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Biomedical subjects

K Mori

Publications and source records attributed to K Mori.

At least 145 records · Page 8Linked to original sources
PubMed2001

Immunohistochemical study of glutathione reductase in rat ocular tissues at different developmental stages.

Glutathione, which is found in high levels in eye tissues, is involved in multiple functions, including serving as an antioxidant and as an electron donor for peroxidases. Although the activities of enzymes related to glutathione metabolism have been reported in the eye, the issue of which cells produce these proteins, where they are produced and at what levels is an important one. Glutathione reductase, an enzyme which recycles oxidized glutathione by transferring electrons from NADPH, was localized immunohistochemically in adult rat eye in this study. The reductase was distributed in the corneal and conjunctival epithelia, corneal keratocytes and endothelium, iridial and ciliary epithelia, neural retina, and retinal pigment epithelium. In addition, it was highly expressed in ganglion cells, which are responsible for transmitting photophysiological signals from the retina to the higher visual centres. To clarify the correlation of glutathione reductase expression and oxidative stress, the enzymatic activity and the level of protein expression at the pre- and postnatal stages was examined. Expression of the enzyme was detected first in the ganglion cell layer of a late prenatal stage, and appeared in the inner plexyform layer after birth. Along with an increasing differentiation between the inner nuclear and outer nuclear layers, glutathione reductase expression became detectable in the outer plexyform layer. Pigment epithelial cells were positively stained only after birth. Expression was also detected in the lens epithelium from the prenatal to early postnatal stages although its level was low in the adult lens. Collectively, these data, except for lens epithelia, suggest the pivotal role of glutathione reductase in recycling oxidized glutathione for the protection of the tissues against oxidative stress, which is caused by eye opening accompanied by the initiation of various ocular processes, such as accession of light and transduction of the photochemical signal.

Animals↗
PubMed2001

Vitamin B-12-deficiency affects immunoglobulin production and cytokine levels in mice.

To clarify the role of B-12 in the immunological function, serum C3, IgM, IgG, IgE contents, splenocytes expression of CD4, CD8, and CD4 positive intracellular IFN-gamma and IL-4 were examined in B-12-deficient mice, and the effect of the administration of CH3-B-12 was also studied. Serum C3, IgM and IgG contents were lower in B-12-deficient mice than in the control mice. On the other hand, serum IgE content was significantly higher in B-12-deficient mice, and the value in CH3-B-12 administered mice, administered CH3-B-12 to B-12-deficient mice for 48 h before the end of feeding period, showed a tendency to recovery. CD4+CD8- cells and CD4+CD8-/CD4-CD8+ ratio in splenocytes were significantly higher in B-12-deficient mice than in control mice. CD4+IFN-gamma+ cells was significantly lower in B-12-deficient mice than in control mice, and CD4+IL-4+ was significantly higher in B-12-deficient mice than in control mice. These results suggest that B-12-deficiency causes CD4+CD8-T cells shift from the T helper type 1 to the T helper type 2, which participate in the IgE production and elevates CD4+CD8-/CD4-CD8+ ratio. Thus, B-12 plays a role in maintaining the immune function in mice.

Animals↗
PubMed2001

Ibudilast attenuates astrocyte apoptosis via cyclic GMP signalling pathway in an in vitro reperfusion model.

We examined the effect of 3-isobutyryl-2-isopropylpyrazolo[1,5-a]pyridine (ibudilast), which has been clinically used for bronchial asthma and cerebrovascular disorders, on cell viability induced in a model of reperfusion injury. Ibudilast at 10 - 100 microM significantly attenuated the H(2)O(2)-induced decrease in cell viability. Ibudilast inhibited the H(2)O(2)-induced cytochrome c release, caspase-3 activation, DNA ladder formation and nuclear condensation, suggesting its anti-apoptotic effect. Phosphodiesterase inhibitors such as theophylline, pentoxyfylline, vinpocetine, dipyridamole and zaprinast, which increased the guanosine-3',5'-cyclic monophosphate (cyclic GMP) level, and dibutyryl cyclic GMP attenuated the H(2)O(2)-induced injury in astrocytes. Ibudilast increased the cyclic GMP level in astrocytes. The cyclic GMP-dependent protein kinase inhibitor KT5823 blocked the protective effects of ibudilast and dipyridamole on the H(2)O(2)-induced decrease in cell viability, while the cyclic AMP-dependent protein kinase inhibitor KT5720, the cyclic AMP antagonist Rp-cyclic AMPS, the mitogen-activated protein/extracellular signal-regulated kinase inhibitor PD98059 and the leukotriene D(4) antagonist LY 171883 did not. KT5823 also blocked the effect of ibudilast on the H(2)O(2)-induced cytochrome c release and caspase-3-like protease activation. These findings suggest that ibudilast prevents the H(2)O(2)-induced delayed apoptosis of astrocytes via a cyclic GMP, but not cyclic AMP, signalling pathway.

