Successful use of vancomycin hydrochloride in the treatment of lactulose-resistant chronic hepatic encephalopathy.
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Drug Resistance↗
Biomedical subjects
A Sakurai
Publications and source records attributed to A Sakurai.
Japanese modified traditional Chinese medicines as preventive drugs of the side effects induced by tumor necrosis factor and lipopolysaccharide.
It was found that the capacity for tumor necrosis factor (TNF) production by Japanese modified traditional Chinese medicines and crude drugs broadly paralleled their antitumor activity. Pretreatment with these drugs prevented the lethal and marked side effects of recombinant human TNF (rhTNF) and lipopolysaccharide (LPS) without impairing their antitumor activity. These drugs are thought to decrease the oxygen radicals and stabilize the cell membranes, with a deep relation to the arachidonic cascade. The release of prostaglandins and leukotriene B4 was suppressed by pretreatment with Shosaiko-to. Thromboxane B2 was transiently increased, followed by suppression. After pretreatment with Hochu-ekki-to or Juzen-taiho-to, suppression of leukotriene B4 could not be observed. The release of prostaglandin D2 was suppressed in mice pretreated with Shosaiko-to, Juzentaiho-to or Ogon (Scutellariae Radix) but it increased following pretreatment with Hochu-ekki-to. Chemicals that could prevent the lethality of rhTNF and LPS also revealed suppression of prostaglandins, leukotriene B4 and thromboxane B2. In general, drugs that prevented the lethality of rhTNF and LPS without impairing the antitumor activity could inhibit the release of leukotriene B4 and/or prostaglandin D2. rhTNF could activate the arachidonic cascade in combination with LPS. The lethality of rhTNF and LPS could be prevented by pretreatment with Japanese modified traditional Chinese medicines and the crude drug, Ogon.
Animals↗
[Results of coronary artery bypass surgery in patients with spastic angina pectoris].
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Angina Pectoris↗
Therapy combining tumor necrosis factor with tumor-specific antibody against Meth A sarcoma.
We have investigated the antitumor activity of tumor necrosis factor (TNF) against numerous. It appears that the efficacy of TNF against highly immunogenic tumor cell lines is greater than that against low immunogenic cell lines. Tumor cells express immunogenic tumor-associated antigen and sometimes shed antigens. Antibody against shedding antigens from Meth A sarcoma cells was prepared by immunizing rabbits seven times. This antibody by itself was not curative. However, in combination with TNF, the antibody was effective even against large and well-established tumors. When the antibody was injected 1 day after administration of TNF, the antitumor activity was stronger than in the case of simultaneous administration of TNF and antibody. We further examined the effect of this antibody against Ehrlich tumors in combination with TNF. The results were similar to those for Meth A sarcoma, although effects were weaker.
Animals↗
Interspecific actions of alpha mating pheromones on the a mating-type cells of three Saccharomyces yeasts.
The alpha mating pheromones synthesized in three Saccharomyces yeasts (S. cerevisiae, S. kluyveri, and S. exiguus) displayed interspecific actions on the a cells of all three species despite the fact that the amino acid sequences of all three alpha pheromones are different. Mating between species, however, did not occur. The interspecific alpha pheromone--a cell reaction was not necessarily more effective than the interspecific one.
Amino Acid Sequence↗
Characterization of a thyroid hormone receptor expressed in human kidney and other tissues.
