Biomedical subjects

N Kuroda

Publications and source records attributed to N Kuroda.

At least 37 records · Page 2Linked to original sources

PubMed2004

Presence of vascular adventitial fibroblastic cells in diffuse-type gastric carcinomas.

AIM: To investigate morphological changes in the tumour vessel adventitia, particularly the distribution of vascular adventitial fibroblastic cells (VAFCs)--namely, CD34 positive fibroblastic cells just outside the vascular media--in diffuse-type gastric carcinomas. METHOD: In total, 18 surgically resected advanced typical diffuse-type gastric carcinomas and their normal tissues were examined. Immunostaining for CD34, CD31, high molecular weight caldesmon (HCD), and cytokeratin 8 (CAM5.2) was performed to detect VAFCs. VAFCs are positive for CD34 but negative for CD31, and are located just outside the vascular media (HCD positive vascular smooth muscle bundle). The areas just outside the vascular media in the whole maximum tumour cut surface were assessed, except the tumour growing edge, which was confirmed by immunostaining with CAM5.2. CD34 positive and CD31 negative cells just outside the vascular media were defined as VAFCs. RESULTS: VAFC containing vessels were seen in 17 of the 18 diffuse carcinoma tissues. Vessels lacking VAFCs were also detected in these 17 tumours. In contrast, all of the vessels lacked VAFCs in the remaining tumour. In the 18 samples of normal tissue, all of the vessels contained VAFCs. CONCLUSIONS: These results suggest that the presence of VAFCs is associated with the infiltration of diffuse scattered gastric carcinoma cells.

Adenocarcinoma↗

PubMed2004

Immunohistochemical identification of intracytoplasmic lumens by cytokeratin typing may differentiate renal oncocytomas from chromophobe renal cell carcinomas.

Renal oncocytomas and chromophobe renal cell carcinomas (RCCs) share a common phenotype and both originate from the intercalated cells of the collecting duct. This makes it very difficult to differentiate between the two tumors immunohistochemically. Therefore, we studied the results of immunohistochemistry focusing on certain characteristic structures that are occasionally present in renal oncocytomas. We carried out Hale's colloidal iron staining and immunohistochemistry for various cytokeratins (cytokeratins 7, 8, 10, 10/13, 14, 18, 19 and 20, and AE1/AE3) in four oncocytomas and six chromophobe RCCs. In addition, one renal oncocytoma and one chromophobe RCC were studied using electron microscopy. Two renal oncocytomas and one chromophobe RCC were completely unstained by colloidal iron. There was no evident difference between the immunohistochemical characteristics of oncocytomas and those of chromophobe RCCs. However, in all four renal oncocytomas we identified intracytoplasmic ring-like positive reactions for some cytokeratins (at least 3 antigens of cytokeratins 7, 8 and 19, and AE1/AE3), which corresponded ultrastructurally to the intracytoplasmic lumens (ICLs). In contrast, no such structures were found in any of the chromophobe RCCs using the antibodies employed. Therefore, immunohistochemical identification of ICLs by cytokeratin typing may be useful for differentiating between renal oncocytomas and chromophobe RCCs and be more sensitive in this respect than colloidal iron staining.

Adenoma, Oxyphilic↗

PubMed2004

The distribution and role of myofibroblasts and CD34-positive stromal cells in normal pancreas and various pancreatic lesions.

