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Biomedical subjects

I Urushizaki

Publications and source records attributed to I Urushizaki.

At least 19 recordsLinked to original sources
PubMed1990

[Palliative therapy in cancer--Significance and practice].

Most of advanced cancer-patients will have suffered symptoms from the local spread or dissemination of the malignancy for a variable time, but possibly for months or years. During recent years, advances in diagnosis and therapy have allowed earlier and most effective intervention, which has served to increase longevity and enhance the quality of life. However, the overall mortality from malignant disease has hardly changed in the last 40 years. There is usually a progression from unsuccessful attempt at cure to symptom palliation and, ultimately, terminal care. There will be some patients in whom appropriate palliation is compatible with cure and others who are terminal, but are amenable to palliation of certain symptoms. Therefore, the objection of palliative therapy in these individuals is to maximise their quality of life. Many differing tumors may produce a given symptom. So palliative therapy can be defined most simply as the alleviation of symptoms. Palliative therapy is most certainly not only the treatment of recurrent, but also of asymptomatic disease. The significance and practice of palliative therapy for advanced cancer will be reported.

Humans↗
PubMed1990

[Palliative therapy in cancer 2. Nutrition control].

Deterioration in nutritional status occurs late in the progress of cancers at certain sites, but at all stages in patients with gastrointestinal cancer. Weight loss with decrease in body fat and muscle wastage, occurs to a varying degree. Superficially, the clinical condition resembles simple food deprivation. However, the derangements in metabolism are often and some patients show an elevated resting energy expenditure, disturbances of carbohydrate, fat and protein metabolism and generally, a failure to adapt to reduced food intake, which is characteristic of cachexia. Cancer cachexia then becomes characterized by signs of marked negative energy and protein balance, including hypoalbuminemia, weight loss, and anemia. On the other hand, toxohormone extracted from tumor tissues was considered as the main cause to produce cancer cachexia. However, it has become clearer that cytokines, e.g. cachectin/TNF, IL-1, LT and IFN gamma play an important role to produce cachexia. Patients who are malnourished have an incidence of postoperative complications double that seen in adequately nourished patients. The effectiveness of cancer-chemotherapy is also different in nutritional status of patients. Although in patients requiring hyperalimentation, enteral nutritional support may feasible and enteral feeding has a distinct metabolic advantage compared with parenteral feeding, there is a definite role for total parenteral nutrition in patients who have severe chronic radiation enteritis, side effect of chemotherapy, weight loss and malabsorption. Tentative weight gain and correction of hypoalbuminemia without improving patient survival may be expected by this intravenous hyperalimentation.

Humans↗
PubMed1990

[Palliative therapy in cancer. 3. Palliation of the symptoms from a malignant tumor (1)].

Most of the symptoms from a malignant tumor are caused by local invasion by the tumor, or obstruction, either at the site of the primary disease or by metastases. However, tumors can produce symptoms at a remote site. Patients with gastrointestinal malignancy may present with symptoms which include dysphagia, nausea, vomiting, abdominal pain, diarrhea, bleeding and ascites. Palliation gastrectomy delays or prevents these symptoms. About 30% of gastric carcinomas are inoperable at the time of presentation. Chemotherapy is rarely effective in the palliation of gastric carcinoma. Laser irradiation can be delivered to assay site accessible to fibreoptic endoscopy, which is an advantage over endocavity irradiation or diathermy fulguration. Ascites is a common and disabling implication in patients with advanced malignant disease. Spironolactone will increase urinary sodium excretion significantly and control their ascites. If spironolactone fails to control, useful control can be achieved by draining the ascites. Patients with carcinoma of the lung may present with symptoms that include cough, bloody sputum and dyspnoea. Pain in the chest wall is usually secondary to invasion of the parietal pleura, ribs or intercostal nerves. Lesions in the medial portion of the right upper lobe, or mediastinal metastases, may invade or compress the superior vena cava, causing venous hypertension with oedema of the head and arms. The patients may complain of dyspnoea, dysphagia, stridor and headaches. Radiotherapy can be expected to improve the quality of life for these patients. Successful palliation of symptoms is almost related to tumor regression. The problems of obstruction and bleeding from malignant tumor is common. Recently, laser techniques have been applied to aid in palliation of these problems. Malignant effusion may occur early and be the first signs of metastases. The aim of therapy is to evacuate the fluid and induce pleural adhesion. One of the sad situations that we have to face is the patient with recurrent cancer which complains of various symptoms. The relief of symptoms is the most important palliative therapy to them.

