Immunoreactive transferrin receptors in sera of 90 pregnant women of various gestational periods were investigated. The mean concentrations of the serum transferrin receptor in normal males and females were 251 +/- 94 ng/ml and 256 +/- 99 ng/ml, respectively. Serum transferrin receptor levels in pregnant women did not show a significant increase in the early stage of gestation. However, a rapid elevation of the mean concentration of transferrin receptor was observed after 20 weeks of pregnancy. The apparent increase with gestation period suggests that this immunoreactive receptor in the sera of pregnant women is derived from the placental syncytiotrophoblast and reflects the activity of maternofetal iron transport.

Female↗

PubMedDate not supplied

The near-infrared electronic endoscope for diagnosis of esophageal varices.

We developed an electronic endoscope sensitive to light delivered by an infrared laser, which makes it possible to visualize submucosal vessels of the gastrointestinal tract. The system consists of a modified electronic endoscope and an image processing unit. A high output laser diode was chosen as the source of the infrared ray with a wavelength of 815 nm, an output of 200 milliwatts, and a band width of 30 nm. Using this instrument, esophageal varices were classified into three categories: venous dilation, dark spot, and diffuse dark area. The venous dilation and dark spot appearances correlated with early esophageal varices, which were rarely seen with visible light. On the other hand, the diffuse dark area appearance was considered to be a high risk sign of future bleeding. This system is useful not only for the early diagnosis of esophageal varices, but also for the localization of optimal puncture sites and the evaluation of the effect of sclerotherapy.

Adult↗

PubMedDate not supplied

Computer-assisted data processing of images of mucosal and submucosal blood vessels of the stomach obtained by visible and infrared endoscopy using a directional-contrast filter.

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Blood Vessels↗

PubMedDate not supplied

Heat-induced apoptosis via caspase-3 activation in tumour cells carrying mutant p53.

Apoptosis plays an important role in heat-induced cell death. However, the mechanism of heat-induced apoptosis has not yet been elucidated. In the present study, the signal transduction pathway underlying heat-induced apoptosis was investigated in heat-resistant HeLa cells carrying mutant p53 gene and heat sensitive HeLa cells that had been transduced with an antisense TNF gene. Induction of mutant p53, but not p21/WAF-1, was observed after heat treatment of both the resistant and sensitive cells. Heat-induced cytotoxicity was not inhibited in either cells with interleukin-1beta-converting enzyme (ICE: caspase-1) like protease inhibitor Ac-YVAD-CHO. In contrast, there was 48% and 63% inhibition of cytotoxicity in HeLa and transfectants, respectively, with a caspase-3 inhibitor (Ac-DEVD-CHO). Heat-induced apoptosis was also prevented by administration of Ac-DEVD-CHO in both cells. In addition, an augmentation of heat-induced cytotoxicity in transfectants was almost completely inhibited by Ac-DEVD-CHO. Further, caspase-3 mRNA expression was increased remarkably in heat-treated HeLa cells and transfectants. Taken together, these results suggest that activation of caspase-3 is involved in the signal transduction pathway of heat-induced apoptosis of the tumour cells carrying mutant p53.

Base Sequence↗

PubMedDate not supplied

Immunochemotherapy in B-16-melanoma-cell-transplanted mice with combinations of interleukin-2, cyclophosphamide, and PSK.

The effect of combination immunochemotherapy using interleukin-2 (IL-2), PSK and cyclophosphamide (CY) was evaluated in a pulmonary metastasis model in BDF1 mice. B-16 melanoma cells were inoculated into a hind limb. On day 3 after inoculation, 20 mg/kg of CY was administered intraperitoneally, and IL-2 (3.75 x 10(4) BRM units/head) was injected into the tail vein on days 7, 8 and 9. PSK (1,000 mg/kg) was administered orally every day from day 1 to day 10 using a stomach tube. This treatment cycle was repeated three times. Using this combination therapy, the cytotoxicity of lymphokine-activated killer cells and tumor-infiltrating lymphocytes was enhanced. Pulmonary metastasis was remarkably suppressed and a prolongation of survival was obtained compared with the nontreated group and an IL-2+CY group. The effect was augmented by repeating the therapy protocol. By analyzing the killer activity and surface markers of tumor-infiltrating lymphocytes, it was recognized that increased numbers of Lyt-2-positive T cells with augmented cytotoxicity were obtained. This treatment modality should have clinical significance.

Animals↗

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Recombinant human tumor necrosis factor causes regression in patients with advanced malignancies.

Fifteen patients with advanced solid tumors of various types were treated by the intratumoral administration of recombinant human tumor necrosis factor (rH-TNF). The treatment appeared to benefit the 4 cases of superficial tumors: there were 1 complete response, 1 partial response and 2 minor responses. In all 11 patients with deep-seated tumors, including 6 cases of pancreatic cancer, 4 of liver cell cancer and 1 of metastatic liver tumor, no tumor regression was observed, but progression stopped in all these tumors. Seven of the 11 with deep-seated tumors showed a decrease in tumor markers and/or the development of tumor necrosis. Fever, hypotension and fatigue were the main clinical side effects. No significant changes were found in hematologic, renal or liver parameters. These results suggest that administration of rH-TNF to the tumor site has the potential for controlling local tumor growth.

