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Biomedical subjects

K Kashima

Publications and source records attributed to K Kashima.

At least 199 records · Page 11Linked to original sources

Relationship between cell proliferation activity and morphological characteristics of papillary microcarcinoma in the thyroid of Graves' disease.

Three hundred and seven lesions of papillary microcarcinoma of the thyroid (PMT), found in 6830 cases of Graves' disease, were reviewed to evaluate the morphological characteristics. The prevalence rate and incidence of multiplicity of PMT in Graves' disease were higher (P < 0.05 and P < 0.005, respectively) in females (4.03% and 0.73%, respectively) than in males (2.68% and 0.12%, respectively). All lesions of PMT were classified histologically into three types: sclerosing non-encapsulated (SNE), non-sclerosing encapsulated (NSE) and non-sclerosing non-encapsulated (NSNE). Comparison of the three types of PMT revealed that the mean age and tumor size of NSNE were less than those of NSE and SNE (P < 0.001 and P < 0.005, respectively), and 13 of 19 lesions less than 1 mm belonged to NSNE. In addition, cell proliferation and expression of estrogen and progesterone receptors were examined immunohistochemically in 257 lesions of PMT. The Ki-67 labeling index of NSE was lower than that of NSNE and SNE (P < 0.005). None of the cases of PMT was positive for estrogen or progesterone receptors. The present study indicated that NSNE may be an early stage in tumor progression, and that fibrous encapsulation has the potential to modify neoplastic cell proliferation.

Adolescent↗

Contribution of Epstein-Barr virus to development of malignant lymphoma of the thyroid.

Epstein-Barr virus (EBV)-related mRNA, their products and apoptosis were investigated in 32 cases of malignant lymphoma of the thyroid (MLT) and 30 cases of Hashimoto's thyroiditis (HT) by in situ hybridization, immunohistochemistry and nick end labeling method on routinely processed tissue sections. In MLT, EBV-encoded small RNA (EBER) were detected in three cases, consisting of a follicular, predominantly large cell type (FL), a diffuse, large cell type (DL) and a large cell, immunoblastic type (IBL). In EBER-positive cases, IBL that was positive for T cell marker, exhibited neither BamHl H Left Frame 1 (BHLF1) transcript, EBV-encoded latent membrane protein (LMP) nor BamHl Z Left Frame 1 (BZLF1) gene product (ZEBRA), whereas both BHLF1 and ZEBRA were found in a small portion of the tumor cells in the FL and DL that expressed B cell marker and LMP. Apoptotic cells were observed in only a few lymphocytes in HT, and in a few non-neoplastic lymphocytes and various numbers of lymphoma cells in MLT. The apoptotic cell ratio of MLT tended to be higher in lower grade lymphomas. These results suggest that EBV may participate in the malignant transformation from HT to MLT.

Adult↗

Morule with biotin-containing intranuclear inclusions in thyroid carcinoma.

One thousand and sixty cases of thyroid carcinoma were reviewed to compare morules with squamous metaplasia clinicopathologically and immunohistochemically. Morules and squamous metaplasia were found in five (0.47%) and 32 cases (3.0%) respectively. The five patients with morules were all female (age 20-36 years) including four with papillary carcinoma and one with follicular carcinoma. The 32 patients with squamous metaplasia consisted of 30 females and 2 males (age 14-78 years), all of whom had papillary carcinoma except for one follicular carcinoma. The morules demonstrated characteristic 'optically clear nuclei' (OCN), which ultrastructurally showed filamentous structures in the nuclei. The OCN were immunohistochemically demonstrated to contain intranuclear biotin. Furthermore, the morule often accompanied with the OCN was positive for Ulex Europaeus agglutinin l (UEA-l) but negative for bovine muzzle epidermal keratin (EK). On the contrary, squamous metaplasia unaccompanied with the OCN was negative for UEA-l, but positive for EK. Follow-up information revealed that one of the five patients with morules had died of the disease, one was alive with pulmonary metastasis, and three were disease-free. Eight of 32 patients with squamous metaplasia had died of the disease; of the others who were alive, four patients have had recurrence.

Adenocarcinoma, Follicular↗

Expression of cytokine mRNA in gastric mucosa with Helicobacter pylori infection.

