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N Eguchi

Publications and source records attributed to N Eguchi.

At least 55 records · Page 3Linked to original sources
PubMed1997

Prostaglandin D synthase (beta-trace) in human arachnoid and meningioma cells: roles as a cell marker or in cerebrospinal fluid absorption, tumorigenesis, and calcification process.

Glutathione-independent prostaglandin D synthase (PGDS) is an enzyme responsible for biosynthesis of prostaglandin D2 in the CNS and is identical to a major cerebrospinal fluid protein, beta-trace. Although PGDS has been identified recently in rat leptomeninges, little information is available about human meninges or meningiomas. Here, we report PGDS to be expressed consistently in 10 human arachnoid and arachnoid villi and in 21 meningiomas by immunohistochemistry, Western blot, and reverse transcription (RT)-PCR analyses. In arachnoid, PGDS immunoreactivity was seen in arachnoid barrier cells but was negligible in arachnoid trabecula and pia mater. In contrast, in arachnoid villi, PGDS was seen in core arachnoid cells rather than in the cap cell cluster or arachnoid cell layer. Meningioma cells also showed intense immunoreactivity in the perinuclear region, and it was often concentrated within meningocytic whorls and around calcifying psammoma bodies. Immunoelectron microscopic data, when compared with the ultrastructure, showed that PGDS was localized at rough endoplasmatic reticulum of arachnoid and meningioma cells. Western blot showed a 29 kDa immunoreactive band indicating PGDS, but the extent of expression was variable from case to case, which was compatible with immunohistochemical data. RT-PCR revealed PGDS gene expression in all meningiomas studied, regardless of histological subtypes, and also in human arachnoid villi. Because human arachnoid and meningioma cells exclusively express PGDS, it can be considered their specific cell marker. These results show functional differences in various types of meningeal cells attributable to differences in PGDS expression.

Animals↗
PubMed1997

Metabolites of arsenic induced tetraploids and mitotic arrest in cultured cells.

The toxic effects of arsenic compounds on cell divisionwere studied, using Chinese hamster V79 cells. Seven arsenic compounds weretested. Inorganic arsenic compounds (arsenite and arsenate), which have beenfound in drinking water, inhibited cell growth at very low concentrations. Monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), and trimethylarsineoxide (TMAO), which are methylated metabolites of inorganic arsenics, wereless cytotoxic than the inorganic arsenics themselves. The cytotoxicity ofthe three methylated metabolites decreased as the number of methyl groupsincreased. Arsenobetaine (AsBe) and arsenocholine (AsC), which have beenfound in some marine products, did not show any cytotoxicity. Threemethylated metabolites; MMA, DMA and TMAO induced mitotic arrest. Tetraploidyproduction was observed in cells exposed to DMA or TMAO. Arsenite, arsenate,AsBe and AsC did not induce mitotic arrest or tetraploids. These resultssuggest that MMA, DMA and TMAO exert some effect on cell division inmetaphase and may thereby give some clue as to the carcinogenic mechanism ofarsenic.

Animals↗
PubMed1997

TP53 mutations in stage I gallbladder carcinoma with special attention to growth patterns.

32 stage I cases of gallbladder carcinoma (GC) were examined to evaluate TP53 mutations with special attention to growth patterns. Their growth patterns were classified into two types: polypoid (P-type) and flat (F-type). 16 cases of GC were classified as P-type and 16 as F-type. p53 immunohistochemistry was performed using a mouse monoclonal anti-p53 antibody. Mutations in exons 5-8 were examined by polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) and direct sequencing. The incidence of p53 immunoreactivity was greater in the cases of F-type (11/16, 69%) than those in P-type (14/16, 25%) (P < 0.05). PCR-SSCP or direct sequencing revealed that TP53 mutations were detected in all cases positive for p53 protein. These results suggest that TP53 mutations may contribute to the carcinogenesis of the F-type GC, and than this pathway in the F-type may differ from that in the P-type GC.

Adenocarcinoma↗
PubMed1997

Changes in contrast enhancement of hepatocellular carcinoma and liver: effect of temporary occlusion of a hepatic vein evaluated with spiral CT.