Alkaloids↗
PubMed2001

Recombinant adeno-associated virus vector-transduced vascular endothelial cells express the thrombomodulin transgene under the regulation of enhanced plasminogen activator inhibitor-1 promoter.

We were able to facilitate plasminogen activator inhibitor 1 (PAI-1) promoter activity approximately by 14-fold using an enhancer element. This enhanced PAI-1 promoter has a strong basal activity, comparable to CAG promoter activity, and has a response similar to the PAI-1 promoter with respect to TGFbeta 1 and TNFalpha stimulation. The characteristics of the enhanced PAI-1 promoter are thought to be suited to timely and tissue-specific expression of anticoagulant molecules in the vascular cells. Thus, we developed recombinant adeno-associated virus (rAAV) vectors using the enhanced PAI-1 promoter and were successful in transducing vascular endothelial cells to express the thrombomodulin transgene under the regulation of the enhanced PAI-1 promoter in vitro. Thromobomodulin transgene expression driven by the enhanced PAI-1 promoter in rAAV vector-transduced cultured endothelial cells was between 600- and 1000-fold higher than constitutive thrombomodulin gene expression in cultured human umbilical vein endothelial cells and was up-regulated by TGFbeta1 and TNFalpha stimulation which may down-regulate endogenous thrombomodulin gene expression in endothelial cells. The brain vascular endothelial cells of Mongolian gerbils could also be transduced by the same rAAV vector in vivo. Transduction of endothelial cells by rAAV vectors to express enhanced PAI-1 promoter-driven transgenes may be a useful gene therapy approach for vascular diseases.

Animals↗
PubMed2001

Effects of ten year body weight variability on cardiovascular risk factors in Japanese middle-aged men and women.

OBJECTIVE: The purpose of the present study was to determine the effects of weight variability on cardiovascular risk factors (CRF) based on a large sample of community-resident Japanese males and females. METHOD: A total of 3564 men and 1955 women, all Japanese, aged 30-69 y in the baseline year (1987), were followed-up for up to 10 y (end-point in 1996). Height, body weight, systolic and diastolic blood pressure, fasting serum total cholesterol, triglyceride and fasting plasma glucose were measured as an annual health check-up. At least six times in 10 y, body mass index (BMI) mean was calculated as an index of the BMI level of each subject (BMI mean). Direction and magnitude of the change in a subject's BMI was determined by a regression slope of BMI values over time (BMI slope). BMI fluctuation was defined as the root mean square error (BMI RMSE) of a regression line. The slopes of the five CRF were calculated using each regression equation over time. RESULTS: The BMI slope strongly correlated to each CRF slope independent of baseline age, baseline CRF value, smoking habit, BMI mean and BMI RMSE. BMI RMSE did not correlate to any CRF slopes. CONCLUSION: This study indicates that weight gain and weight loss have a much greater effect on CRF change than does weight fluctuation in Japanese middle-aged men and women.

Adult↗
PubMed2001

Exon 3 of tyrosine hydroxylase gene: lack of association with Japanese schizophrenic patients.

Tyrosine hydroxylase (TH) is the rate-limiting enzyme in dopamine (DA) biosynthesis. Exon 3 of the human TH gene encodes the sequence from Ser31 to Glu104 of type 1 enzyme, which contains the critical parts for regulation of the catalytic activity. The amino acid residues Gly36-Arg37-Arg38 were identified as a key sequence for DA to exert its inhibitory effect on catalytic activity. Therefore, we screened the nucleotide sequences of exon 3 from 201 Japanese patients with schizophrenia to explain the elevation in the synaptic or presynaptic DA concentrations in the schizophrenic brain, based on the hypothesis that any mutation changing the amino acid sequence Gly36-Arg37-Arg38 would result in the elevation of DA synthesis, due to a reduced inhibitory effect of DA on the catalytic activity. However, no mutated sequences of exon 3 and both exon-intron boundaries were detected in any of the patients examined. Polymorphisms generating Val81 and Met81 were compared of the distributions of genotype and allele between the patients and 175 Japanese healthy controls, which did not suggest an association between the polymorphism and schizophrenia. These results indicate that exon 3 of the human TH gene lacks association with schizophrenia in Japanese patients.