BACKGROUND: We have studied the cytokine production patterns in gastric mucosal biopsy specimens with and without the Helicobacter pylori infection, using a reverse transcription-polymerase chain reaction (RT-PCR) method capable of detecting low levels of specific mRNA. METHODS: Total RNA was prepared from biopsy specimens with the acid guanidinium thiocyanate-phenol-chloroform method. cDNA was synthesized by M-MLV RTase and amplified using the oligonucleotide primers specific for interleukin-1 beta (IL-1beta), IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, tumor necrosis factor-alpha (TNF-alpha), interferon-alpha (IFN-alpha), IFN-beta, and IFN-gamma by PCR methods. RESULTS: Although IL-1 beta and IFN-gamma mRNA were detected in most specimens, IL-2, IL-3, IL-4, IL-5, IL-9, TNF-alpha, and IFN-beta mRNA were not detected at all. The expressions of IL-7 and IL-8 mRNA were significantly higher in H. pylori-positive gastritis than in H. pylori-negative normal controls. There was a significant correlation between the expression of IL-8 mRNA and the severity of gastritis both in the antrum and in the corpus. On the other hand, there was a significant correlation between the expression of IL-7 mRNA and the severity of gastritis only in the corpus. CONCLUSIONS: These findings suggest that some cytokines, especially IL-7 and IL-8, play some roles in H. pylori-associated gastritis.

Adult↗

[A combined consecutive therapy with fosfomycin and sulbactam/cefoperazone for bacterial infections associated with hematological diseases].

A combination antibacterial therapy with fosfomycin (FOM) and sulbactam/cefoperazone (SBT/CPZ) was applied to 78 patients with severe infections associated with hematological diseases. In this protocol, FOM was followed by SBT/CPZ and each drug was administered for 1 hour intravenously and consecutively. Among 72 evaluable patients, 43 patients had acute leukemia, myeloblastic or lymphoblastic, 22 had malignant lymphoma, 3 had multiple myeloma, and 4 had other hematological diseases as underlying diseases. Bacterial infections diagnosed were sepsis in 21 patients, suspected sepsis in 47, and other infections in 4. The overall efficacy rate of this treatment was 72.2%, and those for individual infections were 66.7% for sepsis, 74.5% for suspected sepsis, and 75.0% for other infectious diseases. Among 22 bacteria separated from patients with sepsis, 78.6% (11/14 strains) were eradicated by this treatment. This protocol was also effective in 57.1% (8/14) of patients whose granulocyte count was less than 100/mm3 during the course of treatment as well as in 83.3% (15/18) of patients with granulocyte count over 500/mm3. There was no difference in effectiveness between those patients to whom G-CSF was administered and those to whom it was not (17/24, 70.8% vs 35/48, 72.9%). As an adverse reaction, a transient increase of GOT and/or GPT was observed in 2 patients (2.8%). The consecutive administration treatment of FOM and SBT/CPZ is thus an effective and safe regimen for the treatment of patients with hematological diseases complicated by severe infections.

Adult↗

[A case of pulmonary blastoma composed of histological features of both pulmonary blastoma and pulmonary endodermal tumor resembling fetal lung].

A case of pulmonary blastoma in a 71-year-old male was reported. Chest X-ray and CT scan showed a well demarcated mass lesion in the apical segment of the right lung. A polypoid tumor was detected in the apical branch of the right bronchus by bronchoscopy. The biopsy confirmed the diagnosis of pulmonary blastoma. The patient underwent a right upper lobectomy with lymph nodes dissection on Jan. 26, 1990. The resected tumor was really composed of two parts: a main tumor in the lung parenchyma and polypoid one protruding into the bronchus from the main tumor. The polypoid tumor exhibited typical features of pulmonary blastoma with both carcinomatous and sarcomatous components. The histology of the main tumor was identical to pulmonary endodermal tumor resembling fetal lung (PET). The metastases in the excised lymph nodes consisted entirely of carcinomatous elements. The patient died of brain stem metastasis a year after his operation. The present case, with typical pulmonary blastoma and PET present in the same tumor, supports the idea that pulmonary blastoma and PET belong to the same group neoplasma.

Aged↗

Serum autoantibody against interleukin-1 alpha is unrelated to the etiology or activity of liver disease but can be raised by interferon treatment.

OBJECTIVE: To clarify the clinical significance of serum levels of interleukin-1 alpha autoantibody in liver disease and their change during interferon therapy for chronic hepatitis. METHODS: By radioimmunoassay, we studied the incidence of serum interleukin-1 alpha autoantibody in 838 healthy controls and 180 patients with liver disease and monitored the change in antibody titer during the interferon therapy for chronic hepatitis. RESULTS: We detected the interleukin-1 alpha autoantibody in 12.6% (106/838) of healthy controls. In patients with liver disease, we found the antibody in 15.6% (5/32) in patients with acute hepatitis, 16.3% (13/80) in patients with chronic hepatitis, 18.8% (9/48) in patients with liver cirrhosis, and 15% (3/20) in patients with autoimmune liver disease. The incidence was not related to either etiology or inflammatory activity of liver disease. Two of three chronic hepatitis patients with initially high serum levels of the antibody (> 2000 ng/ml) showed transient increase in antibody titers during interferon therapy. CONCLUSION: The serum level of interleukin-1 alpha autoantibody was unrelated to the etiology or activity of liver disease. Interferon therapy can cause transient elevation of serum interleukin-1 alpha autoantibody levels.

