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H Iizuka

Publications and source records attributed to H Iizuka.

At least 19 recordsLinked to original sources
PubMed2001

Fractures of the posterior part of the body and unilateral spinous process of the axis: a case report.

STUDY DESIGN: A case report and review of the literature. OBJECTIVES: To present a case of the fractures of the posterior part of the body and unilateral spinous process of the axis. SUMMARY OF BACKGROUND DATA: A few authors have described fractures involving the body of the axis. Fractures of the posterior part of the body and unilateral spinous process of the axis are extremely rare. METHODS: A fracture of the posterior part of the body and unilateral spinous process was treated nonsurgically by a halo and a Philadelphia brace. The relevant literature was reviewed. RESULTS: Solid bony union was shown by plain radiographs and computed tomography. The patient was free of pain and obtained a full range of motion. CONCLUSION: The presumed mechanism of injury in the fracture described here was flexion and axial rotation.

Aged↗
PubMed2001

Extensor musculature of the cervical spine after laminoplasty: morphologic evaluation by coronal view of the magnetic resonance image.

STUDY DESIGN: A radiographic study in 22 patients using magnetic resonance imaging was conducted. OBJECTIVE: To describe the relation between postoperative cervical alignment and morphologic evaluation of the cervical extensor musculature, especially semispinalis cervics in laminoplasty. SUMMARY OF BACKGROUND DATA: Cervical laminoplasty has been widely accepted as a treatment for cervical myelopathy. Posterior procedures, however, involve the extensor musculature of the cervical spine. METHODS: In this study, 22 patients who underwent laminoplasty for repair of the extensor musculature were reviewed prospectively. The semispinalis cervics was evaluated by coronal view of the magnetic resonance image 1 month, 12 months, and 24 months after surgery. Cervical alignment at last follow-up assessment was compared with preoperative alignment using the lateral view of cervical radiographs. RESULTS: In 18 patients (82%), morphologic repair of semispinalis cervics had been maintained (Group A), but in 4 patients (18%), but it had not been maintained at the last follow-up assessment (Group B). Cervical alignment in Group A had been maintained, but maximum loss of cervical lordosis occurred in Group B. Moreover, Group B consisted of elderly women. CONCLUSIONS: The findings from this magnetic resonance imaging study suggest that the degree of semispinalis cervics repair affects postoperative cervical alignment, and significant loss of cervical lordosis tends to occur in elderly women who undergo laminoplasty.

Adult↗
PubMed2001

Expression of human cystatin A by keratinocytes is positively regulated via the Ras/MEKK1/MKK7/JNK signal transduction pathway but negatively regulated via the Ras/Raf-1/MEK1/ERK pathway.

Cystatin A, a cysteine proteinase inhibitor, is a cornified cell envelope constituent expressed in the upper epidermis. We previously reported that a potent protein kinase C activator, 12-O-tetradecanoylphorbol-13-acetate, increases human cystatin A expression by the activation of AP-1 proteins. Here, we delineate the signaling cascade responsible for this regulation. Co-transfection of the cystatin A promoter into normal human keratinocytes together with a dominant active form of ras increased the promoter activity by 3-fold. In contrast, a dominant negative form of ras suppressed basal cystatin A promoter activity. Further analyses disclosed that transfection of dominant negative forms of raf-1, MEK1, ERK1, ERK2, or wild-type MEKK1 all increased cystatin A promoter activity in normal human keratinocytes, whereas wild-type raf-1, ERK1, ERK2, or dominant negative forms of MEKK1, MKK7, or JNK1 suppressed the promoter activity. The increased or decreased promoter activity reflected the expression of cystatin A on mRNA and protein levels. These effects were not observed when a cystatin A promoter with a T2 (-272 to -278) deletion was used. In contrast, transfection of dominant negative forms of MKK3, MKK4, or p38 did not affect cystatin A promoter activity. Immunohistochemical analyses revealed that phosphorylated active extracellular signal-regulated kinases and c-Jun N-terminal kinase were expressed in the nuclei of basal cells and cells in the suprabasal-granular cell layer, respectively. These results indicate that the expression of cystatin A is regulated via mitogen-activated protein kinase pathways positively by Ras/MEKK1/MKK7/JNK and negatively by Ras/Raf/MEK1/ERK.

