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Biomedical subjects

Takeshi Inagaki

Publications and source records attributed to Takeshi Inagaki.

27 records · Page 2Linked to original sources

Nerve sparing radical prostatectomy: effects of hemostatic energy sources on the recovery of cavernous nerve function in a canine model.

PURPOSE: To preserve sexual function following radical prostatectomy, one must avoid injury to the neurovascular bundles (NVBs). In the conventional open surgical technique, the use of energy sources for hemostasis is avoided to prevent damage to the cavernous nerves. In contrast, during laparoscopic radical prostatectomy, electrosurgical and ultrasonic energy sources are frequently used for hemostasis during dissection of the prostate. In this study, we evaluated the acute and chronic physiological effects of various hemostatic energy sources on cavernous nerve function in the canine model. MATERIALS AND METHODS: A total of 12 dogs were divided into 4 groups based on the type of energy source used for hemostasis during unilateral dissection of the NVB. The groups included conventional dissection with suture ligatures (group 1), monopolar (group 2) or bipolar (group 3) electrosurgery and ultrasonic shears (group 4). The contralateral NVB was left undissected as a control. Erectile function was assessed acutely and after 2 weeks of survival by measuring peak intracavernous pressures in response to cavernous nerve stimulation. RESULTS: Following conventional techniques of nerve sparing, the erectile response to nerve stimulation was unaffected. In contrast, the use of energy sources in proximity to the NVB during nerve preservation was associated with a substantial decrease in erectile response both acutely (74% to 91% decrease compared to controls) and after 2 weeks (93% to 96% decrease). CONCLUSIONS: In the chronic canine model, use of hemostatic energy sources in proximity to the prostate during dissection of the neurovascular bundle is associated with a significantly decreased erectile response to cavernous nerve stimulation.

Animals↗

[Histoculture drug response assay guided concurrent chemoradiotherapy for lung metastasis from adrenocortical carcinoma--a case report].

A 50-year-old woman underwent surgical resection of a left adrenocortical carcinoma in April 2000. Bilateral pulmonary metastases and abdominal lymph node metastasis were detected in June 2001. After radiation therapy for the abdominal lymph node metastasis, a pulmonary metastatic lesion was thoracoscopically resected. The specimen was subjected to histoculture drug response assay (HDRA), and results revealed that this tumor was sensitive for cisplatin. We therefore performed concurrent chemoradiotherapy including cisplatin for the residual pulmonary metastatic lesion; a complete response was then obtained. Standard protocols of chemotherapy are often absent for malignant tumors, such as in this case, with low incidences. HDRA seems useful for chemotherapy agent selection in cases of rare malignant tumors.

Adrenal Cortex Neoplasms↗

The retinoic acid-responsive proline-rich protein is identified in promyeloleukemic HL-60 cells.

To identify new genes that retinoic acid activates, we employed an mRNA differential display technique and screened for genes that are differentially expressed in promyeloleukemic HL-60 cells incubated in the presence of all-trans-retinoic acid (ATRA) compared with the absence of ATRA. We cloned the coding region of a retinoic acid-induced gene from a human thymus library, which was the mRNA encoding the 666-amino acid human homologue of mouse proline-rich protein 76. We have designated it RARP1 (retinoic acid response proline-rich protein 1). Transcription of an approximately 2.4-kbp mRNA occurred mainly in organs with immune functions, such as thymus, spleen, and peripheral leukocytes. Cycloheximide blocked the ATRA-induced expression. In megakaryocyte-like human erythroleukemia HEL cells, the amount of RARP1 mRNA was high, but it was low in human T-lymphoblastoid Jurkat cells. A specific antibody against RARP1 recognized a 110-kDa protein, which accumulates after incubation of HL-60 cells with ATRA. In immunohistochemical experiments, strong RARP1 staining was observed in the megakaryocytes of bone marrow and spleen, and heterogeneous stain was seen in thymus. Transcriptional studies showed that RARP1 expression impaired the transactivation through activator protein1 and serum response-element in all cell lines we checked, whereas it did not affect the transactivation through cAMP-response element in the same cell lines. Further analysis demonstrated that proline-rich regions of RARP1 are the functional regions regulated for suppression of activator protein1 transactivation. These data suggest that ATRA-inducible RARP1 selectively affects signal transduction and may contribute to myeloid and megakaryocytic differentiation.

Base Sequence↗

Morphologic characterization of green fluorescent protein in embryonic, neonatal, and adult transgenic rats.

Transgenic (Tg) animals with reporter genes are useful models in which to study cell lineage and the process of differentiation into tissues. We developed the green fluorescent protein (GFP)-Tg rat, which is more suitable for transplantation and stem cell research because it is larger than mice. We found that marker gene expression was dependent on each organ and developmental stage. In this study we describe GFP expression in various tissues from embryonic, neonatal, and adult animals. GFP expression in brain, lung, liver, and islet tissues was restricted to early developmental stages, but it was continuously strong in the exocrine pancreas, kidney, and cardiac and skeletal muscles. The CAG promoter that was presumed to induce ubiquitous protein expression might be responsible for the differences in expression.

Animals↗

Cell-specific expression of NADPH-dependent cytosolic 3,5,3'-triiodo-L-thyronine-binding protein (p38CTBP).