Adult↗

PubMedDate not supplied

Endogenous tumor necrosis factor functions as a resistant factor against hyperthermic cytotoxicity in pancreatic carcinoma cells via enhancement of the heart shock element-binding activity of heart shock factor 1.

To elucidate the relationship between two distinct resistant factors, endogenous tumor necrosis factor (enTNF) and heat shock proteins (HSPs), against hyperthermia, we assessed whether enTNF enhances HSP72 expression. Although there was a variability in the sensitivity of pancreatic carcinoma cell lines to heat, enTNF and HSP72 expression as well as MnSOD activity correlated positively with heat resistance. When MIAPaCa-2 pancreatic carcinoma cells, which had the lowest enTNF expression and highest heat sensitivity, were transfected with a nonsecretory-human TNF gene (pTNF delta pro), intracellular manganous superoxide dismutase (MnSOD) activity, HSP72 expression, and heat resistance were significantly increased. Furthermore, in these cells, enTNF expression correlated with the binding activity of heat shock factor 1 (HSF 1) to an oligonucleotide containing the human heat shock element. These results indicate that enTNF participates in the intrinsic resistance against heat via induction of MnSOD, enhances HSF1-binding activity, and augments of HSP72 expression. Therefore, inhibition of enTNF expression in pancreatic carcinoma cells would improve the efficacy of hyperthermia for pancreatic carcinoma.

DNA-Binding Proteins↗

PubMedDate not supplied

Protein kinase C inhibitors augment tumor-necrosis-factor-induced apoptosis in normal human diploid cells.

In this report we show augmentation of tumor necrosis factor (TNF)-induced apoptosis by protein kinase C (PKC) inhibitors in human embryonic lung fibroblast (HEL) cells. Staurosporine (STS) reportedly potentiates TNF-mediated cytotoxicity in cancer cell lines via inhibition of PKC. We investigated whether STS or another potent PKC inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7), augmented TNF-induced apoptosis in normal human diploid cells and examined the effects of the PKC inhibitors on the expression of endogenous TNF (enTNF) and manganous superoxide dismutase (MnSOD) as possible cell resistance factors opposing TNF-induced apoptosis. Both PKC inhibitors augmented TNF-mediated DNA fragmentation in HEL cells, which are normally TNF resistant and constitutively express high amounts of enTNF and MnSOD activity. Neither the number nor the affinity of TNF receptors were altered by STS and H7. The expression of enTNF and MnSOD was suppressed by the presence of STS or H7 along with TNF. The results indicate that PKC inhibitors augment TNF-induced apoptosis not only in tumor cells but also in normal cells by inhibitory effects on cellular resistance factors such as enTNF and MnSOD.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMedDate not supplied

Mineralogical analysis of sputum lith from an apparently healthy subject.

The sputum lith, 1 to 3 mm in diameter, were examined by microanalyser and by the method of X-ray diffraction, which revealed that the lith was composed of calcium carbonate and calcite in crystalline style. A composition of bronchial liths is often associated with different underlying diseases so that these nondestructive analyses seem to provide useful information for differential diagnosis. The present case is the first one to expectorate bronchial lith without marked pulmonary diseases.

Adult↗

PubMedDate not supplied

Diffuse infiltrating T-cell lymphoma of the colon associated with polyclonal hypergammaglobulinemia and hepatocellular carcinoma: report of a case.

A 55-year-old man with a chief complaint of melena had diffusely infiltrated lymphoma from the rectum to the sigmoid colon and polyclonal hypergammaglobulinemia. Biopsy specimen obtained from the rectum revealed diffuse medium-sized lymphoma cell with plasmocytosis. Histochemical analysis with monoclonal antibodies indicated that the origin of the tumor cell to be T-lymphocyte. Chemotherapy with cyclophosphamide, vincristine and prednisolone (VEP regimen) was effective for mucosal bleeding of the colonic lesion and reduction of polyclonal hypergammaglobulinemia. Five yrs later he showed recurrence of the disease and elevation of serum alphafetoprotein, and died of pulmonary infections. Autopsy finding confirmed the diagnosis of malignant lymphoma of the colon and disclosed the association of hepatocellular carcinoma.

Antineoplastic Combined Chemotherapy Protocols↗

PubMedDate not supplied

Endogenous tumour necrosis factor regulates heat-inducible heat shock protein 72 synthesis.

Endogenous tumour necrosis factor (enTNF) acts as a resistant factor against cytotoxicity of heat by induction of manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals. On the other hand, it is also well known that heat shock proteins (HSPs), which are induced by heat-stress, behave as cytoprotecting factor against this stress. However, the relationship of these two resistant factors is not yet elucidated. In the present study we would therefore propose the possibility that enTNF enhances HSP72 expression. Heat-sensitive L-M (mouse tomourigenic fibroblast) cells, which normally do not express enTNF, were transfected with a nonsecretory-type human TNF expression vector to produce enTNF. Stable transfectants showed resistance to heat treatment and an increase of HSP72 expression. Conversely, when HeLa (human uterine cervical cancer) cells, which normally produce an appreciable amount of enTNF, were transfected with an antisense TNF mRNA expression vector to inhibit enTNF synthesis, their heat sensitivity was enhanced and HSP72 expression was reduced by half. In conclusion, these findings indicate that enTNF regulates heat-inducible HSP72 synthesis.

Animals↗