Adenoviridae↗
PubMed2001

Mutations of either or both Cys876 and Cys888 residues of sarcoplasmic reticulum Ca2+-ATPase result in a complete loss of Ca2+ transport activity without a loss of Ca2+-dependent ATPase activity. Role of the CYS876-CYS888 disulfide bond.

Disulfide-containing peptides in pepsin digest of sarcoplasmic reticulum vesicles were identified by using a fluorogenic thiol-specific reagent 4-fluoro-7-sulfamoylbenzofurazan and a reductant tributylphosphine. Sequencing of the purified peptides revealed the presence of a Cys(876)-Cys(888) disulfide bond on the luminal loop connecting the 7th and 8th transmembrane helices (loop 7-8) of the Ca(2+)-ATPase (SERCA1a). We substituted either or both of these cysteine residues with alanine and made three mutants (C876A, C888A, C876A/C888A), in which the disulfide bond is disrupted. The mutants and the wild type were expressed in COS-1 cells, and functional analysis was performed with the microsomes isolated from the cells. Electrophoresis performed under reducing and non-reducing conditions confirmed the presence of Cys(876)-Cys(888) disulfide bond in the expressed wild type. All the three mutants possessed high Ca(2+)-ATPase activity. In contrast, no Ca(2+) transport activity was detected with these mutants. These mutants formed almost the same amount of phosphoenzyme intermediate as the wild type from ATP and from P(i). Detailed kinetic analysis showed that the three mutants hydrolyze ATP in the mechanism well accepted for the Ca(2+)-ATPase; activation of the catalytic site upon high affinity Ca(2+) binding, formation of ADP-sensitive phosphoenzyme, subsequent rate-limiting transition to ADP-insensitive phosphoenzyme, and hydrolysis of the latter phosphoenzyme. It is likely that the pathway for delivery of Ca(2+) from the binding sites into the lumen of vesicles is disrupted by disruption of the Cys(876)-Cys(888) disulfide bond, and therefore that the loop 7-8 having the disulfide bond is important for formation of the proper structure of the Ca(2+) pathway.

Adenosine Triphosphate↗
PubMed2001

Differential phosphorylation of mitogen-activated protein kinase families by epidermal growth factor and ultraviolet B irradiation in SV40-transformed human keratinocytes.

SV-40 transformed human keratinocytes (SVHK cells) were stimulated with epidermal growth factor (EGF) and ultraviolet B (UVB) irradiation. Following the stimulation, cell growth, apoptosis, and the activities of mitogen-activated protein (MAP) kinase families were analyzed. EGF (100 ng/ml) increased SVHK cell number compared with control cells cultured in serum-free DMEM medium. The EGF-stimulated cells did not show DNA fragmentation. In contrast, UVB irradiation (40 mJ/cm(2)) markedly decreased viable cell number that was accompanied with DNA fragmentation. EGF stimulated extracellular signal-regulated kinase (ERK) and stress-activated protein kinase/c-Jun N-terminal kinase (JNK). Following the EGF stimulation, phosphorylated ERK and JNK were detected by phospho-p42/44 MAP kinase antibody and phospho-SAPK/JNK antibody, respectively. On the other hand, UVB irradiation stimulated the phosphorylation of p38 and JNK but not of ERK. The stimulation of ERK and JNK induced by EGF was observed earlier than the stimulation of p38 and JNK induced by UVB. PD98059, a specific MAP kinase kinase (MAPKK) 1 (also referred to as MEK1) inhibitor, inhibited EGF-dependent cell proliferation, that was associated with the inhibition of ERK and JNK phosphorylation. In contrast, UVB-induced overall cell death was not significantly affected by PD98059, that inhibited phosphorylation of JNK but not of p38. PD98059, however, significantly augmented UVB-induced cell death earlier time points (30 min--2 h). These results indicate that ERK and JNK are activated following EGF stimulation that might be associated with cell proliferation. On the other hand, UVB-induced apoptosis seems to be mostly associated with the activation of p38. JNK stimulation might provide an anti-apoptotic tonus during the UVB-induced, p38-associated SVHK cell death.

Cell Death↗
PubMed2001

RCAS1 antigen is highly expressed in extramammary Paget's disease and in advanced stage squamous cell carcinoma of the skin.