A cDNA encoding a specific form of thyroid hormone receptor expressed in human liver, kidney, placenta, and brain was isolated from a human kidney library. Identical clones were found in human placenta and HepG2 cDNA libraries. The cDNA encodes a 490-amino acid protein (Mr, 54,824). When expressed and translated in vitro, the protein product binds triiodothyronine with Ka of 2.3 X 10(9) M-1. This protein, designated human thyroid hormone receptor type alpha 2 (hTR alpha 2), has the same domain structure as other members of the v-erbA-related superfamily of receptor genes. It is similar to thyroid hormone receptor type alpha described in chicken and rat and less similar to human thyroid hormone receptor type beta (formerly referred to as c-erbA beta) from placenta. However, it is distinguished from these receptors by an extension of the C-terminal hormone binding domain making it 80 amino acids longer than rat thyroid hormone receptor type alpha 1 [Thompson, C.C., Weinberger, C., Lebo, R. & Evans, R. M. (1987) Science 237, 1610-1614]. Different sizes of mRNA found in liver (2.5 kilobases) and kidney (2 kilobases) suggest there may be tissue-specific processing of the primary transcript of this gene. Identification of human thyroid hormone receptor type alpha 2 indicates that two or more forms of thyroid hormone receptor exist in human tissues and may explain the normal variation in thyroid hormone responsiveness of various organs and the selective tissue abnormalities found in the thyroid hormone resistance syndromes.
Amino Acid Sequence↗
An experimental study of craniofacial growth in a heterotopic rat head transplant.
In order to examine whether or not facial bones are themselves able to regulate their own growth, we devised a new experimental model in which we transplanted the whole head of an infant rat to the body of an isohistogeneic adult rat by means of microvascular anastomoses. The advantage of this model is that the transplanted head has neither scars nor any moving soft tissues that could modify growth around facial bones. Using this model, we conducted a study of the nasomaxillary region that has led us to conclude that facial bones do in fact regulate their own growth. The results also suggested that facial bone sutures play a more active role in the growth process than presently suspected.
Animals↗
Effect of thyroid hormone on the protein inhibitors for Ca2+-dependent proteinase in brain: evidence for the induction by thyroidectomy of irreversible changes in immature rats.
The effects of thyroid hormone on the levels of protein inhibitors for Ca2+-dependent proteinase were studied in rat brain. Four different inhibitory proteins (I, II, III, and IV) were isolated from immature (7-day-old) rat brain. The molecular weights of these inhibitory proteins, which were estimated by gel-exclusion chromatography on Sephacryl S-200 column, were approximately 280,000 (I), 70,000 (II), 50,000 (III), and 35,000 (IV). All of these inhibitory proteins were decreased by thyroidectomy. Four-day T4 administration (100 micrograms/kg daily) to thyroidectomized-immature animals restored proteins I, II, and IV. However, protein III was not recovered with the same treatment of the rats. In mature rats (40-day-old), four different inhibitory proteins were identified in the brain. The molecular weights were identical to those obtained in immature rat brain. As observed in immature rats, all of these inhibitory proteins were decreased by thyroidectomy. In contrast to the results obtained in immature animals, however, inhibitory protein III, as well as I, II, and IV, was restored by T4 administration (100 micrograms/kg daily) to thyroidectomized mature rats. The results suggested that thyroid hormone increases protein inhibitors for Ca2+-dependent proteinase in brain, and that irreversible decrease in one of the inhibitors is induced by thyroid hormone deficiency in immature animals. The phenomenon may be related to the neonatal hypothyroidism-induced irreversible damage to the central nervous system in patients with cretinism.
Aging↗
Characterization of a third human thyroid hormone receptor coexpressed with other thyroid hormone receptors in several tissues.
A cDNA that encodes a third type of human thyroid hormone receptor (hTR alpha 1) has been isolated from a skeletal muscle library. The cDNA encodes a 410 amino acid protein, Mr = 46,820. When expressed and translated in vitro, hTR alpha 1 binds T3 with an association constant (ka) of 1.8 x 10(9) M-1. Comparison of the DNA sequence of hTR alpha 1 and a previously identified alpha type thyroid hormone receptor (hTR alpha 2) suggests that they could be transcribed from the same gene, and that alternative RNA splicing results in the synthesis of either hTR alpha 1 or hTR alpha 2. Two mRNA (3.2 kilobases and 6 kilobases) of hTR alpha 1 have been detected in several tissues. At least three types of thyroid hormone receptors (hTR alpha 1, alpha 2, beta), which possess similar affinities for hormone ligands, can be expressed in the same tissue.