Adult↗
PubMed2001

Musashi1, an evolutionarily conserved neural RNA-binding protein, is a versatile marker of human glioma cells in determining their cellular origin, malignancy, and proliferative activity.

Tumor cells often express phenotypic markers that are specific to the cells from which they originated. A neural RNA-binding protein, Musashil, is an evolutionarily well-conserved marker for neural stem cells/ progenitor cells. To examine the origin of gliomas, we examined the expression of the human Musashil homolog, MSI1, in human glioma tissues and in normal human adult and fetal brains. As we had seen previously in rodents, in the normal human brain, MSI1 was expressed in cells located in the ventricular and subventricular zones, in GFAP-negative glial cells, and in GFAP-positive astrocytes. In glioblastomas, MSI1 was expressed in GFAP-negative tumor cells forming foci that were clearly demarcated and surrounded by GFAP-positive cells. Tumor cells arranged in pseudopalisades were also strongly immunoreactive with MSI1 antibodies. The percentage of MSI1-labeled tumor cells increased in higher-grade astrocytomas and correlated with proliferative activity, as estimated by an MIB-1 staining index. Our results indicate that MSI1 is an excellent marker for neural progenitor cells including neural stem cells in normal human brains. Furthermore, the expression of MSI1 correlates well with the immature nature as well as the malignancy of tumor cells in human gliomas. Thus, we expect the analysis of MSI1 expression to contribute to the understanding of the cellular origin and biology of human gliomas.

Adult↗
PubMed2001

Vascular calcification and inorganic phosphate.

Vascular calcification is highly correlated with elevated serum phosphate levels in uremic patients. To shed light on this process, we examined the ability of extracellular inorganic phosphate (Pi) levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro. When cultured in media containing normal physiological levels of Pi (1.4 mmol/L Pi), HSMC grew in monolayers and did not mineralize. In contrast, HSMC cultured in media containing Pi levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L), showed dose-dependent increases in cell culture calcium deposition. Mechanistic studies showed that elevated Pi treatment of HSMC also enhanced the expression of the osteogenic markers, osteocalcin and Cbfa-1. The effects of elevated Pi on HSMC were mediated by a sodium-dependent phosphate cotransporter (NPC), as indicated by the ability of the specific NPC inhibitor, phosphonoformic acid (PFA), to dose-dependently inhibit Pi-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. Using polymerase chain reaction and Northern blot analyses, the NPC in HSMC was identified as Pit-1 (Glvr-1), a member of the type III NPCs. Interestingly, platelet-derived growth factor-BB (PDGF-BB), a potent atherogenic stimulus, increased the maximum velocity (Vmax) but not the affinity (Km) of phosphate uptake, enhanced the expression of Pit-1 mRNA, and induced HSMC culture calcification in a time- and dose-dependent manner. Importantly, in the presence of PDGF, HSMC culture calcification occurred under normophosphatemic conditions. These data suggest that elevated Pi may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification and may help explain both the phenomena of human metastatic calcification under hyperphosphatemic conditions as well as increased calcification in PDGF-rich atherosclerotic lesions.

Actins↗
PubMed2001

Mönckeberg's medial sclerosis and inorganic phosphate in uremia.

Mönckeberg's medial sclerosis (MMS) is one of the characteristic calcified lesions of uremic artery disease and often exhibits osseous metaplasia. Although its pathogenic mechanism is largely unknown, MMS may contain two different pathologic processes: degenerative process leading to apoptosis or necrosis of medial smooth muscle cells and osteogenic process leading to formation of bone-like structures. It has long been known that calcification follows necrosis. Apoptotic/necrotic cells often release matrix vesicles or membranous cellular degradation products resulting from disintegration of the cells that frequently serve as the nidus of calcification. On the other hand, vascular cells may exhibit osteoblastic phenotype in vitro, and some of the markers for osteoblastic differentiation and noncollagenous proteins regulating mineralization have been demonstrated in calcified arterial lesions. As a possible etiologic factor inducing these two responses, hyperphosphatemia among various metabolic disturbances recognized in uremia may play an important role in the development of MMS in uremia.