Abdominal Pain↗
PubMed1990

[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)].

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.

Humans↗
PubMed1990

[Palliative therapy in cancer. 5. Side effects by anticancer drugs and their treatments].

Many chemotherapeutic agents have been evaluated during the last 40 years and some have now an established place in the management of malignant disease. However these agents have a level of toxicity well above any other group of drugs. Chemotherapeutic agents do not discriminate between normal and neoplastic tissue. Chemotherapeutic regimens that are toxic to rapidly dividing malignant cells, are liable to be particularly harmful to lymphoid tissues, bone marrow and the epithelium of the gastrointestinal tract. The side effects due to chemotherapy are classified as immediate, early, delayed and late. Immediate side effects are those that may occur within the first 24 hours of treatment. The most common immediate side effect is nausea and vomiting, due to direct central effect on the vomiting center of the brain. Cisplatin and nitrogen mustard are particularly prone to this complication. The antiemetics usually used are metoclopramide, domperidone and steroid. The efficacies of these drugs are not so good for nausea and vomiting due to cisplatin administration, however several blockades against serotonin M-receptor recently developed are quite effective to nausea and vomiting of chemotherapeutic regimens including cisplatin. Early side effects commence within about one month of therapy. The most common is bone marrow toxicity and can occur after therapy with the vast majority of anticancer drugs. The relative importance of leukopenia and thrombocytopenia vary between the drugs and their route of administration. Recently, hematopoietic cytokines, such as granulocyte-colony stimulating factor (G-CSF) and granulocyte-macrophage-colony stimulating factor (GM-CSP) have been introduced to granulocytopenia developed by cancer chemotherapy. In the phase II study of G-CSF, a rapid recovery of granulocytes after chemotherapy and marked efficacy on infection in granulocytopenic patients were observed. In addition to this, autologous bone marrow transplantation after chemotherapy has been described in patients with solid tumors.

Antiemetics↗
PubMed1990

[Palliative therapy in cancer. 6. Quality of life and BRM therapy in cancer-patients].

Almost all of anti-cancer drugs developed, injured not only the tumor cells but also the normal cells. For this reason, immunotherapy which injures specifically the tumor cells, has been developed. However, the clinical studies conducted in the past 20 years tend to indicate that even though the immunotherapy does not produce any serious side effect, the anti-tumor effect are not totally satisfactory in spite of marked prolongation of survivals. In recent years, various fields of cancer therapy have seen the development and application of treatment modalities which take into account the quality of the patients. Several patient's self-assessment questionnaires are widely used practical at the aims to assess what happens in the cancer-patients and to improve the cancer treatment. The measurements of quality of life have been performed on both immunochemotherapy group and chemotherapy group. The results showed the remarkable improvement of QOL in the immunochemotherapy group. The biotechnological advances have been made in the last 10 years. Various cytokines which participate in the immunological response between cancer and host. Many of these biologicals that will be called as biological response modifiers (BRM) are cell products of lymphocytes or macrophage. Systemic administration of exogenous cytokines to act against a tumor at a distant site may not be as successful as more localized therapy in situation. In most circumstances, cytokines are produced transiently at a local site acting in an autocrine or paracrine manner. Cytokines, whether naturally produced, or administered therapeutically, are rapidly clear from the circulation, both as a result of finding to often ubiquitous cell surface receptors, and by active excretion. So, the local injections of TNF and LAK cells are effective to decrease tumor size without the side effects. Finally, the serum level of IL-2 and TNF-alpha were determined for 24 healthy volunteers and 42 patients with advanced or terminal cancer, and the relationship between these levels and the QOL was investigated. In the cancer-patients who showed a higher serum level of IL-2 than the healthy volunteers, it was elucidated that there was an inverse correlation between the serum IL-2 level and the QOL. This finding cannot be explained at present, but it is surmised that, for this subpopulation of cancer-patients, the serum IL-2 level can probably serve as an objective biochemical index for use in evaluating the QOL.