Adult↗

Effectiveness of bovine gallstone (Goou) and bear gall powder (Yutan) on chronic liver diseases: a preliminary report.

The author reports 23 cases of chronic liver disease which showed remarkable improvement with the administration of bovine gallstone (Goou) and bear gall powder (Yutan). The concomitant administration of both Goou at 200 mg/day and Yutan at 60 mg/day resulted in marked improvement of liver function as well as subjective complaints in all the patients within one month. The administration of Goou alone was also effective, but concomitant administration of Goou and Yutan tended to be more effective than administration of Goou alone in cases of liver cirrhosis. These results suggest that animal crude drugs (Goou and Yutan) are reliable medicines for intractable chronic liver diseases.

Adult↗

Mechanisms for pancreatic hypertrophy induced by long-term administration of bethanechol.

Mechanisms for the hypertrophy of rat pancreas induced by long-term administration of bethanechol were investigated. The administration of bethanechol, an acetylcholine receptor agonist, to male Wistar rats for 14 days induced significant increases in the pancreatic weight and contents of protein, amylase and RNA in the pancreas without altering the content of DNA and the incorporation of [3H]thymidine into DNA. Simultaneous administration of atropine with bethanechol suppressed the bethanechol-induced pancreatic hypertrophy. Long-term administration of other acetylcholine receptor agonists also showed similar effects as produced by bethanechol. CR1505 (loxiglumide; D,L-4-(3,4-dichlorobenzoyl-amino)-5-(N-3-methoxypropyl-pentylam ino)-5- oxopentanoic acid), an antagonist of cholecystokinin receptors, inhibited pancreatic growth induced by long-term administation of pentagastrin, whereas pancreatic hypertrophy induced by bethanechol was not inhibited by CR1505. These results suggest that long-term administration of bethanechol induces pancreatic hypertrophy through direct activation of muscarinic receptors in the pancreas.

Amylases↗

Detection of 14q32 translocations in B-cell malignancies by in situ hybridization with yeast artificial chromosome clones containing the human IgH gene locus.

Partner sites of 14q32 translocations found in B-cell malignancies were detected by fluorescence in situ hybridization (FISH) using yeast artificial chromosome (YAC) clones, Y20 and Y6, containing the human Ig heavy chain (IgH) gene locus. Y20 spans a 160-kb upstream and 40-kb downstream region of the JH segments on chromosome band 14q32.33. Y6 is 300-kb upstream of Y20, and spans a further 320-kb telomeric region. The human DNA sequences amplified by Alu polymerase chain reaction of the YAC clones were used as probes for FISH to study six patients with non-Hodgkin's lymphoma (NHL), one patient with acute lymphoblastic leukemia, and one cell line FR4 established from a plasmacytoma. Three telomeric YAC clones each specific for 3q, 8q, and 18q were also used to further characterize 14q32 translocations. The IgH YACs were successfully applied to detect cytogenetically invisible subtelomeric translocation of the IgH gene locus to each partner site in t(14;18), t(8;14), and t(14;19), and to identify t(3;14) (q27;q32.33) in three patients with 14q32 translocation of unknown origin. Furthermore, complex translocations involving more than three chromosomes were detected in an NHL patient with t(8;14), and t(3;12), and in the FR4 with der(14)t(8;14), der(8)dic(1;8), and del(1)(q21). The technique would be a useful tool in elucidating the mechanisms of a 14q32 translocation in B-cell malignancies.

Aged↗

Regulation of hepatocyte albumin and alpha 1-acid glycoprotein secretion by monokines, dexamethasone, and nitric oxide synthase pathway: significance of activated liver nonparenchymal cells.

To clarify the mechanism involved in regulating the secretion of albumin and alpha 1-acid glycoprotein by rat hepatocytes, we studied hepatocyte culture and cocultures of hepatocyte and liver nonparenchymal cells. The secretion of alpha 1-acid glycoprotein by hepatocytes was stimulated and that of albumin was inhibited by combinations of dexamethasone and monokines, especially by dexamethasone and interleukin-6. The secretion of these proteins was equally inhibited during stimulation by lipopolysaccharide in cocultures. The inhibitory effect of sinusoidal endothelial cells was smaller than that of Kupffer cells. This inhibition was partially abolished by blocking the nitric oxide synthase pathway in cocultured cells and was completely abolished by dexamethasone. In conclusion, the secretion of albumin and alpha 1-acid glycoprotein by hepatocytes was regulated by monokines, dexamethasone, and the inducible nitric oxide synthase pathway in hepatocytes and liver nonparenchymal cells in vitro.