Amino Acid Sequence↗
Antitumor activity of combination therapy with traditional Chinese medicine and OK432 or MMC.
To examine the effects of combination therapy with traditional Chinese preparations (Syô-saiko-tô, Zyûzen-taiho-tô or Cinnamomum cortex) and OK432 or mitomycin C on the antitumor activities and TNF producibility, an investigation was carried out using mice transplanted with Ehrlich or Meth A tumor cells. Development of the transplanted tumors was strongly inhibited by the combination therapy, and the tumor necrosis factor (TNF) producibility was increased with the combination of a traditional Chinese preparation and OK432. A significant negative correlation was observed between the TNF activities and tumor weight, and there was a positive correlation between the TNF activities and spleen weight in the Ehrlich-bearing DDY mice receiving traditional Chinese preparations or OK432. Marked lymphocytosis, hyperplasia, and hypertrophy of Kupffer's cells in the liver were noted in the tumor-bearing DDY mice receiving traditional Chinese preparations or OK432. In two-step carcinogenesis experiments involving treatment with DMBA and TPA to induce skin papillomas, Zyûzen-taiho-tô appeared to be effective in inhibiting carcinogenesis. These results suggest that the antitumor activities and capacity for TNF production of the preparations are probably due in part to stimulation of the reticuloendothelial system, including macrophages, and induction of a host-mediated antitumor substance like TNF as one of the immunopotentiators.
Animals↗
[Changes in liver and spleen volume in various types of compensated liver cirrhosis--measurement by computed tomography].
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Adult↗
Preventive effects of several chemicals against lethality of recombinant human tumor necrosis factor.
Toxicity has been observed in mice receiving recombinant human tumor necrosis factor (rhTNF). In the present experiments, several chemicals were used to determine whether they could prevent the lethality of rhTNF without impairing its antitumor activity. Injection of phospholipase A2, cyclooxygenase, and lipoxygenase inhibitors at the same time as rhTNF administration could prevent the lethality of rhTNF, but the antitumor activity was also reduced. Urinastatin and reduced glutathione could prevent the lethality while reducing the activity. In contrast, by pretreatment with O2 scavengers, the lethality of rhTNF was markedly reduced without impairment of the antitumor activity of rhTNF. Antihistamines exerted no influence on the lethality of rhTNF. Histopathologic examinations have demonstrated that the capillaries of the tumor tissue show aggregation of platelets and formation of fibrin adherent to the vascular surface after TNF administration. Heparin or protamine revealed no effects against the lethality of rhTNF. These results strongly suggest that the arachidonic cascade is deeply related to the antitumor activity of TNF and its side effects. Pretreatment with O2 scavengers, especially bismuth subnitrate, could prevent the lethality of rhTNF without impairing its antitumor activity.
Animals↗
Antitumour effects of tumour necrosis factor: cytotoxic or necrotizing activity and its mechanism.
The antitumor activity of murine, rabbit and recombinant human tumour necrosis factor (TNF) was examined in an experimental animal model. TNF showed an excellent curative effect against the murine and human tumours tested. Strong antitumour activity was obtained by combining a small dose of TNF with moderate hyperthermia (40 degrees C for 40 min). TNF was also active against metastatic tumours, especially after repeated administration. The necrotizing action of TNF in vivo mainly relates to capillary injury. TNF causes necrosis not only in tumour tissue but also in granulation tissue. It causes morphological changes in, growth inhibition of, and cytotoxicity against cultured vascular endothelial cells. TNF inhibits endothelial motility evoked by the tumour. The mechanism of the cytotoxic action of TNF was examined using a microspectrophotometric assay for the lysosomotropic probe, acridine orange. The results suggest that TNF exerts its effect by enhancing endogenous tumour lysosomal activity. The increment in cellular respiration paralleled the susceptibility to TNF.