Combined Modality Therapy↗
PubMed1989

[Recent trends in cancer treatment using cytokines].

Recent progress in biotechnology has uncovered the presence of trace substances which participate in the immunological response between cancer and host; They are cytokines, monoclonal antibodies, and immunomodulating agents produced by effector cells which are called macrophage, NK cells and lymphocytes of cancer patients. Recent genetic engineering enables mass production of these substances, and their clinical application in treating human cancers is expected to take place in the near future. In this paper, the recent trend of cancer treatment, using various cytokines are briefly introduced, namely interferon, interleukin-2, tumor necrosis factor and colony stimulating factor. Although IL-2 is effective for the activation of T-lymphocyte, intravenous injection of IL-2 is not so effective for treatment of cancer-patients. On the other hand, IL-2-activated killer cells (LAK cells) are potent effectors of adoptive immunotherapy in advanced cancer patients. The clinical study was conducted in 25 patients with advanced carcinomas. Therapeutic efficacy was obtained in patients for whom local transfer was undertaken rather than systemic administration. Tumor necrosis factor, a cytotoxin derived from macrophages shows much promise for application in cancer therapy because of its marked antitumor effects and its high specificity to tumors. Clinical study was performed on leukemia patients who showed marked decreases of percentage of leukemic cells in peripheral blood. Moreover, local injection of TNF was very effective for the decrease of tumor size in patients with hepatoma and subcutaneous tumor. In addition, to clinical results using CSF and interferon are reported.

Colony-Stimulating Factors↗
PubMed1989

[Therapy by biological response modifiers].

Recent progress in biotechnology has uncovered the presence of trace substances which participate in the immunological response between cancer and host, they are cytokines, monoclonal antibodies, and immunomodulating agent which are called as biological response modifiers (BRM). The genetic engineering enables mass production of these substances, and their clinical application in treating hematological malignancies is expected. The role of biologically active substances as important pharmacological reagents was initially explored in human with purified interferon. The most recent example of such rapid progress has been with IL-2 and TNF. Clinical trials with recombinant IL-2 and TNF have begun in 1984. Although IL-2 is effective for the activation of T lymphocyte, intravenous injection of IL-2 was not so effective for treatment of hematological malignancies. On the other hand, IL-2 activated Killer cells were potent effectors of adoptive immunotherapy. Tumor necrosis factor, a cytotoxin derived from macrophages showed marked decreases in percentage of leukemic cells of peripheral blood in treating leukemic patients.

Humans↗
PubMed1988

Toxic effect of tumor necrosis factor on tumor vasculature in mice.

Stereoscopic observation via an implanted sight glass in mice bearing transplanted methylcholanthrene-induced A-cells showed tumorivascular hemorrhage at 1-2 h after tumor necrosis factor (TNF) administration, congestion at 4-6 h, and hemorrhage, congestion, and blood circulation blockage at 24 h. Histological examination after TNF administration to mice bearing similar methylcholanthrene-induced A-cell transplants showed thrombus formation in the tumor vasculature at 4 h and thereafter. Suppression of this thrombus formation with heparin had no apparent influence on the necrotic response, tumor growth inhibition or complete cure rate following TNF administration to mice bearing the methylcholanthrene-induced A-cell tumors. The results suggest that direct toxicity of TNF on tumor vasculature is a factor in the overall antitumor mechanism of TNF.

Animals↗
PubMed1988

Synergistic effects of recombinant human tumor necrosis factor and hyperthermia on in vitro cytotoxicity and artificial metastasis.

Synergy in cytotoxic effect between recombinant human tumor necrosis factor and hyperthermia (incubation at 38.5 degrees C or 40 degrees C) was observed to occur against L-M (mouse tumorigenic fibroblast) cells and shown to be related to an accelerated turnover rate of recombinant human tumor necrosis factor-receptor complex under elevated temperatures rather than to changes in number of cell receptors or binding strength. However, no synergy in cytotoxic effect was observed to occur against human embryonic lung (HEL) cells. A clearly synergistic inhibition of metastatic tumor growth by combined administration of recombinant human tumor necrosis factor (300 units) and whole-body hyperthermia (40 degrees C, 30 min) was also observed in BALB/c mice previously given injections of 1 x 10(6) Meth-A (MH) cells/mouse via tail vein, neither of which alone resulted in significant inhibition.