Animals↗
PubMed2001

Role of connective tissue growth factor in profibrotic action of transforming growth factor-beta: a potential target for preventing renal fibrosis.

Tubulointerstitial fibrosis is a crucial process determining the progression and prognosis of various renal diseases. Connective tissue growth factor (CTGF), a novel fibrogenic protein induced by transforming growth factor-beta (TGF-beta), is upregulated in various clinical and experimental nephropathies, but the significance of CTGF in the profibrotic action of TGF-beta is still poorly defined. To explore the implication of CTGF in renal fibrosis, we investigated gene expression of CTGF, fibronectin, and alpha1(I) collagen in an obstructive nephropathy model in rats. Furthermore, to elucidate the role of CTGF in TGF-beta-stimulated extracellular matrix accumulation, we analyzed the effects of blockade of endogenous CTGF using antisense oligodeoxynucleotides (ODNs) in cultured rat renal fibroblasts. After unilateral ureteral obstruction, TGF-beta1 and CTGF messenger RNA (mRNA) expression in the obstructed kidney was coordinately upregulated from the early stage of interstitial fibrosis, followed by marked induction of fibronectin and alpha1(I) collagen mRNA expression. In cultured normal rat kidney fibroblast (NRK-49F) cells, CTGF antisense ODN transfection significantly attenuated TGF-beta1-induced fibronectin and alpha1(I) collagen mRNA expression compared with control reverse ODNs. These results indicate that CTGF has a crucial role in the profibrotic action of TGF-beta in renal fibroblasts, providing a potential therapeutic target against tubulointerstitial fibrosis.

Animals↗
PubMed2001

CD45RC gammadelta T-cell infiltration is associated with immunologic unresponsiveness induced by prior donor-specific blood transfusion in rat hepatic allografts.

Little is known regarding the role of gammadelta(+) T cells in organ transplantation. We previously reported that immunologic unresponsiveness is induced by prior donor-specific blood transfusion (DST) in rat hepatic allografts. We investigated the phenotype and distribution of gammadelta(+) T cells in the hepatic allograft, spleen, and peripheral blood of recipient rats with immunologic unresponsiveness induced by DST. gammadelta(+) T cells were enumerated in allograft livers and spleens by immunostaining and in blood by flow cytometric analysis. The phenotype of gammadelta(+) T cells was determined using CD45RC isoforms derived from alternative mRNA splicing. The cytokine profile of CD45RC(+) and CD45RC(-) gammadelta(+) T cells was analyzed by reverse transcription polymerase chain reaction. The number of gammadelta(+) T cells in hepatic infiltrates in recipient rats pretreated with DST was significantly greater than in untreated animals. This correlated with significantly higher levels of gammadelta T cell receptor (TCR) mRNA in hepatic allografts of DST-treated rats as compared with untreated animals. The gammadelta(+) T cell/alphabeta(+) T-cell ratio increased in hepatic infiltrates in DST-treated recipient rats but not in untreated animals. CD45RC(-)gammadelta(+) T cells were predominantly increased in DST-treated hepatic allografts compared with untreated allografts. Most of the intestinal intraepithelial T cells were CD45RC(-)gammadelta(+). Interleukin (IL)-10 and IL-4 mRNA were detected more in CD45RC(-)gammadelta(+) T cells than CD45RC(+)gammadelta(+) T cells. CD45RC(-)gammadelta(+) T cells infiltrating liver allografts produce Th2-type cytokines and are associated with immunologic unresponsiveness induced by DST.

Acute Disease↗
PubMed2001

Pulmonary epithelial cell maturation in hyperplastic lungs associated with fetal tracheal agenesis.