To elucidate the distribution and role of myofibroblasts and CD34-positive stromal cells in various pancreatic lesions, we performed an immunohistochemical study using a streptoavidin-biotin immunoperoxidase technique. We selected 43 pancreatic lesions from 1 biopsied, 22 surgically resected and 12 autopsied specimens: acute pancreatitis (n=3), chronic non-obstructive pancreatitis (n=4), obstructive pancreatitis (n=7), islet cell tumor (n=4), serous cystadenoma (n=7), mucinous cystadenoma (n=6), and invasive ductal carcinoma (n=12). In normal pancreas, myofibroblasts and CD34-positive stromal cells were predominantly present in the peridcutal and periacinar areas, respectively. Both myofibroblasts and CD34-positive cells were observed in the stroma of chronic pancreatitis. In four islet cell tumors, myofibroblasts were present in the stroma of the tumor center, but no CD34-positive stromal cells were identified. Additionally, myofibroblasts and CD34-positive stromal cells were located in the inner layer and the outer layer of the capsule of three islet cell tumors, respectively. In nine of the thirteen cystadenomas, only myofibroblasts were recognized in the cyst wall. In the remaining four cystadenomas, a small number of CD34-positive cells were observed in the cyst wall. In 12 invasive ductal carcinomas, the stroma possessed a lot of myofibroblasts, but there were no or few CD34-positive stromal cells. In conclusion, it seems that the abundant amount of CD34-stromal cells in the main lesions is characteristic of chronic inflammatory lesions. Myofibroblasts and CD34-positive stromal cells may play a role in regulating the tumor growth in the capsule of islet cell tumors of the pancreas.

Acute Disease↗

PubMed2004

The disappearance of CD34-positive and alpha-smooth muscle actin-positive stromal cells associated with human intra-uterine and tubal pregnancies.

In order to elucidate the change in alpha-smooth muscle actin (ASMA)-positive and CD34-positive stromal cells associated with pregnancy, we examined endometrial and Fallopian tube tissues from 40 patients including normal endometrium (n=10), intra-uterine pregnancy (n=10), normal Fallopian tube (n=10), and tubal pregnancy (n=10), using immunohistochemistry. In normal endometrium, only a few ASMA-positive cells were focally observed. Additionally, a wide range of CD34-positive stromal cell abundance was observed. In normal Fallopian tube mucosa, a small to moderate number of both ASMA-positive and CD34-positive stromal cells was observed. Neither ASMA-positive nor CD34-positive stromal cells were observed anywhere in the decidual stroma during both intra-uterine and tubal pregnancies. Likewise, a varying abundance of ASMA-positive cells but no CD34-positive stromal cells were observed at the fetal side during both intra-uterine and tubal pregnancies. In conclusion, the disappearance of CD34-positive and ASMA-positive stromal cells may be an indicator of decidualisation induced change in the stroma during both intra-uterine and tubal pregnancies. ASMA-positive stromal cells at the fetal side associated with pregnancy may play a role in the production of villous extracellular matrix or regulation of blood flow.

Actins↗

PubMed2004

Distribution and role of CD34-positive stromal cells and myofibroblasts in human normal testicular stroma.

CD34-positive stromal cells are distributed in various organs including breast, Fallopian tubes, thyroid gland, colon, pancreas, and uterine cervix. To elucidate the distribution of CD34-positive stromal cells, smooth muscle cells, and myofibroblasts in normal human testis, we examined 48 testes obtained by autopsy and operation, including five fetal, one neonatal, and 42 adult cases without evident testicular lesions, using a streptavidin-biotin immunoperoxidase technique. The expression of alpha-smooth muscle actin (ASMA), h-caldesmon, CD34, and CD31 were immunohistochemically examined in all cases. The tunica albuginea and the inner layer of seminiferous tubules in adult testis were predominantly composed of myofibroblasts. Smooth muscle cells were also scattered throughout these sites in some cases. CD34-positive stromal cells were abundant, and they formed a reticular network around the seminiferous tubules and Leydig cells as well as the outer layer of seminiferous tubules. Moreover, myofibroblasts and the CD34 reticular network were already present in the testicular stroma during fetal or neonatal development. Double immunostaining of fetal, neonatal and adult testes using ASMA and CD34 confirmed that myofibroblasts and CD34-positive stromal cells were present in the inner and outer layers of peritubular tissue, respectively. This distribution and cytological identification was also confirmed by an ultrastructural study of four cases. Finally, CD34-positive stromal cells and myofibroblasts are major components of human testicular stroma.

Actins↗

PubMed2003

Fascin-positive dendritic cells and fibroblastic reticulum cells build a framework of T-cell areas in lymph nodes.