PURPOSE: To assess the hemodynamics of the liver and of hepatocellular carcinomas (HCCs) with hepatic vein occlusion. MATERIALS AND METHODS: Selected hepatic veins were temporarily occluded with a balloon catheter in 21 patients with 28 nontreated nodular HCCs. Computed tomographic (CT) arteriography was performed without and with temporary occlusion of a hepatic vein that drained the blood from segmental liver parenchyma containing tumor by using a unified spiral CT and angiography system. The degree of enhancement and change in appearance of the HCC in each condition were compared. RESULTS: All HCCs were well-enhanced, almost round masses at CT arteriography. At CT arteriography with hepatic vein occlusion, however, HCCs were changed as follows: (a) the absolute attenuation of the HCC was decreased in 27 (96%) of 28 tumors compared with that at CT arteriography without hepatic vein occlusion, while attenuation of the surrounding liver parenchyma was increased; (b) the size of the highly enhanced area in HCC became smaller in 17 (61%) tumors (of these, two disappeared); and (c) the shape was changed in 12 (43%) tumors. CONCLUSION: Hepatic vein occlusion resulted in reciprocal hemodynamic changes in the liver parenchyma relative to HCCs: Enhancement of the liver increases and that of HCCs decreases.

Adult↗
PubMed1996

Lipocalin-type prostaglandin D synthase (beta-trace) is located in pigment epithelial cells of rat retina and accumulates within interphotoreceptor matrix.

Glutathione-Independent prostaglandin D synthase, identical to beta-trace, (a major CSF protein), is localized in the CNS. This enzyme, lipocalin-type prostaglandin D synthase, is a member of the lipocalin family of secretory proteins that transport small lipophilic substances. This enzyme's activity in adult rat retina was enriched sixfold in retinal pigment epithelium (RPE) and even more in interphotoreceptor matrix (IPM), all higher than brain. Western blots with anti-lipocalin-type prostaglandin D synthase showed three distinct immunoreactive bands. In the retinal cytosolic fraction, only one band was observed (M(r) 25,000); in IPM, the larger component occurred (M(r), 26,000). The RPE membrane-bound fraction showed two bands (M(r) 20,000 and 23,000), indicating synthesis, and the cytosolic fraction contained two bands (M(r) 23,000 and 26,000), indicating modification for release into IPM. At least two glycosylation sites occurred on the prostaglandin D synthase moiety, explaining the three immunoreactive bands in Western blots. Immunohistochemistry with polyclonal antibodies against this lipocalin-type enzyme showed intense localization in RPE, but less in photoreceptor outer and inner segments. In situ hybridization showed mRNA specifically expressed in RPE. Thus, lipocalin-type prostaglandin D synthase is predominantly expressed in RPE and actively accumulated in IPM. This may demonstrate gene sharing because, while catalyzing prostaglandin D2 synthesis, it may perform an additional, unrelated role in IPM. This enzyme is secreted from the RPE into IPM from which it is then taken up by photoreceptors. However, the nature of its ligand(s) is not known; they may be retinoids and/or docosahexanoic acid.

Animals↗
PubMed1996

Seasonal variation in levels of prostaglandins D2, E2 and F2(alpha) in the brain of a mammalian hibernator, the Asian chipmunk.

Seasonal changes in the in vivo levels of the prostaglandins (PGs) PGD2, PGE2, and PGF2(alpha) were measured in the brain of the male Asian chipmunk, Tamias asiaticus (n = 111), which underwent hibernation during the period between November and March. The mean level of PGD2 ranged from 36.0 to 85.2 pg/g tissue from June to October and remained essentially unchanged (80.5 pg/g tissue) in December. However, the mean PGD2 level rose significantly to 128.6 pg/g tissue in February, and returned to 75.2 pg/g tissue in the following April, suggesting a correlation between PGD2 and hibernation phenomenon. While PGE2 level did not vary significantly throughout the year, PGF2(alpha), which appeared to be the most abundant among the three prostanoids, showed a marked circannual rhythm with a trough of 51.6 pg/g tissue in July, rising to 391.6 pg/g tissue in February and reaching the peak value of 492.7 pg/g tissue in April, the reproduction period.

Animals↗
PubMed1996

Pathology and cellular kinetics of gallbladder with an anomalous junction of the pancreaticobiliary duct.