We have previously shown that cytosolic 3,5,3'-triiodo-L-thyronine (T3)-binding protein (CTBP) possesses a high affinity for T3 binding in the presence of nicotinamide adenine dinucleotide phosphate in vitro, and that p38CTBP increases intracellular content of T3, and suppresses T3-mediated transactivity. Screening of mRNA expression in 73 different human tIssues has demonstrated that p38CTBP mRNA is expressed at high levels in brain and heart. We have examined the intracellular localization and tissue-specific distribution of this protein by using a specific antibody against human p38CTBP. Western blotting and immunoprecipitation studies have shown that the antibody recognizes human p38CTBP. Interaction of p38CTBP with the antibody did not affect the T3-binding activity of p38CTBP, and its dimer formation in vitro. Western blotting analysis has shown that p38CTBP is expressed in brain and heart predominantly, similar to the distribution of mRNA. Immunohistochemical studies have demonstrated p38CTBP in neural cells and cardiac muscle cells. p38CTBP localizes in cytoplasm rather than in nuclei in neural cells. The evidence for the presence of tIssue-specific localization of p38CTBP has indicated that p38CTBP has a tIssue-specific function, such as the regulation of T3 delivery from cytoplasm to nuclei.

Animals↗

Rat encodes the paralogous gene equivalent of the human histo-blood group ABO gene. Association with antigen expression by overexpression of human ABO transferase.

We cloned a rat ABO homologue and established human A- and B-transferase transgenic rats. A DNA fragment corresponding to exon 7 of the human ABO gene was amplified from Wistar rat genomic DNA and sequenced. Using the amplified fragments as a probe for Southern blotting, multiple hybridized bands appeared on both EcoRI- and BamHI-digested genomes of seven rat strains, which showed variations in the band numbers among the strains. Four cDNAs were cloned from a Wistar rat, three of which showed A-transferase activity and one of which showed B-transferase activity. These activities were dependent on the equivalent residues at 266 and 268 of human ABO transferase. Wild Wistar rats expressed A-antigen in salivary gland, intestine, and urinary bladder tissue, but B-antigen was not stained in any organs studied, whereas a transcript from the ABO homologue with B-transferase activity was ubiquitous. Human A-transferase and B-transferase were transferred into Wistar rats. A-transgenic rats expressed A-antigen in ectopic tissue of the brain plexus, type II lung epithelium, pancreas, and epidermis. B-antigen in the B-transgenic rat was expressed in the same organs as A-transgenic rats. These results may shed light on the function and evolution of the ABO gene in primates.

ABO Blood-Group System↗

Nicotinamide adenine dinucleotide phosphate-dependent cytosolic T(3) binding protein as a regulator for T(3)-mediated transactivation.

Nicotinamide adenine dinucleotide phosphate (NADPH)- dependent cytosolic T(3) binding protein (CTBP) plays a role in the regulation of nuclear transport of T(3) in vitro. However, it is not known whether CTBP regulates the T(3) action. In this study, we examined the effects of CTBP on cellular translocation of T(3) and on transcriptional activation using established CTBP-expressing CHO or GH3 cells. The expression of CTBP increased cellular and nuclear uptake of T(3) in the CTBP-expressing cells. The efflux rate was decreased by induction of CTBP. Efflux from nuclei also inhibited by induction of CTBP. Expression of CTBP suppressed the T(3)-regulated luciferase activity in GH3 cells. Suppression was observed to be related to the expression level of CTBP. T(3) induction of rat GH mRNA was lower in the cells expressing CTBP than that in CTBP-null cells. These results suggest that CTBP regulates the T(3)-induced gene expression, with which an increase in the nuclear content of the T(3) is associated. Because we observed that a part of CTBP could be transported into nuclei and that acceptor protein for CTBP is present in nuclei as previously reported, interaction of CTBP with certain proteins, including transcription factors or nuclear T(3) receptor, may contribute to the regulation.

Animals↗

Fulminant diabetes mellitus associated with pregnancy: case reports and literature review.

We report two cases of type 1 diabetes mellitus fulminantly developed as diabetic ketoacidosis (DKA) at 19 weeks of gestation and immediately after delivery. Development of type 1 diabetes around pregnancy is not rare, but its fulminant development is highly uncommon. We also review the relevant literature concerning mostly Japanese cases. In our cases, the group of patients with fulminant progressive diabetes mellitus associated with pregnancy required insulin replacement therapy even after the acute period and showed high value of pancreatic exocrine enzymes, i.e. amylase, elastase, and lipase. The phenotype of this group was similar to "nonautoimmune, fulminant type 1 diabetes" described by Imagawa et al., where the laboratory data of type 1 diabetes-related autoantibodies showed negative. It is well known that autoimmune diseases are in good control during pregnancy. Our present finding suggests that this type of fulminant type 1 diabetes mellitus associated with pregnancy might develop as a consequence of a nonautoimmune mechanism.

Adult↗

[A case of renal cell carcinoma with heterotopic bone formation].

We report a case of renal cell carcinoma with heterotopic bone formation in a 28-year old woman. The patient was referred to our hospital with a complaint of left lumbargo. Laboratory data were within normal limits. Radiography (KUB) suggested a calcification in the left kidney and abdominal computed tomographic (CT) scan confirmed the presence of a renal mass which contained a calcification. Selective renal angiography revealed a hypervascular (microaneurysm-like change) tumor at the lower part of the kidney. Left nephrectomy was performed. Histopathological diagnosis was renal cell carcinoma with heterotopic bone formation (clear cell carcinoma, G1 > G2, pT1b). There has been neither metastasis nor any recurrence during the 7 months since her operation.

Adult↗