Fascin, a 55-kDa actin-bundling protein, and alpha-smooth muscle actin (ASMA) were immunohistochemically examined in murine normal and stimulated lymph nodes. In specific pathogen-free young female mice, a few fascin-positive cells (FPCs) were located in the sinus and surrounding tissues, but ASMA-positive cells were undetectable. Following a subcutaneous injection of sheep red blood cells, the numbers of FPCs and their dendrites increased in the paracortex, with the accumulation of activated lymphocytes. Fibroblastic reticulum cells (FRCs), endothelial cells, histiocytic cells and lymphocytes in various stages of maturation were all fascin negative. These results indicated that fascin could be a reliable marker of paracortical dendritic cells in murine lymph nodes. However, FRCs became ASMA positive. Immunoelectron microscopy showed that the FPCs were interdigitating cells and that they closely contacted with FRCs. These two types of cells and reticular fiber formed a network in the paracortex and contacted with each other. In active paracortical response, both FPCs and FRCs are also stimulated and might play a significant role in the maturation of the lymphocytes.

Actins↗

PubMed2003

Phylogeny of antigen-processing enzymes: cathepsins of a cephalochordate, an agnathan and a bony fish.

Cathepsins are enzymes that have been cleaving peptide bonds of lysosomal proteins probably since lysosomes appeared in early eucaryotes. When the adaptive system emerged in gnathostomes, cathepsins were recruited to produce peptides for loading onto the major histocompatibility complex class II molecules and for degrading the class II-associated invariant chain just before the loading. The circumstances under which this recruitment took place are unclear because the knowledge about vertebrate cathepsins is limited largely to mammals. To shed light on the recruitment, 10 amphioxus, one lamprey and one cichlid fish cathepsin cDNA clone were characterized and analysed phylogenetically. Disregarding cathepsin O, whose phylogenetic position is uncertain, the analysis confirms the existence of two old lines of descent, the B and the L lineages of cathepsins, which diverged from each other early in the evolution of eucaryotes. The B lineage encompasses cathepsins B, C and Z (X). The L lineage splits off sublineages encompassing cathepsins F and W before the plant-animal separation and cathepsin H early in the evolution of the metazoa. The remaining cathepsins belonging to the L lineage diverged from one another during the evolution of vertebrates: S, K and L before the emergence of bony fishes, and the group of rodent placentally expressed cathepsins [J (P), M, Q, R, 3, 6, 7 and 8] as well as the testis/ova-expressed cathepsins (testins) probably after the divergence of rodents from primates. The part possibly played by the adaptive immune system in some of these divergences is discussed.

Amino Acid Sequence↗

PubMed2003

Validation and verification of the ICRP biokinetic model of 32P: the criticality accident at Tokai-Mura, Japan.

Regrettably, a criticality accident occurred at a uranium conversion facility in Tokai-mura, Ibaraki, Japan, on 30 September 1999. Radioactivities of 32P in urine, blood and bone samples of the victims, who were severely exposed to neutrons, were measured. 32P was induced in their whole bodies at the moment of the first nuclear release by the reaction 31P (n, gamma) 32P and 32S (n, p) 32P. A realistic biokinetic model was assumed, as the exchange of 32P between the extracellular fluid compartment and the soft tissue compartment occurs only through the intracellular compartment, and the model was used for preliminary calculations. Some acute excretion of 32P, caused by decomposition or elution of tissues which occurred at the time of the accident, may have happened in the victims' bodies in the first few days. The working hypotheses in the present work should initiate renewed discussion of 32P biokinetics.

Bone and Bones↗

PubMed2003

Transfer of 14C to prenatal and neonatal rats from their mothers exposed to 14C compounds by ingestion.

The transfer of 14C through placenta or milk was investigated and the radiation dose to fetal and newborn rats was estimated. Female rats at different gestational stages or after delivery were exposed to 14C in the form of sodium bicarbonate, thymidine and lysine by a single ingestion. Radioactivity in maternal tissues and conceptuses (placenta, fetal membrane and fetus) and in the newborn was determined at various times after ingestion. After exposure to these 14C compounds, there was no significant difference between the 14C concentration in the fetus and that in the maternal tissues, suggesting that the placenta has no effect in preventing or accelerating the placental transfer of 14C. The concentration and content of 14C in the fetus and newborn were, however, dependent on the chemical form of 14C and on the prenatal or neonatal stage at the time of ingestion. The result of the dose estimation showed that 14C-lysine gave significantly higher prenatal and neonatal doses than 14C-sodium bicarbonate or 14C-thymidine.