Albumins↗

Morphological alterations of gap junctions in phalloidin-treated rat livers.

Morphological alterations in the pattern of liver cell gap junctions were examined in phalloidin-treated rats to assess the role of gap junctions in experimental intrahepatic cholestasis. Double-labelled fluorescent staining of gap junctions and F-actin were performed using a monoclonal antibody against rat hepatocyte connexin 32 and rhodamine-phalloidin. Immunoelectron microscopy, using the anti-connexin 32 antibody, freeze-fracture replica electron microscopy, and conventional electron microscopy were also performed. In phalloidin-treated rat livers, the specific immunofluorescent staining of connexin 32 was markedly decreased in the pericentral area after 1 day of phalloidin treatment and, after 5 days of phalloidin treatment, there was a decrease in connexin 32 staining in the entire hepatic lobule. On the other hand, F-actin staining at the cell periphery and at the bile canaliculi was markedly increased in the pericentral area of the hepatic lobule after 1 day of phalloidin treatment and in the entire lobule after 5 days of treatment. Immunoelectron microscopy showed that both sides of the cytoplasmic domains of gap junctions were stained with anti-connexin 32 antibody in controls, whereas, in cholestatic rats, only one side of the cytoplasmic domain of some gap junctions was stained with anti-connexin 32 antibody after 1 or 3 days of phalloidin treatment. No gap junctions were observed after 5 days of phalloidin treatment either by freeze-fracture replica electron microscopy or by conventional electron microscopy. These results indicate that with phalloidin treatment, hepatocyte gap junctions decrease, first in the pericentral area, and finally throughout the entire lobule.

Actins↗

Evaluation of hepatic proliferative activity in chronic liver diseases and hepatocellular carcinomas by proliferating cell nuclear antigen (PCNA) immunohistochemical staining of methanol-fixed tissues.

The proliferative activity of chronic liver diseases and hepatocellular carcinomas (HCCs) was studied by PCNA immunohistochemistry. Human liver tissues were obtained by surgical operation or needle biopsy, and PCNA was detected by immunohistochemistry. PCNA-labelling indices (PCNA-LIs) of methanol-fixed tissues corresponded with the incidence of S-phase cells previously reported, whereas paraformaldehyde-fixed tissues showed extremely high PCNA-LIs in all specimens. Therefore, methanol-fixed tissues were used for evaluation. The PCNA-LIs of the methanol-fixed tissues were: normal liver 0.78 +/- 0.38%, chronic persistent hepatitis 1.06 +/- 0.86%, chronic aggressive hepatitis 2A 1.01 +/- 0.50%, chronic aggressive hepatitis 2B 4.20 +/- 1.79%, inactive cirrhosis 0.81 +/- 0.49%, active cirrhosis 1.96 +/- 0.93%, HCC of Edmondson's type I 4.83 +/- 1.98%, type II 6.65 +/- 1.69%, and type III 38.7 +/- 30.6%. PCNA-positive cells showed little specific distribution; in periportal areas in chronic hepatitis, at the margins of pseudolobules in cirrhosis, and throughout the tumor in HCC. These findings indicated that proliferative activity increased during the progression of chronic hepatitis, but that it decreased at the stage of cirrhosis. In chronic liver diseases, the PCNA-LIs reflected hepatitis activity. HCC showed higher proliferative activity than liver cirrhosis, and the histological grade was correlated with the PCNA-LI.

Analysis of Variance↗

Hemodynamic effects of combined treatment with somatostatin analogue (SMS 201-995) and low-dose isosorbide dinitrate on portal hypertension in conscious cirrhotic rats.