OBJECTIVES: Anomalous junction of the pancreaticobiliary duct (AJPBD) is thought to be an important risk factor for gallbladder carcinoma in Japan. In this report, we examine histopathology and cellular kinetics of gallbladder mucosae of patients with AJPBD and the possible risk of gallbladder carcinoma. METHODS: We examined 62 gallbladders from patients with AJPBD (group A), 16 gallbladder carcinomas from patients with AJPBD (group B), 60 gallbladder carcinomas from patients without AJPBD (group C), and six normal gallbladders from patients without AJPBD (group D). Histopathology, mucosal heights, and proliferative cell nuclear antigen-labeling index were obtained from routinely processed tissue specimens. RESULTS: The incidence of hyperplastic changes in group A and in the noncancerous regions (NCRs) of group B was greater than in the NCRs of group C (p < 0.05). The incidence of dysplastic changes in the NCRs of group B was greater than in the NCRs of group C (p < 0.05). The mucosal heights in group A and in the NCRs of group B were higher than in the NCRs of group C (p < 0.05). A high proliferative cell nuclear antigen-labeling index was observed in group A and in the NCRs of group B, where hyperplastic changes were frequently observed. CONCLUSIONS: These results suggest that a sequence of hyperplastic changes with a corresponding increase in cellular kinetics with progression through dysplasia to carcinoma may be important in carcinogenesis in gallbladders of patients with AJPBD. AJPBD itself may be a possible risk for gallbladder carcinoma.

Adolescent↗
PubMed1995

Structural and functional significance of cysteine residues of glutathione-independent prostaglandin D synthase. Identification of Cys65 as an essential thiol.

Glutathione-independent prostaglandin D synthase in rat brain is composed of 189 amino acid residues and catalyzes the isomerization of prostaglandin H2 to prostaglandin D2, an endogenous sleep-promoting substance. This enzyme is the only enzyme among members of the lipocalin superfamily composed of various secretory lipophilic ligand-carrier proteins and is recently identified to be a beta-trace protein, a major constituent of human cerebrospinal fluid. We expressed the active enzyme in Escherichia coli and then systematically substituted all cysteine residues of the delta 1-29 enzyme at positions of 65, 89, and 186 with alanine or serine. The parent and mutant enzymes were purified to apparent homogeneity with a recovery of approximately 30% by chromatography with Sephadex G-50 and S-Sepharose, by which all the enzymes showed identical elution profiles. The purified enzymes, irrespective of the mutation, showed almost the same circular dichroism spectral characteristics as displayed by a highly ordered beta-structure. The recombinant enzymes containing Cys65 showed the activity comparable with that of the enzyme purified from rat brain (approximately 3 mumol/min/mg of protein) in the presence, but not in the absence, of sulfhydryl compounds. However, all of the single, double, and triple mutants without Cys65 lost the enzyme activity. The purified delta 1-29 Ala89,186 enzyme was inactivated reversibly by conjugation with glutathione at Cys65 and irreversibly by the stoichiometric chemical modification with N-ethylmaleimide. These results indicate that Cys65 is an essential thiol of the enzyme and that both the intrinsic and extrinsic sulfhydryl groups are necessary for nonoxidative rearrangement of 9,11-endoperoxide of prostaglandin H2 to produce prostaglandin D2 catalyzed by the enzyme.

Amino Acid Sequence↗
PubMed1995

A novel deletion mutation in the beta-myosin heavy chain gene found in Japanese patients with hypertrophic cardiomyopathy.

Mutations in the cardiac beta-myosin heavy chain (MHC) gene of 50 Japanese patients with hypertrophic cardiomyopathy (HCM) were investigated by polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP) analysis. A novel deletion mutation was detected in exon 3 of the cardiac beta-MHC gene in a Japanese family with HCM. Sequencing analysis revealed a three nucleotide deletion at codon 10 leading to a deletion of a glycine residue, which has been conserved in the myosin gene from birds to humans. Because this deletion mutation was not detected in other healthy family members, it was suggested that this 10Gly deletion is the cause of HCM in this family. The same deletion mutation has been found in three other unrelated patients with HCM. This is the first report of a one codon deletion in the beta-MHC gene in patients with HCM.

Adult↗
PubMed1995

Effect of temporary occlusion of the hepatic vein on dual blood in the liver: evaluation with spiral CT.