Absorption↗

PubMed2003

Review of chromophobe renal cell carcinoma with focus on clinical and pathobiological aspects.

In recent years, the concept of chromophobe renal cell carcinoma (RCC) has been established. Chromophobe RCCs account for about 4-6% of all renal tumors. Macroscopically, the cut surface of the tumor is generally grey-beige in color. Histologically, there are two variants (typical and eosinophilic). In the typical variant, large tumor cells with architecture of a compact tubulo-cystic pattern proliferate. The cytoplasm is abundant and shows a fine reticular translucent pattern. The cell border is thick, prominent and eosinophilic. In the eosinophilic variant, tumor cells are smaller and markedly eosinophilic, and a perinuclear halo is often seen. Histochemically, the tumor cells generally show a diffuse and strong reaction for Hale's colloidal iron staining. Ultrastructurally, tumor cells contain many cytoplasmic microvesicles (150-300 nm). In chromosomal analysis, a low chromosome number is characteristic of chromophobe RCCs, due to the frequent occurrence of a combined loss of chromosomes 1, 2, 6, 10, 13, 17, and 21. In differential diagnosis, histological distinction from oncocytomas, which share a common phenotype (intercalated cells of the collecting duct system), is most important. In this diagnostic setting, recent studies have given rise to several problems. Firstly, some cases of coexistent chromophobe RCC and oncocytoma (so-called renal oncocytosis) or cases of oncocytoma with metastasis have recently been reported. Secondly, the existence of chromophobe adenoma, which is the benign counterpart of chromophobe RCC, and an oncocytic variant of chromophobe RCC has recently been suggested. Therefore, further studies are needed to elucidate the relationship between chromophobe RCCs and oncocytomas, to confirm whether chromophobe adenoma actually exists or not, and to identify the key gene that causes chromophobe RCCs.

Carcinoma, Renal Cell↗

PubMed2003

Review of metanephric adenoma of the kidney with focus on clinical and pathobiological aspects.

The concept of metanephric adenoma has become established in recent years. Metanephric adenoma is a rare neoplasm. Macroscopically, the cut surface of the tumor displays a tan to gray or yellow color, and tumors generally form well-circumscribed masses. Histologically, tumors are composed of small epithelial cells that form small acini. Glomeruloid bodies, which are composed of lobulated papillary projections, are occasionally seen. Although there have been few studies using chromosomal analysis, two recent studies have shown partial monosomy or LOH of 2p. On the other hand, the concept of metanephric tumors has recently become broadened. These tumors include metanephric adenomas, adenofibromas and stromal tumors, and they compose a continuous histological spectrum. Therefore, further studies on various aspects are needed to identify the gene responsible for the occurrence of metanephric tumors and, furthermore, to clarify the association among the three types of metanephric tumors.

Adenoma↗

PubMed2003

Review of papillary renal cell carcinoma with focus on clinical and pathobiological aspects.

Recent studies have shown that papillary renal cell carcinoma (RCC) is clinically and genotypically a distinct entity. Papillary RCCs account for about 10-15% of renal parenchymal neoplasms. Macroscopically, the cut surface is yellow or brown in color and large tumors frequently show cystic change. Hemorrhage and necrosis are common. Histologically, Delahunt and Eble have classified papillary RCCs into type 1 (small cells, single layer) and type 2 (large cells, pseudostratification) according to the cytoplasmic volume and thickness of the lining cells. In chromosomal analysis, gain of chromosomes 7 and 17, loss of Y chromosome and additional gains (chromosome 3q, 8p, 12q, 16q and 20q) are frequently found in type 1 papillary RCCs, but the chromosomal aberration of type 2 papillary RCCs seems to be more heterogenous than that of type 1 papillary RCCs. Mutations of MET proto-oncogenes in some cases of both hereditary and sporadic papillary RCCs have recently been detected. Furthermore, all hereditary and sporadic papillary RCCs with MET proto-oncogene show type 1 histological features. Type 1 papillary RCCs generally seem to have a favorable prognosis, but type 2 tumors have a worse prognosis than do type 1 tumors. Papillary RCCs with involvement of the X chromosome and cancer syndrome with predisposition to cutaneous/uterine leiomyomas and papillary RCCs, the histological features of which are basically different from those of usual papillary RCCs, have also been recently reported. Since papillary RCCs seem to constitute clinically, histologically, and even genetically more heterogenous groups than previously thought, further investigations are needed to characterize the subtype of papillary RCC.