Animals↗
Effects of tumor necrosis factor (TNF) on transplanted tumors induced by methylcholanthrene in mice. A histopathologic study.
The effects of a highly purified tumor necrosis factor (TNF) on transplanted methylcholanthrene (Meth A)-induced murine tumors were compared with those of lipopolysaccharide (LPS). TNF caused immediate subepidermal edema and hyperemia followed 2 h later by fibrin thrombi in tumor blood vessels. Finally hemorrhagic necrosis with dispersal of tumor cells occurred. LPS produced similar hemorrhagic necrotizing changes. However, the necrotic action of LPS was delayed and complete tumor regression was not achieved with LPS. These findings suggest that tumor necrosis induced by TNF is due to circulatory disturbance associated with a microvascular injury in the tumor manifested by hyperemia and multiple fibrin thrombi.
Animals↗
Necrotizing activity of tumor necrosis factor: histopathological investigation using Meth A sarcoma and granulation tissue.
The action of tumor necrosis factor (TNF) was investigated histopathologically in mice using methylcholanthrene A (Meth A)-induced sarcomas and granulation tissue induced by autotransplantation of fragments of liver and spleen. Highly purified murine TNF caused hemorrhagic necrosis of both the tumors and the granulation tissue. Proliferation of tumor capillaries, demonstrated microangiographically, occurred 2 h after TNF administration and hyperemia of tumor vessels was obvious after 3-6 h. Hyperemia and capillary leakage were also observed in the granulation tissue 6 h after TNF injection and hemorrhage was noted in the epidermis after 12 h. These results strongly suggest that the in vivo necrotizing action of TNF is mainly related to capillary injury.
Animals↗
Neurilemoma of the ansa cervicalis.
A case of neurilemoma originating from the ansa cervicalis is presented. Available literature is reviewed, and the rarity of the tumor is discussed. It is believed that some cases of neurilemoma in which the nerve of origin was not identified may in reality have originated from the ansa cervicalis.
Child↗
Problems encountered with the ratchet lock of the Mathieu needle holder.
It is necessary to modify the Mathieu needle holder by reversing the arms of the ratchet so that it will become better suited for right hand use than the present design. Such an improvement would decrease the possibility of the ratchet pinching gloves and causing tears during operative procedures.
Equipment Design↗
Antitumor activity of recombinant human tumor necrosis factor in combination with hyperthermia, chemotherapy, or immunotherapy.
The antitumor activity of recombinant human tumor necrosis factor (rhTNF) against methylcholanthrene A-induced sarcoma (Meth A sarcoma) and human tumors in vivo was studied. On systemic administration of rhTNF to Meth A sarcoma-bearing mice, tumor regression was achieved with a large dose or with repeated administration of a small dose. Strong antitumor activity could be achieved in the Meth A sarcoma model by administration of a small dose of rhTNF in combination with moderate temperature hyperthermia (p less than 0.005). rhTNF (1,000 U/mouse) combined with moderate hyperthermia (40 degrees C for 40 min) within 2 h after the TNF administration effected 100% complete regression. In contrast, the rhTNF or moderate hyperthermia alone revealed 0% complete regression. The antitumor activity of rhTNF was decreased in combination with cyclophosphamide (0.6 or 1.2 mg/mouse) (p less than 0.005). However, in combination with mitomycin C (30 or 120 micrograms/mouse), the antitumor activity of rhTNF was enhanced (p less than 0.005). In combination with immunotherapy (lentinan or OK 432), the antitumor activity was mostly enhanced. Repeated rhTNF administration also displayed antitumor activity in heterotransplanted human tumors (p less than 0.005). The antitumor activity of TNF was enhanced by repeated administration of even small dosages, in combination with hyperthermia, or in combination with immunotherapy.
Animals↗