PURPOSE: To evaluate the contribution of hepatic veins to the dual blood supply in the liver under temporary hepatic venous occlusion. MATERIALS AND METHODS: Selected hepatic veins in 23 patients with liver tumors were temporarily occluded with a balloon catheter. Computed tomography (CT) arteriography, CT during arterial portography (CTAP), or both were performed with a spiral technique with and without temporary occlusion of a hepatic vein. RESULTS: After hepatic vein occlusion, a well-demarcated, wedge-shaped area of hypoattenuation was seen at CTAP and/or hyperattenuation was seen at CT arteriography in the following regions: left lobe (left hepatic vein), ventral part of the anterior segment and the medial segment except for the ventromedial part (middle hepatic vein), dorsal part of the anterior segment and the ventral part of the posterior segment (right hepatic vein), and dorsocaudal part of the right lobe (inferior right hepatic veins). CONCLUSION: After hepatic venous occlusion, the portal veins become draining veins and the occluded area is supplied with arterial blood alone.

Adult↗
PubMed1995

Hepatobiliary cysts in patients with autosomal dominant polycystic kidney disease: prevalence and CT findings.

OBJECTIVE: Hepatobiliary (intrahepatic and peribiliary) cysts have been described for patients with autosomal dominant polycystic disease. The purpose of this study was to determine the prevalence of these cysts and to describe the wide variation in their appearance on CT scans. MATERIALS AND METHODS: We studied CT scans for 64 patients (31 men and 33 women) who either had known autosomal dominant polycystic kidney disease or had renal cysts and a family member with polycystic kidney disease. Contrast enhancement was used for 31 patients. CT scans were retrospectively evaluated by consensus by two experienced radiologists. The presence, number, and size of hepatobiliary cysts and the presence and appearance of the two variations, peribiliary and intrahepatic cysts, were analyzed. Peribiliary cysts were determined to be present when many small (< or = 10-mm) cysts were seen adjacent to the larger (up to the third order) portal triad. Cysts present in the hepatic parenchyma but not in contact with the larger portal triad were regarded as intrahepatic cysts. RESULTS: CT showed hepatobiliary cysts in 56 of the 64 patients (24 men and 32 women; 88%). Intrahepatic cysts were noted in all 56 patients; peribiliary cysts were definitely seen on CT scans for 22 patients and were probably seen (fewer than five cysts and/or cysts located only on one side of the portal vein) on CT scans for 19 patients (73% of all patients with hepatobiliary cysts). Peribiliary cysts appeared as discrete cysts in 31 patients, as a string of cysts in six patients, and as a tubular structure in four patients. Intrahepatic cysts generally were round but occasionally were polygonal. They were variable in number, size, and location. CONCLUSION: Hepatobiliary cysts were noted in 56 of 64 patients (intrahepatic cysts in all cases and peribiliary cysts in 73% of positive cases). Intrahepatic cysts varied widely in number, size, and location, whereas peribiliary cysts were small and appeared as discrete cysts, a string of cysts, or a tubular structure adjacent to the larger portal triad. It is important to be aware of the wide variety of findings for hepatobiliary cysts so that they are not confused with other abnormalities.

Bile Duct Diseases↗
PubMed1995

[Spatial and temporal alteration of the dual supply of the hepatic circulation with transient occlusion of the hepatic veins: spiral volumetric CT during arterial portography and arteriography].

To elucidate the contribution of hepatic veins to the blood flow of liver, CT arterial portography and/or arteriography was performed in eight patients having hepatocellular carcinoma with transient occlusion of the hepatic vein and eight without occlusion. In each patient with occlusion of the hepatic vein, CT showed a well-demarcated fan-shaped area of low density during arterial portography and increased density during arteriography in the corresponding area. Hepatic vein occlusion could result in the pooling of arterial blood in the liver parenchyma. Transient segmental hepatic venous occlusion might improve the results of transcatheter arterial infusion and transcatheter arterial embolization for liver tumors.

Adult↗
PubMed1994

Relationship between occurrence of tremor/convulsion and level of beta-carbolines in the brain after administration of beta-carbolines into mice.