BACKGROUND/PURPOSE: Cellular differentiation of pulmonary hyperplasia has not been reported in human cases. The authors studied surfactant protein expression and ultrastructure of pulmonary epithelial cells in fetal hyperplastic lungs associated with congenital tracheal agenesis. METHODS: The maturation of pulmonary epithelial cells was assessed by immunohistochemical examination for surfactant proteins (SP-A, mature SP-B, proSP-B, proSP-C, and SP-D) and transmission electron microscopy. As controls normal lung portions of 8 fetuses born at 21 weeks gestation were used. RESULTS: Mature SP-B and SP-D was detected in terminal airways in this case, but not in controls. In electron microscopy, lamellar bodies were recognized, and glycogen granules were less abundant in terminal airway cells. CONCLUSION: The differentiation of pulmonary epithelial cells appeared to be more advanced for the gestational age in pulmonary hyperplasia with congenital tracheal agenesis. J Pediatr Surg 36:1845-1848.

Adult↗
PubMed2001

Heparin modulates integrin function in human platelets.

PURPOSE: Heparin binds to human platelets and can cause activation and aggregation, although the mechanisms are unknown. To determine how heparin alters platelet function, we identified platelet-binding sites for heparin and measured heparin's influence on the function of platelet integrin alpha(IIb)beta(3) (glycoprotein IIb/IIIa). METHODS: Photoaffinity cross-linking and affinity chromatography experiments were performed to identify platelet membrane proteins that bind heparin. Heparin's effect on fibrinogen binding to platelets was measured with a radioligand-binding assay. The translocation to the cytoskeleton of Rap2, a guanosine triphosphate-binding protein, was measured from platelets aggregating in response to heparin and other agonists. RESULTS: Cross-linking and affinity chromatographic experiments positively identified the integrin alpha(IIb)beta(3) as a heparin-binding site. Heparin aggregation was calcium dependent. Low concentrations of unfractionated porcine mucosal heparin (2-5 U/mL) significantly increased fibrinogen I 125 binding to activated platelets, whereas higher doses did not. Heparin-mediated platelet aggregation was completely blocked by GRGDS peptide (5 mmol/L), a competitive inhibitor of fibrinogen binding, and was blocked by EDTA (2 mmol/L), which dissociates the functional integrin complex. Aggregation was associated with Rap2 translocation to the cytoskeleton, a sign of outside-in signaling. CONCLUSIONS: Heparin binds to the alpha(IIb)beta(3) integrin in vitro and ex vivo, and heparin increases fibrinogen binding to the integrin. Heparin-mediated aggregation requires an intact integrin and ligand and leads to Rap2 translocation to the cytoskeleton-an outside-in signal of ligand engagement. Heparin may directly modulate platelet integrin function, most likely through direct binding and modulation of integrin function.

Binding Sites↗
PubMed2001

Determination of aldose reductase activity in the eye by localized magnetic resonance spectroscopy.

The polyol pathway plays an important role in the formation of diabetic complications of the eye. Due to variations in the pharmacokinetic properties of aldose reductase inhibitors and variations in the degradation of the blood-ocular barrier, it is often difficult to determine the proper intraocular levels of aldose reductase inhibitor required for inhibition of aldose reductase activity in ocular tissues. Utilizing localized magnetic resonance spectroscopy (MRS), the present method can determine adequate inhibition of aldose reductase activity in the lens by noninvasively measuring polyol pathway activity in the eye. New Zealand White rabbits, under anesthesia, were administered an intravitreal injection of 3-fluoro-3-deoxy-D-glucose (3FDG). Localized MRS was then used to assess polyol pathway activity by determining the levels of 3-fluoro-3-deoxy-D-sorbitol (3FS) and 3-fluoro-3-deoxy-D-fructose (3FF) metabolite formation from 3FDG in the eye. MRS was able to follow the loss of 3FDG from the vitreous into the anterior segment of the eye and particularly into the lens and aqueous. The primary metabolism of 3FDG observed by MRS was the formation of 3FS in the lens that is catalyzed by aldose reductase. Production of 3FS was linear in time and decreased with the oral administration of an aldose reductase inhibitor.

Aldehyde Reductase↗
PubMed2001

Comprehensive comparison between locations of orthologous genes on archaeal and bacterial genomes.