Receptor-binding cancer antigen expressed on SiSo cells (RCAS1), which is a type II membrane protein expressed on cervical carcinoma cells, induces apoptosis in RCAS1 receptor expressing cells. RCAS1 is thus presumed to protect tumor cells from immune surveillance by infiltrating RCAS1 receptor-positive immunocytes (Sonoda et al. Int J Oncol 1995; 6: 1899-1904; Nakashima et al. Nature Med 1999; 5: 938-942). We performed immunohistochemical analysis of RCAS1 expression in various skin tumors. RCAS1 was not detected in normal human epidermis. One of 21 seborrheic keratosis (4.8%), one of 12 actinic keratosis (8.3%), two of 16 keratoacanthomas (12.5%), and two of 14 basal cell carcinomas (14.2%) expressed RCAS1. RCAS1 was not detected in Bowen's disease (0/17). RCAS1 was positive in 45 of 61 (73.8%) squamous cell carcinomas. Interestingly, the expression of RCAS1 was mostly correlated with clinical stages of squamous cell carcinoma. It was found that 46.1% of stage I, 61.1% of stage II, 85.7% of stage III, and 83.3% of stage IV squamous cell carcinomas were RCAS1-positive. In addition, RCAS1 was found to be highly expressed in extramammary Paget's disease. Fifty nine of 63 extramammary Paget's disease samples (93.7%) were positive for RCAS1. Fifty eight (92%) showed co-expression of RCAS1 and carcinoembryonic antigen (CEA). While two of 24 cases of melanoma (8.3%) expressed RCAS1 antigen, none of 20 cases of nevus pigmentosus showed positive staining. These results indicate that RCAS1 is a highly sensitive marker for extramammary Paget's disease. RCAS1 is also expressed in various skin tumors including squamous cell carcinoma, where positive correlation with clinical staging was documented.

Antigens, Neoplasm↗
PubMed2001

Novel mutations of ATP2A2 gene in Japanese patients of Darier's disease.

Darier's disease (DD) is a rare, dominantly inherited skin disorder with abnormal keratinization and acantholysis. Recently, mutations of ATP2A2 encoding the sarco/endoplasmic reticulum Ca(2+)-ATPase type 2 isoform (SERCA2) have been reported in Caucasian DD families. In the present study, we examined the ATP2A2 gene mutations of three sporadic (AS1,AS3,AS4) and one familial (AS2) Japanese DD patients. Sequence analysis revealed that the patients had novel mutations, one nonsense mutation (AS1 (C613X)) and three single base changes leading to amino acid substitutions (AS2 (L321F), AS3 (I274V), and AS4 (M719I)). These results demonstrate that distinct ATP2A2 gene mutations are present in Japanese DD patients.

Aged↗
PubMed2001

Nuclear localization of beta-catenin in the hair matrix cells and differentiated keratinocytes.

Beta-catenin is a structural component of adherens junctions and also a downstream effector of Wnt signaling pathway. Beta-catenin has been detected in the adherens junctions in almost all normal tissues including the epidermis. Only in some malignant tumor cells was it found in the cytoplasm and nuclei. Recently pilomatricoma was found to be caused by mutations of amino-terminal segment of beta-catenin, normally involved in phosphorylation-dependent ubiquitin-mediated degradation of the protein. Since nuclear beta-catenin has not been detected in pilomatricoma or any other benign follicular tumors, we investigated localization of beta-catenin in the normal hair follicle, follicular tumor cells, normal and psoriatic epidermis by using immunohistochemical method with a high temperature antigen unmasking technique. The nuclear localization of beta-catenin was detected not only in the matrix cells of follicular tumors including pilomatricoma but also in the normal hair matrix cells and the differentiated keratinocytes of the upper layers of the epidermis. Cell membrane staining of beta-catenin and E-cadherin was decreased in these differentiated keratinocytes. This coincided with the emergence of nuclear beta-catenin. The present immunohistochemical method has revealed hitherto unproven nuclear localization of beta-catenin in hair matrix cells. Our results also provided evidence suggesting that beta-catenin plays an important role in keratinocyte differentiation.

Cell Differentiation↗
PubMed2001

Corneodesmosin expression in psoriasis vulgaris differs from normal skin and other inflammatory skin disorders.