Carcinoma, Papillary↗

PubMed2003

Review of sarcomatoid renal cell carcinoma with focus on clinical and pathobiological aspects.

In sarcomatoid renal cell carcinoma (RCC), it is generally accepted that the sarcomatoid portion is derived from metaplastic transformation of carcinoma. Sarcomatoid RCCs account for about 1-8% of all renal tumors. Macroscopically, tumors generally form encapsulated masses and show invasive growth. Sarcomatoid RCCs originate from all subtypes of RCCs, including conventional, papillary, chromophobe, and collecting duct carcinomas. With regard to the growth pattern of the sarcomatoid component, malignant fibrous histiocytomatous, fibrosarcomatous and unclassified sarcomatous patterns are frequently seen. Immunohistochemically, sarcomatoid RCCs are generally positive for AE1/AE3, epithelial membrane antigen (EMA) and vimentin and negative for desmin, actin and S-100. Little is know about genetic alterations in sarcomatoid RCCs. Further studies are therefore needed to identify the key gene involved in sarcomatoid transformation of RCCs.

Animals↗

PubMed2003

Review of renal oncocytoma with focus on clinical and pathobiological aspects.

Renal oncocytomas account for about 3-7% of all renal tumors. Macroscopically, the cut surface of the tumor is generally mahogany brown or dark red in color. A central scar is occasionally observed. Histologically, tumor cells with finely granular cytoplasm proliferate in an edematous, myxomatous or hyalinized stroma with a nested, tubulocystic, solid or trabecular pattern. Ultrastructurally, tumor cells contain many mitochondria with lamellar cristae. Mitochondrial DNA alterations are consistently observed in renal oncocytomas. In chromosomal analysis, renal oncocytomas comprise a heterogenous group. Combined loss of chromosomes Y and 1, rearrangements affecting band 11q12-13, involvement of 12q12-13, loss of 14q, and the lack of combination of LOH at specific chromosomal sites have been reported. In differential diagnosis, the histological separation from chromophobe RCCs is of great importance. In such a setting, ultrastructural or chromosomal analysis is very useful. However, there are several findings suggesting a close relationship between chromophobe RCC and oncocytoma. First, both tumors share a phenotype of intercalated cells of the collecting duct system and mitochondrial DNA alterations. Second, some cases of coexistent oncocytoma and chromophobe RCC, designated as "renal oncocytosis", have recently been reported. Third, oncocytic variants of chromophobe RCCs that have similar ultrastructural features to those of oncocytomas have been reported. Fourth, the existence of chromophobe adenoma, which is the benign counterpart of chromophobe RCC and shows loss of chromosomes Y and 1, has recently been suggested. Finally, although almost all oncocytomas behave in a benign fashion, some cases of oncocytoma that caused metastasis or resulted in death have also been reported. Therefore, further studies are needed to resolve these problems and also to elucidate the genetic mechanisms responsible for the occurrence of oncocytomas.

Adenoma, Oxyphilic↗

PubMed2002

Electron cooling of high-energy protons in a multiring trap with a tank circuit monitoring the electron-plasma oscillations.

Electron cooling of energetic protons in a multiring trap was investigated experimentally with a tank circuit monitoring electron-plasma oscillations in the trap. The energy of protons was determined by time-of-flight measurements. It is found that a simple model can explain the qualitative behavior of both electron and proton energy when the initial energy of protons is less than 2 keV. Monitoring the electron-plasma temperature with a tank circuit can be an effective tool when energetic particles are electron cooled in a multiring trap.