MOTIVATION: Following an extensive search for orthologous genes between the complete genomes from archaea and bacteria, the spatial association of the orthologs has been investigated in terms of synteny, the conservation of the order of neighboring genes. However, the relationships between the relative locations of remote orthologs over entire genomes have not been shown. RESULTS: Comprehensive comparisons between the locations of orthologs on nineteen archaeal and bacterial genomes are presented by the location to location correspondence based on the gene-location distance. When the two genomes are rotated such that a pair of orthologs with the shortest distance is set in the same angle, a statistically significant number of orthologs maintain their relative locations between the genomes. Even by the short distances at the 5% significance level, the rotations are restricted within a narrow range, suggesting an intrinsic angle for realizing similar locations between the orthologs in each genome pair. Furthermore, the rotations in the restricted range agree with the replication origin and terminus sites for the analyzed genomes where such sites are known. The relationship between location-maintained orthologs and gene function is also discussed.

Chromosome Mapping↗
PubMed2001

Randomized phase I study of standard-fractionated or accelerated-hyperfractionated radiotherapy with concurrent cisplatin and vindesine for unresectable non-small cell lung cancer: a report of Japan Clinical Oncology Group Study (JCOG 9601).

BACKGROUND: We attempted dose escalation of standard-fractionated and accelerated-hyperfractionated radiotherapy combined with concurrent cisplatin and vindesine to improve local control and survival in unresectable non-small cell lung cancer. METHODS: Twenty-one patients were enrolled between June 1996 and August 1997. There were 19 males and two females and their median age was 65 years (range 45-74 years). Performance status was 0 in 10 cases and 1 in 11 cases. Disease stage was IIIA in three cases and IIIB in 18 cases. The cases were randomized to a standard-fractionated arm (n = 10) or an accelerated-hyperfractionated radiotherapy arm (n = 11) with two or three cycles of concomitant cisplatin 80 mg/m(2) on day 1 and vindesine 3 mg/m(2) on days 1 and 8 every 4 weeks in both arms. Dose escalation from 60 Gy/30 fractions/6 weeks to 70 Gy/35 fractions/7 weeks was planned in the standard-fractionated radiotherapy group and from 54 Gy/36 fractions/3.6 weeks to 60 Gy/40 fractions/4 weeks and then 66 Gy/44 fractions/4.4 weeks in the accelerated-hyperfractionated radiotherapy group. RESULTS: Grade 3 or 4 hematological toxicities were observed as follows: in the standard-fractionated/accelerated-hyperfractionated radiotherapy group, leukocytopenia 9/10, anemia 2/3 and thrombocytopenia 0/2. Grade 3 non-hematological toxicity consisted of esophagitis 0/3, increased serum total bilirubin 2/0 and hypoxia 0/1. Two patients died of radiation pneumonitis in the standard-fractionated radiotherapy group. Dose-limiting toxicity was observed in four of the 10 and seven of the 11 patients at initial dose level of standard-fractionated radiotherapy, 60 Gy/30 fractions/6 weeks, and of accelerated-hyperfractionated radiotherapy, 54 Gy/36 fractions/3.6 weeks, respectively. Thus, we failed to escalate the dose of radiotherapy in both arms. The overall response rate in the standard-fractionated group and the accelerated-hyperfractionated radiotherapy group was 70 and 73% and the 1-year survival rate was 70 and 64%, respectively. CONCLUSIONS: We concluded that these schedules of radiotherapy with concurrent cisplatin and vindesine were unacceptable for use in patients with unresectable non-small cell lung cancer. Further modifications of the schedule for radiotherapy and evaluation of combination with new chemotherapy are warranted.

Aged↗
PubMed2001

Reliable, minimally invasive oromandibular reconstruction using metal plate rolled with pectoralis major myocutaneous flap.

The purpose of this study was to minimize the surgical invasiveness to the donor site and the amount of the primary reconstruction time after oromandibular tumor resection. Oromandibular reconstruction was performed only using a pectoralis major myocutaneous flap and a metal plate. The pectoralis major myocutaneous flap was grafted to the oral cavity defect by rolling and wrapping around the metal plate with the muscle of the flap. No early postoperative complications have been noted in all seven patients. An average of 2 years and 1 month has past since surgery, and to date no infections, plate exposure, or plate breakage have been observed in any of the patients. The safety of the oromandibular reconstruction using a metal plate was improved by rolling the muscle of the pectoralis major myocutaneous flap around the metal plate. The present method was shown to be a rational technique that allowed primary reconstruction of the oral cavity and mandible in a minimally invasive manner in a short time.

Adult↗