Fifteen beta-carboline derivatives, including those found in the South American hallucinogenic plant Banisteriopsis caapi, were injected IP and IVC into mice. Subsequent behavioral changes were observed and the levels of the compounds in brain tissue were determined. It was found that following IP administration, tremors and/or convulsions were induced by beta-carbolines having aliphatic alkyl groups, but not by those with carbonyl and oxo groups substituted at carbon-1 of the C ring. These effects were potentiated by the presence of a methoxy group at carbon-7 of the A ring, and their duration of actions were prolonged by 3,4-dihydro derivatives. When induced, tremors/convulsions correlated with levels of beta-carbolines in the brain. The smaller ED50 values of beta-carbolines that cause tremors/convulsions showed lower levels of beta-carbolines in brain tissue.

Animals↗
PubMed1992

Biochemical and immunohistochemical demonstration of a tightly bound form of prostaglandin E2 in the rat brain.

Basal levels of prostaglandin E2 in the rat brain were determined by radioimmunoassay to be 0.68-0.79 pmol/g brain. About one-third of the prostaglandin E2 (0.23-0.28 pmol/g) was resistant to extraction with ethanol, but could be recovered with a mixture of ethanol and 1 N HCl (9:1, v/v), indicating that a tightly bound form of prostaglandin E2 exists in the brain. The amount of the bound form of prostaglandin E2 was almost unchanged by pentylenetetrazole-induced convulsion or by transcardial perfusion with a formaldehyde solution, although these treatments resulted in 40- to 80-fold increases in prostaglandin E2 content extracted with ethanol at neutral pH. A polyclonal antibody against prostaglandin E2-albumin conjugates recognized the bound form of prostaglandin E2, giving a punctate appearance in many neuronal cell bodies in the brain. Although almost all of the neuronal perikarya were immunoreactive for prostaglandin E2, intense immunoreactivity was observed in the mitral cell layer of the olfactory bulb, layer V of the cerebral neocortex, anterodorsal and reticular nuclei of the thalamus, supraoptic, paraventricular, accessory neurosecretory and lateral mammaillary nuclei of the hypothalamus, mesencephalic trigeminal nucleus, nucleus of the trapezoid body and deep cerebellar nuclei. When the cerebral neocortical regions were observed electron microscopically, immunoreaction products were seen as fine granules which were clustered into small patches in the cytoplasm of neuronal cell bodies and proximal dendrites. No immunoreaction products were seen in glial cells or endothelial cells. These results suggest that prostaglandin E2 is involved in fundamental processes of neurons.

Animals↗
PubMed1992

Permeability of brain structures and other peripheral tissues to prostaglandins D2, E2 and F2 alpha in rats.

Parenchymal tissue-uptake (TU) and permeability-surface area (PS) product of [3H]prostaglandins (PG) D2, E2 and F2 alpha [1.85 MBq, 0.5 mg/kg (270 nmol)] were examined in 98 regions of the brain and in 19 other tissues of urethane-anesthetized male rats (180-200 g) 15 sec after i.v. administration with [14C]dextran [0.185 MBq, 0.6 mg/kg (2 nmol)] used as a blood spacer. Slight and insignificant change in blood volume was observed in most of the tissues and brain regions between vehicle- and PG-administered groups. TU for the three PG was markedly high in kidney and lung (2388-3952 ng/g), exceeding the blood concentration (2021-2320 ng/ml), but low (less than 10% of the blood concentration) in epididymis, epididymal fat, testis (59-163 ng/g), brain and spinal cord (33-67 ng/g). TU in brain were detected about 0.1% of the administered PG. Based on a two-compartment model, the PS product for the three PG ranged from 0.75 to 4.16 microliters/g/sec in the latter tissues. The value of brain was 1.22 +/- 0.18 microliters/g/sec for PGD2, 1.69 +/- 0.05 for PGE2 and 1.33 +/- 0.13 for PGF2 alpha, indicating that PGE2 enters the brain more readily than PGD2 and PGF2 alpha. In various brain structures, the ranges of the PS product were large and completely overlapped among the three PG (PGD2, 0.14-1.56 microliters/g/sec; PGE2, 0.05-1.78; PGF2 alpha, 0.05-1.82). The highest PS product for the three PG was found in olfactory bulb and cerebellum (0.96-1.82 microliters/g/sec) and the lowest was in septum (0.05-0.53). However, the level of the PS product was different among the PG in each brain region as follows: PGD2 greater than PGE2, PGF2 alpha in septum and anterior part of pyriform cortex; PGE2 greater than PGD2, PGF2 alpha in olfactory bulb, frontal cortex, basal forebrain, middle part of pyriform cortex, thalamus, hippocampus and lateral neocortex; and PGF2 alpha greater than PGD2, PGE2 in posterior part of pyriform cortex, hypothalamus, amygdala and entorhinal and retrosplenial cortices. Low correlation coefficients (0.708, 0.522 and 0.562 for PGD2, PGE2 and PGF2 alpha, respectively) between the PS product and cerebrovascular volume in various regions revealed heterogeneous cerebrovascular permeabilities of PG.