The authors investigated whether combined treatment with the somatostatin analogue, SMS 201-995, and low-dose isosorbide dinitrate enhanced the hemodynamic effects of the individual agents on rats with thioacetamide-induced cirrhosis. Four groups of cirrhotic rats received SMS 201-995 (0.1 microgram.min-1.kg-1), isosorbide dinitrate (10 micrograms.min-1.kg-1), both agents, or placebo, respectively. Hemodynamics were measured serially in conscious rats, using a radioactive microsphere method. SMS 201-995 reduced portal venous inflow 21 +/- 4% and portal pressure 17 +/- 3%. Isosorbide dinitrate decreased portal venous inflow 20 +/- 4%, by inducing splanchnic vasoconstriction mediated by low pressure baroreflexes, and this agent also decreased portal pressure, by 14 +/- 2%. Portal venous resistance rose 7.6 +/- 3% with isosorbide dinitrate alone, but decreased 18 +/- 4% with combination therapy. This effect may have been induced by the pronounced vasodilatory effect of isosorbide dinitrate on the venous vasculature, since the reflex splanchnic vasoconstriction that occurs with low-dose isosorbide dinitrate disappears when this agent is combined with SMS 201-995. The decrease in portal pressure was more marked (22 +/- 4%) and changes in systemic hemodynamics were milder with the combined treatment. It was concluded that combination therapy with SMS 201-995 and low-dose isosorbide dinitrate may be beneficial for portal hypertension in liver cirrhosis.

Analysis of Variance↗

A case of metastatic chondrosarcoma of the stomach.

A case of metastatic chondrosarcoma of the stomach in a 34-year-old female is reported. This patient had been diagnosed as having chondrosarcoma of the right knee and was operated on in 1984. Thereafter, there was repeated local recurrence and operations were performed on multiple metastases, including those of the lung, brain, ovary and spleen. In September, 1990, the patient was readmitted because of advanced anemia. Gastroendoscopy disclosed a firm elevated lesion with central irregular erosion. Histologically, there was cellular atypical cartilage with pleomorphic chondrocytes, which showed the same staining reactions as those in the primary lesion. Therefore this case was diagnosed as metastatic chondrosarcoma. This may be the first documentation of a case of gastric metastasis of chondrosarcoma.

Adult↗

Subcortical impairment in subclinical hepatic encephalopathy.

We have used short latency somatosensory evoked potential (SEP) in 108 patients with liver cirrhosis by viral hepatitis to evaluate hepatic encephalopathy. Short-latency SEPs were recorded by the MEM-4104 apparatus (Nihon Kohden Inc., Tokyo) in response to median nerve stimulation. For a precise analysis of the early components, we averaged 1000 responses during a 30-msec period. Early SEP components were prolonged in patients with decompensated, but not in those with compensated, cirrhosis. We also examined the relationship between consciousness level and interpeak latency (IPL) N13-N20 of SEP and between consciousness level and electroencephalograph in 51 patients among 108 patients with liver cirrhosis. The IPL N13-N20 was prolonged in the decompensated stage with normal consciousness, but EEG findings had not deteriorated in this stage. EEG grade became worse in the stage of abnormal consciousness. The prolongation of the IPL N13-N20 was attributed to the central conduction impairment. We postulate that subcortical impairment may occur in patients with subclinical hepatic encephalopathy. when the cortex is little affected.

Aged↗

Serum levels of macrophage colony stimulating factor (M-CSF) in liver disease.

We investigated the serum level of macrophage colony stimulating factor in acute and chronic liver disease. Levels of macrophage colony stimulating factor (mean +/- SD, ng/ml) were significantly higher in acute hepatitis (5.67 +/- 1.01, p < 0.01) and chronic active hepatitis (3.34 +/- 1.19, p < 0.01) than in healthy volunteers (1.90 +/- 0.25), asymptomatic hepatitis B virus carriers (1.98 +/- 0.40), and chronic persistent hepatitis (2.34 +/- 0.43). Levels of macrophage colony stimulating factor showed a highly significant correlation with the serum alanine aminotransferase levels in acute hepatitis (p < 0.01, rs = 0.903) and in chronic active hepatis (p < 0.01, rs = 0.672). Levels of macrophage colony stimulating factor in patients with cirrhosis (cirrhosis; 3.11 +/- 0.93 and hepatocellular carcinoma; 3.30 +/- 0.74) were significantly higher than in patients with chronic persistent hepatitis although the alanine aminotransferase levels were not significantly different. In cirrhosis, levels of macrophage colony stimulating factor correlated positively with the serum alanine aminotransferase levels (p < 0.05), total bilirubin levels (p < 0.05), and indocyanine green clearance (p < 0.05). An immunohistochemical study showed an increased number of macrophage colony stimulating factor positive mononuclear cells in portal areas in acute hepatitis. Our findings suggest that; (a) the serum levels of macrophage colony stimulating factor represent ongoing hepatocellular necrosis in acute and chronic liver disease, (b) the source of the increase in the serum macrophage colony stimulating factor levels in hepatic inflammation may be, in part, its production by infiltrating mononuclear cells in the liver, and (c) cirrhosis also causes elevated serum levels of macrophage colony stimulating factor.

Acute Disease↗