of hippocampal long-term potentiation in this line of mutant mice.

Animals↗

PubMed2001

Classical eyeblink conditioning in glutamate receptor subunit delta 2 mutant mice is impaired in the delay paradigm but not in the trace paradigm.

In mice lacking glutamate receptor subunit delta 2 (GluR delta 2(-/-_ mice), cerebellar long-term depression (LTD) at the parallel fibre-Purkinje cell synapses is disrupted. Unlike the cerebellar LTD-deficient mice previously used for eyeblink conditioning, however, the abnormalities of the GluR delta 2(-/-) mice are restricted to the cerebellar cortex. In delay eyeblink conditionings (interstimulus interval of 252 and 852 ms), in which the conditioned stimulus (CS) overlaps temporally with a coterminating unconditioned stimulus (US), GluR delta 2(-/-) mice are severely impaired in learning, strongly supporting the hypothesis that cerebellar cortical LTD is essential for delay conditioning. In the trace paradigm, in which a stimulus-free trace interval of 500 ms intervened between the CS and US, GluR delta 2(-/-) mice learned as successfully as wild-type mice, indicating that cerebellar LTD is not necessary for trace conditioning. Thus, the present study has revealed a cerebellar LTD-independent learning in eyeblink conditioning.

Animals↗

PubMed2001

Impairment of eyeblink conditioning in GluRdelta2-mutant mice depends on the temporal overlap between conditioned and unconditioned stimuli.

Mice lacking the glutamate receptor subunit delta2 (GluRdelta2) are deficient in cerebellar long-term depression (LTD) at the parallel fibre-Purkinje cell synapses. We conducted delay and trace eyeblink conditioning with these mice, using various temporal intervals between the conditioned stimulus (CS) and unconditioned stimulus (US). During trace conditioning in which a stimulus-free trace interval (TI) of 250, 100 or 50 ms intervened between the 352-ms tone CS and 100-ms US, GluRdelta2-mutant mice learned as successfully as wild-type mice. Even in the paradigm with TI = 0 ms, in which the end of CS and onset of US are simultaneous, there was no difference between the GluRdelta2-mutant and wild-type mice in their acquisition of a conditioned response. However, in the delay paradigm in which the 452-ms CS overlapped temporally with the coterminating 100-ms US, GluRdelta2-mutant mice exhibited severe learning impairment. The present study together with our previous work [Kishimoto, Y., Kawahara, S., Suzuki, M., Mori, H., Mishina, M. & Kirino, Y. (2001) Eur. J. Neurosci., 13, 1249-1254], indicates that cerebellar LTD-independent learning is possible in paradigms without temporal overlap between the CS and US. On the other hand, GluRdelta2 and cerebellar LTD are essential for learning when there is CS-US temporal overlap, suggesting that the cerebellar neural substrates underlying eyeblink conditioning may change, depending on the temporal overlap of the CS and US.

Animals↗

PubMed2001

Mechanism of opioid dependence and interaction between opioid receptors.

Clinical studies have demonstrated that when opiates are used to control cancer pain, psychological dependence and analgesic tolerance are not a major concern. The present study was, therefore, designed to investigate the modulation of rewarding effects of opiates under inflammatory chronic pain. Formalin or carrageenan was injected into the plantar surface of the rat paw. Formalin and carrageenan reduced the paw pressure threshold. The hyperalgesia lasted for 9-13 days. The rewarding effect of morphine was evaluated by conditioned place preference paradigm. Morphine produced a significant place preference. This effect was significantly attenuated in inflamed groups compared with the respective non-inflamed groups. Furthermore, the morphine-induced place preference in the inflamed group gradually recovered to the respective control level as the inflammation healed. We also found that kappa-receptor agonists markedly inhibited the rewarding effect of mu-receptor agonists. Therefore, to elucidate the mechanism of this attenuation, the effects of pretreatment with kappa- and delta-receptor antagonists, nor-binaltorphimine (nor-BNI) and naltrindole (NTI), on the development of the morphine-induced place preference under inflammation were examined. Nor-BNI, but not NTI, eliminated the suppression of the morphine-induced place preference in inflamed groups. The morphine-induced increase in dopamine (DA) turnover in the limbic forebrain was suppressed under inflammation, and the suppression was abolished by the pretreatment with nor-BNI. These results suggest that endogenous kappa-opioid systems may be activated by chronic inflammatory nociception, and then the activation of kappa-opioid system may inhibit DA release in nucleus accumbens, resulting in the suppression of the development of rewarding effects produced by morphine.

Analgesics, Opioid↗

PubMed2001

Reduced Fhit expression occurs in the early stage of esophageal tumorigenesis: no correlation with p53 expression and apoptosis.

The FHIT gene, encompassing the FRA3B fragile site at chromosome 3p14.2, is a candidate tumor suppressor gene involved in multiple tumors, including esophageal carcinoma. We analyzed Fhit expression using an immunohistochemical method in invasive carcinoma, carcinoma in situ (CIS) and dysplasia, in paraffin sections of 75 esophageal squamous cell carcinomas (ESCs) to further elucidate the role of Fhit protein in esophageal carcinogenesis. In addition, we also examined whether Fhit expression correlated with p53 expression and apoptosis. Compared to adjacent normal mucosa, significant loss or reduction of Fhit expression was noted in 67 of 75 (89.3%) invasive ESCs, in 13 of 19 (68.4%) CIS lesions, and in 10 of 23 (43.5%) dysplastic lesions. There was a progressive loss or reduction of Fhit expression with progressive increases in the severity of histopathological changes (p < 0.001). However, there was no association between Fhit expression and clinicopathological findings, including tumor stage, lymph node metastasis, or overall survival. Moreover, Fhit expression was not significantly associated with p53 expression and apoptosis. These results indicate that abnormal Fhit expression is a common event in the early stage of ESC development and may occur independently of p53 expression and apoptosis mechanisms.

Acid Anhydride Hydrolases↗

PubMed2001

Circular stapling procedure for mucosal prolapse of the rectum associated with outlet obstruction.

The aim of this study was designed to investigate the outcome from using the new circular stapling device in the surgical treatment for mucosal prolapse of the rectum associated with outlet obstruction. The treatment consisted of resection of the mucosal prolapse through a transverse incision and resecting a suitable part of the mucosa between the rectum and the anal canal, using an HCS33 circular stapler. Eleven patients successfully underwent this operation without morbidity or mortality, and were assessed clinically and by rectoanal manometry and defecography pre- and post-operation. The mean operating time was 39 (range 22-49) min. The postoperative proctalgia and complications were mild, and the patients were discharged at 4 days after the operation. The pre-operative constipation was improved, and the patient's satisfaction was increased at one month after operation in comparison with the preoperative level. Rectoanal function test at 6 months after the operation demonstrated normalization of the maximum resting and squeezing pressures of the anal canal and rectal compliance to the normal levels. No patient has had recurrence of symptoms during the follow-up period. Our data suggest that this procedure may be a useful surgical treatment, as it causes little postoperative complication and enables early discharge of the patients. However, long-term outcomes of recurrence, continence, and constipation need to be evaluated in a more extended follow-up.

Female↗