Animals↗
PubMed1991

Human brain prostaglandin D synthase has been evolutionarily differentiated from lipophilic-ligand carrier proteins.

cDNAs for glutathione-independent prostaglandin D synthase were isolated from cDNA libraries of human brain. The longest cDNA insert was 837 base pairs long and contained a coding region of 570 base pairs corresponding to 190 amino acid residues with a calculated Mr of 21,016. Between two cDNA inserts isolated from the two different libraries, nucleotide substitutions were observed at 16 positions, including conservative amino acid substitutions at 2 positions and nonconservative substitutions at 5 positions, indicating genetic heterogeneity of this enzyme in humans. The computer-assisted homology search revealed that the enzyme is a member of the lipocalin superfamily, comprising secretory hydrophobic molecule transporters, showing the greatest homology (28.8-29.4% identity; 51.3-53.1% similarity) to alpha 1-microglobulin among the members of this superfamily. In a phylogenetic tree of the superfamily, this enzyme, alpha 1-microglobulin, and the gamma chain of the complement component C8 form a cluster separate from the other 14 members. The two distinctive characteristics of glutathione-independent prostaglandin D synthase, as compared to the other members of this superfamily, are its enzymatic properties and its association with membranes that were probably acquired after evolutionary divergence of the two lipocalins. Based on the observed sequence homology, the tertiary structure of the enzyme was deduced to consist of an eight-stranded anti-parallel beta-barrel forming a hydrophobic pocket. Furthermore, the Cys-65 residue in the pocket, which is conserved only in the human and rat enzymes but not in other lipocalins, was considered to be a putative active site of the enzyme.

Amino Acid Sequence↗
PubMed1990

9 alpha,11 beta-prostaglandin F2 formation in various bovine tissues. Different isozymes of prostaglandin D2 11-ketoreductase, contribution of prostaglandin F synthetase and its cellular localization.

9 alpha,11 beta-prostaglandin F2 was formed from prostaglandin D2 by its 11-ketoreductases in 100,000 x g supernatants of various bovine tissues in the presence of an NADPH-generating system. The reductase activities were high in liver (51.09 nmol/h/mg of protein), lung (24.99), and spleen (14.20); moderate in heart and pancreas (3.09-3.61); weak in stomach, intestine, colon, kidney, uterus, adrenal gland, and thymus (0.11-2.63); and undetectable in brain, retina, carotid artery, and blood (less than 0.10). No formation of prostaglandin F2 alpha from prostaglandin D2 was detected in all tissues. In immunotitration analyses with a polyclonal antibody specific for prostaglandin F synthetase, the reductase activities in lung and spleen showed identical titration curves to that of the purified synthetase and decreased to less than 15% of the initial activity under the condition of antibody excess. Prostaglandin F synthetase-immunoreactive protein in these two tissues showed peptide fingerprints identical to that of the purified enzyme after partial digestion with Staphylococcus aureus V8 protease. The antibody was partially cross-reactive to the reductase in liver (about 20% of that to the synthetase) but not to the reductase(s) in other tissues. The Km value for prostaglandin D2 of the reductase activity was the same in lung and spleen as that of the purified prostaglandin F synthetase (120 microM) but differed in liver (6 microM), heart, and pancreas (15 microM). The predominant distribution of prostaglandin F synthetase in lung and spleen was confirmed by radioimmunoassay (2.8 and 1.0 micrograms/mg protein, respectively) and Northern blot analyses. In immunoperoxidase staining, this enzyme was localized in alveolar interstitial cells and nonciliated epithelial cells in lung, histiocytes and/or dendritic cells in spleen, and a few interstitial cells in kidney and adrenal cortex.

Animals↗