SUMMARY: Corneodesmosin (Cdsn) is a late differentiation epidermal glycoprotein putatively involved in keratinocyte adhesion. The Cdsn gene lies within the susceptibility region on chromosome 6p21.3 (PSORS1) for psoriasis, a common chronic disfiguring skin disease. A particular allelic variant of Cdsn has a strong association with psoriasis. Therefore, genetically and biologically, Cdsn is a possible candidate gene for psoriasis susceptibility. To investigate a potential role for Cdsn in psoriasis pathogenesis, protein expression studies were performed by quantitative immunohistochemistry on normal skin, psoriatic skin (lesional and nonlesional), and other skin disorders using monoclonal antibodies (G36-19 and F28-27). In normal and nonlesional skin, Cdsn was expressed in stratum corneum and one or two layers of superficial stratum granulosum. In lesional psoriasis, there was a significant increase in Cdsn expression, which was observed in multiple layers of stratum spinosum and in stratum corneum. The expression pattern varied from granular, cytoplasmic immunoreactivity to cell surface labeling with weakly immunoreactive cytoplasm. In chronic atopic dermatitis, lichen planus, mycosis fungoides, and pityriasis rubra pilaris, Cdsn immunoreactivity was confined to stratum corneum and upper stratum granulosum with no stratum spinosum immunoreactivity. Immunoelectron microscopy of normal and lesional psoriatic skin demonstrated Cdsn release concomitant with involucrin incorporation into cell envelopes and completed before mature envelope formation. Extracellular release of Cdsn occurred at a lower level of the epidermis in psoriasis than normal skin. These protein expression studies provide evidence of altered Cdsn expression in psoriasis consistent with a role of Cdsn in disease pathogenesis. Further functional and genetic studies of Cdsn are justified to determine its role as a potential psoriasis-susceptibility factor.

Chromosomes, Human, Pair 6↗
PubMed2001

Effect of oesophagectomy on monocyte-induced apoptosis of peripheral blood T lymphocytes.

BACKGROUND: Surgical stress has been reported to induce immunosuppression. The mechanisms giving rise to T-cell dysfunction following surgery are still unclear. The cellular mechanisms behind T-cell dysfunction following surgery were investigated, based on the induction of T-cell apoptosis and downregulation of T-cell signalling molecules. METHODS: Peripheral blood T cells were collected and separated before and after surgery in patients who had oesophagectomy, gastrectomy or cholecystectomy, and studied for their ability to produce cytokines, the induction of T-cell apoptosis with terminal deoxynucleotidyl transferase-mediated dUPT-biotin nick end labelling methods, and the expression of T-cell signalling zeta (TCR zeta) molecules with intracellular staining. RESULTS: The increased degree of T-cell apoptosis, downregulation of TCR zeta molecules and impaired cytokine production of T cells were significant on days 1 and 3 after operation in patients who had oesophagectomy, but not after gastrectomy or cholecystectomy. A higher level of T-cell apoptosis was observed in the co-culture with postoperative monocytes than with preoperative monocytes. CONCLUSION: Peripheral blood T cells obtained after oesophagectomy underwent apoptosis that correlated with the downregulation of TCR zeta molecules. Postoperative monocytes induced by surgical stress were able to mediate the T-cell apoptosis.

Aged↗
PubMed2001

Loricrin keratoderma: a cause of congenital ichthyosiform erythroderma and collodion baby.

A group of hereditary palmoplantar keratodermas due to heterozygous mutation in the loricrin gene has recently been identified. Of five reported pedigrees, four presented as mutilating keratoderma with ichthyosis (variant Vohwinkel syndrome), and one as progressive symmetric erythrokeratoderma. We report a new Japanese pedigree of loricrin keratoderma. A 14-year-old male and his 11-year-old female sibling had both been born as collodion babies and were initially diagnosed as having non-bullous congenital ichthyosiform erythroderma, but later developed palmoplantar keratoderma with pseudoainhum. Their father was similarly affected. Direct sequencing of genomic DNA revealed a G residue insertion at codon 230-231 of the loricrin gene. Antibody studies confirmed the presence of mutant loricrin in the retained nuclei. We conclude that loricrin gene mutation may present as congenital ichthyosiform erythroderma, and should be included in the differential diagnosis of collodion baby.

Adolescent↗
PubMed2001

Syringocystadenocarcinoma papilliferum: case report and immunohistochemical comparison with its benign counterpart.