Journal Article↗

PubMed2002

Exertion of the suppressive effects of IFN-gamma on experimental immune mediated blepharoconjunctivitis in Brown Norway rats during the induction phase but not the effector phase.

BACKGROUND/AIMS: Interferon gamma (IFN-gamma) knockout mice exhibit severe allergic conjunctivitis (AC), indicating that IFN-gamma regulates the development of AC. The authors examined whether this inhibitory effect of IFN-gamma is exerted during the induction or effector phase of experimental AC. METHODS: Experimental immune mediated blepharoconjunctivitis (EC) was induced in Brown Norway (BN) rats, using ovalbumin (OVA) as the antigen. To investigate the role of IFN-gamma in the induction phase, EC was induced by active immunisation and IFN-gamma (10 micro g/time, total 70 micro g), or phosphate buffered saline (PBS) as a control, was injected intraperitoneally every other day from the day of immunisation. The rats were challenged with OVA eye drops 13 days after immunisation, and 24 hours later, the eyes were harvested for histology. To examine the effects of IFN-gamma in the effector phase, OVA specific T cells were transferred into syngeneic rats and IFN-gamma (10 micro g/time, total 50 micro g) or PBS was injected each day after the transfer until induction of EC 4 days later with an OVA challenge. To investigate the role of endogenous IFN-gamma during the effector phase, an anti-IFN-gamma monoclonal antibody (3 mg/time) was injected on days 3 and 4. RESULTS: Injection of IFN-gamma into actively immunised rats suppressed eosinophilic infiltration but not infiltration of mononuclear cells. In contrast, neither IFN-gamma nor anti-IFN-gamma affected EC in passively immunised rats. CONCLUSION: IFN-gamma is a suppressive cytokine for the development of EC and exerts this suppressive effect during the induction phase.

Adoptive Transfer↗

PubMed2002

Microinvasive lobular carcinoma associated with intraductal spread arising in a mammary hamartoma.

A 53 year old woman presented with a lump in the inner lower quadrant of the left breast. Histological examination of the breast tumour confirmed that the lesion was a mammary hamartoma. Carcinoma with foci of microinvasion was observed in the lobules of the hamartoma concomitant with the intraductal spread of lobular carcinoma. Immunohistochemically, the cancer cells were negative for beta-catenin, which generally stained normal breast ducts and ductal carcinomas. This is only the sixth case of breast carcinoma arising in a mammary hamartoma to be reported and, moreover, the fourth case of lobular carcinoma occurring within a hamartoma. Despite the apparent rarity of this case, pathologists should be aware of the possibility of carcinomas arising within mammary hamartomas.

Breast Diseases↗

PubMed2002

High molecular weight caldesmon positive stromal cells in the capsule of thyroid follicular tumours and tumour-like lesions.

AIMS: To investigate the smooth muscle nature of the spindle stromal cells in the capsule of thyroid tumours and tumour-like lesions. METHODS: Immunostaining for high molecular weight caldesmon (HCD), a highly specific marker for smooth muscle differentiation, was performed in 70 primary thyroid tumours and tumour-like lesions (21 hyperplastic nodules, 29 follicular adenomas, five minimally invasive follicular carcinomas, six widely invasive follicular carcinomas, and nine encapsulated papillary carcinomas). RESULTS: HCD positive stromal cells (HCD+ cells) were detected in the capsule of 20 of the 21 hyperplastic nodules, and all of the 29 follicular adenomas and five minimally invasive follicular carcinomas, whereas HCD+ cells were seen in the capsule of only four of the six widely invasive follicular carcinomas and no HCD+ cells were seen in the capsule of the nine encapsulated papillary carcinomas examined. CONCLUSIONS: The presence of HCD+ cells in the capsule is characteristic of thyroid follicular tumours and tumour-like lesions. The stromal cells in the capsule of thyroid follicular tumours and tumour-like lesions are different from those of encapsulated papillary carcinoma.

Adenocarcinoma, Follicular↗