Animals↗
PubMed1988

Synergistic cytotoxic and antitumor effects of recombinant human tumor necrosis factor and hyperthermia.

A synergistic increase in the cytotoxic effects of recombinant human tumor necrosis factor (rH-TNF) and hyperthermia was demonstrated both in vitro and in vivo. The cytotoxicity of rH-TNF against L-M cells in incubation for 12 h at 38.5 and 40 degrees C based on the concentration necessary for 50% cytotoxicity was, respectively, 125 and more than 500 times as high as in similar incubation at 37 degrees C. As observed 18 days after implantation of Meth-A fibrosarcoma cells in mice, single i.v. administration of rH-TNF at 1000 units/mouse resulted in complete cures in five mice when performed in combination with hyperthermia (40 degrees C), whereas rH-TNF alone in the same dose resulted in 27.1% inhibition of tumor growth and hyperthermia alone had no appreciable effect on tumor growth. The i.v. administration of rH-TNF three times at 100 or 300 units/mouse together with hyperthermia (40 degrees C) resulted in 41.2 and 89.0% tumor growth inhibition, respectively; similar administration without hyperthermia appeared to have little or no appreciable effect on tumor growth. The results suggest that combination therapy including rH-TNF and hyperthermia may be of value in the treatment of malignancy in human patients.

Animals↗
PubMed1988

Immunohistochemical identification of type I procollagen in tumour cells of scirrhous adenocarcinoma of the stomach.

Human gastric carcinomas were tested for their immunohistochemical reactivity with anti-type I procollagen antiserum. In all specimens of scirrhous carcinomas, staining of the tumour cells was strongly positive, while in medullary carcinomas staining of the tumour cells was generally poor. These results suggest that the tumour cells in scirrhous carcinomas produce collagen in their stroma.

Adenocarcinoma, Scirrhous↗
PubMed1988

Successful treatment of a VIPoma by continuous subcutaneous infusion of somatostatin analogue (SMS 201-995).

A case with WDHA syndrome due to VIPoma is reported. Injection of somatostatin analogue SMS 201-995 was followed by prompt suppression of vasoactive intestinal polypeptide levels (VIP), decreased stool volume, and restoration of the serum potassium concentration to normal. Long-term treatment with SMS 201-995 for up to 20 weeks produced excellent clinical control and a decrease in tumour size. No adverse effects were noted except for localized pain at the site of injection. This was overcome by using a continuous subcutaneous infusion pump which also enabled the effective daily dosage to be reduced and thereby adverse reactions to be avoided.

Female↗
PubMed1988

Quantitation and characterization of serum transferrin receptor in patients with anemias and polycythemias.

Serum transferrin receptor concentration in patients with anemias and polycythemias was determined. The mean normal value was 258 +/- 82 ng/ml. Comparing with normal values, the higher values were obtained in patients with iron deficiency anemia, autoimmune hemolytic anemia, and polycythemias, while the lower values were obtained in patients with aplsatic anemia. During treatments of patients with iron deficiency anemia and autoimmune hemolytic anemia, serial change of serum receptor was paralleled with that of peripheral reticulocyte counts, suggesting that the circulating receptor values may reflect the activity of bone marrow erythropoiesis. The immunoreactive receptor was migrated at the position of alpha 1-globulin by agarose gel electrophoresis and the isoelectric point(pl) was 3.57 by isoelectric focusing. SDS-polyacrylamide gel electrophorogram of various patients' sera revealed that the autoradiographed band was migrated at the molecular weight of 110,000 daltons in the non-reducing condition and 46,000 and 23,000 daltons in the reducing condition. These bands were also capable of binding to 131I-labelled diferric transferrin. The proposed model of circulating transferrin receptor may be the nicked dimers of 55,000 daltons in which inter- and intra-disulfide bridges were present.

Anemia↗