Syringocystadenocarcinoma papilliferum (SCACP) is the malignant counterpart of syringocystadenoma papilliferum (SCAP), although only a few cases have been reported in the literature and its clinical and histologic characteristics are not well known. We report a case of SCACP that started as an enlarging nodule over 10 years in the perianal area of a 61-year-old man. Macroscopically, the lesion was a black exophytic tumor, 6 cm in diameter, with a granular surface. Histologically, it was an in situ adenocarcinoma, showing cytologic atypia and pagetoid spread in the surrounding epithelia, although the clinicopathologic features were distinct from extramammary Paget's disease. The tumor lacked the typical double-layered pattern of SCAP but had some similar histopathologic features to SCAP. Decapitation secretion was apparent and there was positive immunoreactivity to epithelial membrane antigen and human milk fat globules subclass 2. SCACP is a rare cutaneous tumor but nevertheless represents a specific dermatopathologic entity.

Adenocarcinoma↗
PubMed2001

Interposed colon between remnants of the small intestine exhibits small bowel features in a patient with short bowel syndrome.

We describe herein the case of a 48-year-old man who underwent emergency massive resection of the small intestine due to a strangulated ileus, which led to short bowel syndrome (SBS), as he was left with only 7 cm of jejunum and 8 cm of ileum with ileocecal valve. He then received interposition of a colon segment between the jejunum and ileum remnants isoperistaltically. For 24 months after the operation, he has been able to tolerate oral intake, but still requires partial home parenteral nutritional support during the night on a bimonthly basis. Biochemical and nutritional parameters, including the analysis of minerals and trace elements, indicated that the patient was in relatively good health. Histological examination revealed that the mucosa of the interposed colon showed hypertrophy and hyperplasia of the crypt glands, and cells resembling Paneth cells which are usually seen in the small intestine, suggesting that the colon segment exhibits adaptive changes to the small intestine. Colon interposition may be a useful technique in patients with SBS when the small bowel is too short for the other surgical considerations.

Anastomosis, Surgical↗
PubMed2001

Pigmented Paget's disease of the male breast: report of a case.

An 83-year-old man with pigmented Paget's disease of the breast is reported. He had a blackish swollen right nipple with bloody discharge that lasted for 8 months. Histopathology of the lesion disclosed intraepidermal and dermal atypical cells forming small clusters and underlying intraductal carcinoma. Melanocytes were dispersed in the epidermis. Dermal melanophages were also detected. The atypical cells were positive for carcinoembryonic antigen, human-milk fat globule protein and a recently described new antigen, RCAS-1, but negative for S-100 or HMB-45. We diagnosed this case as Paget's disease of the male breast. Paget's disease of the breast is usually nonpigmented and occurs almost exclusively in women. Pigmented Paget's disease of the male breast is extremely rare, and only a few cases have been reported. Albeit rare, pigmented Paget's disease has to be included in the differential diagnosis of pigmented lesions of the nipple.

Aged↗
PubMed2001

In vitro and in vivo transfer of bcl-2 gene into keratinocytes suppresses UVB-induced apoptosis.

Bcl-2 is a member of the large Bcl-2 family and protects cells from apoptosis. Ultraviolet B (UVB) irradiation induces apoptosis of keratinocytes that is known as "sunburn cells." Previously we reported that UVB irradiation induces apoptosis accompanied by sequential activation of caspase 8, 3 and 1 in keratinocytes, and that the process is inhibited by various caspase inhibitors. Using bcl-2-expressing adenovirus vector we investigated the effect of Bcl-2 on UVB-induced apoptosis. Adenovirus vector efficiently introduced bcl-2 gene in cultured normal mouse keratinocytes (NMK cells); almost all NMK cells (1 x 10(6)) were transfected at 1 x 10(8) plaque-forming unit (PFU)/mL. Bcl-2-transfected NMK cells were significantly resistant to UVB-induced apoptosis with the suppressive effect dependent on the Bcl-2 expression level. Following UVB irradiation caspase 8, 3 and 9 activities were stimulated in NMK cells, whereas in bcl-2-transfected cells only caspase 8, but not caspase 3 or 9, activity was stimulated. In order to investigate the effect of Bcl-2 in vivo topical application of Ad-bcl-2 on tape-stripped mouse skin was performed. Following the application Bcl-2 was efficiently overexpressed in almost all viable keratinocytes. The expression was transient with the maximal expression of Bcl-2 on the first day following the application of 1 x 10(9) PFU in 200 microL. The introduced Bcl-2 remained at least for 6 days. UVB irradiation (1250 J/m2) induced apoptosis within 12 h and the maximal effect was observed at 24 h in control mouse skin. Both bcl-2-transfected and topical caspase 3 inhibitor-treated mice skin were resistant to UVB-induced apoptosis. The suppressive effect of Bcl-2 was more potent than that of caspase 3 inhibitor application. Topical application of empty adenovirus vector alone had no effect on Bcl-2 expression or UVB-induced apoptosis. These results indicate that adenovirus vector is an efficient gene delivery system into keratinocytes and that Bcl-2 is a potent inhibitor of UVB-induced apoptosis both in vitro and in vivo.

Adenoviridae↗
PubMed2001

Elevated caspase-3 activity in peripheral blood T cells coexists with increased degree of T-cell apoptosis and down-regulation of TCR zeta molecules in patients with gastric cancer.

To evaluate the mechanisms of T-cell dysfunction in patients with gastric cancer, we investigated the caspase activity of T cells, the induction of spontaneous T-cell apoptosis, the expression of T-cell receptor (TCR) zeta molecules, and the ability of T cells to produce cytokines in peripheral blood lymphocytes from patients (n = 22) and healthy controls (n = 14). The caspase-3 activity of T cells was studied as the protease activity of caspase-3 using the cell-permeable substrate of PhiPhiLux G1D2. Flow cytometric analysis was performed with triple staining by annexin V-FITC, propidium iodide, and CD3-R-phycoerythrin-Cy5 for the detection of T-cell apoptosis and with intracellular staining using permeabilized cells for the expression of TCR-zeta molecules. IFN-gamma and tumor necrosis factor alpha production from T cells was evaluated in response to anti-CD3 stimulation. Caspase-3 activity of peripheral blood T cells from patients with advanced disease was significantly increased compared with that from controls [15.5 +/- 3.6 mean fluorescence intensity (MFI) versus 11.5 +/- 3.3 MFI; P = 0.0068]. Parallel to this, the apoptosis of peripheral blood T cells from patients with advanced disease was significantly higher than for those from controls (16.5 +/- 15.5% versus 4.8 +/- 2.7%; P = 0.010). Furthermore, the expression of TCR-zeta molecules in patients with advanced disease was significantly decreased in comparison with that of the controls (41.0 +/- 13.9 MFI versus 56.7 +/- 16.3 MFI; P = 0.014), and this decreased expression coexisted with impaired IFN-gamma (42.4 +/- 43.2 pg/ml versus 1,757.4 +/- 2449.0 pg/ml; P = 0.031) and tumor necrosis factor alpha (682.6 +/- 519.3 pg/ml versus 1,686.0 +/- 1,533.7 pg/ml; P = 0.041) production of T cells. Thus, peripheral blood T cells from gastric cancer patients simultaneously exhibit an elevated caspase-3 activity, an increased degree of T-cell apoptosis, a down-regulation of TCR-zeta molecules, and impaired cytokine production. These observations suggest that induction of T-cell apoptosis coexisting with a down-regulation of TCR-zeta molecules may be responsible for T-cell dysfunction in patients with gastric cancer.

Apoptosis↗
PubMed2001

[A case of central nervous system anomalies (agenesis of corpus callosum, colpocephaly, hydrocephalus, congenital dermal sinus) associated with congenital heart disease(double-outlet right ventricle, complete endocardial cushion defect, atrial septal defect, pulmonary arterial stenosis, patent ductus arteriosus)].

A case of central nervous system anomalies(agenesis of corpus callosum, colpocephaly, hydrocephalus, congenital dermal sinus) associated with congenital heart disease(double-outlet right ventricle, complete endocardial cushion defect, atrial septal defect, pulmonary arterial stenosis, patent ductus arteriosus) is reported. Female patient had been already diagnosed as hydrocephalus during pregnancy and ventricular drainage was performed soon after the delivery. Prostaglandin E 1 was also applied for heart disease, but saturation of O2 decreased to 80% on arterial blood gas analysis. Blalock-Taussig operation and ligation of ductus arteriosus was done 41 days after the delivery and ventricle-peritoneal shunt was also made for the progressive hydrocephalus on the same day. Chromosome analysis showed no abnormality. The genesis of this complicated brain and heart anomaly is discussed from the viewpoint of neural crest cell abnormality.

Abnormalities, Multiple↗