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Biomedical subjects

S Tsuji

Publications and source records attributed to S Tsuji.

At least 1,027 records · Page 57Linked to original sources
PubMed1976

The problem of the treatment of sarcoidosis: Report of the Subcommittee on Therapy.

Stage I: Hilar Adenopathy With normal lung function observe, as it often resolves. With reduced lung function observe for 6-12 months. Treat if there is progression or persistence. With erythema nodosum use mild anti-inflammatory agents such as salicylates or like drugs. Stage II: Adenopathy + Pulmonar Infiltrates With normal or slightly reduced lung function observe; treat if it worsens. Treat if there is no remission in 6-12 months. With reduced lung function treat, possibly for many years or a lifetime. Stage III: Pulmonary Infiltrates +/- Fibrosis Without Adenopathy There is reduced lung function. Treat, demonstrate improvement, follow patients with serial measurements of vital capacity at least. Other Indications for Treatment Other indications for treatment include myocardial sarcoidosis, cerebral sarcoidosis (although the outcome is less certain), serious hepatic or renal sarcoidosis, hypercalcemia, persistent systemic symptoms, or other serious organ or functional impairment. Assess each patient individually and completely. Use good clinical judgement. It is clear that treatment that is too little or too late is of little benefit. Even the statistical results form a perfectly controlled study cannot provide absolute direction for the individual patient. As clinicians we are frequently called upon to apply considered judgements without hard data to predict the outcome. We also maintain the flexibility to change our therapeutic programs when circumstances change, either in the patient or in our knowledge. We can be grateful we have a treatment as good as corticosteroids and must try to exercise our best judgement as to when it should be instituted.

Adrenal Cortex Hormones↗
PubMed1975

In vitro culture of the proximal tubule of the bovine nephron: transmission and scanning electron microscopy.

By means of a previously described method, viable pure tubules of the nephron were isolated in high yield from the outer cortex of the near-term foetal bovine kidney. The tubular suspension obtained was constituted almost exclusively of proximal segments (about 95%), whose cells were dispersed and grown as confluent primary cultures. The cultured proximal cells were shown to maintain in vitro, on glass or plastic surfaces, the same orientation as on the tubular basement membrane in vivo, with interdigitations extending from the base of the cells and along their full height. Numerous mitochondria and the typical cytoplasmic bodies of the proximal cell were retained in cells grown in vitro. A flagellum was seen in every cultured cell and was shown to be present in the proximal cell in vivo. There is a progressive change, in vitro, of the microvilli of the brush border, from a close-packed to a sparse distribution and to a decrease in height and a reduction in number. This in vitro regression to an earlier embryonic state was correlated with the ability of the proximal cells to synthesize in vitro an alpha-fetoprotein and with the loss in vitro of histiospecific antigen synthesis, confined in vivo to the brush border area. The confluent proximal cells became filled with microfilaments and microtubules, the significance of which is discussed.

Animals↗
PubMed1975

[The ultrastructure of Electrophorus electricus spinal electromotoneurons, with or without acetylcholinesterase activity].

The acetylcholinesterase-rich neurons existing in the electromotor nucleus (EMN or "CMD") of the spinal cord of the Electrophorus electricus exhibit the presence of numerous chemical synapses on their surfaces, whereas the neurons without enzymatic activity which occupy the major part of the grey matter of the EMN are characterized by electrical synapses.

Acetylcholinesterase↗
PubMed1975

[Genetic relationship of two mutant genes which producing three different syndromes in the mouse (author's transl)].

We determined that leaner gene (la) is located in the linkage group XVIII and closely linked to Es-1, which is known to be located closely to tottering gene (tg). Double heterozygote (la/tg) produced by mating between la heterozygote and tg heterozygote showed an intermediate syndrome between those seen in tottering (tg/tg) and leaner (la/la) mice. Both leaner and tottering mice showed neuromuscular disorders, but their clinical and pathological characteristics were different. Leaner mice were found to represent a so-called cerebellar mutant having the reduced size of cerebellum and severe cytoarchitectonic abnormalities with focal losses of Purkinje and granular layer cells. Tottering was, however, another mutation having epileptiform seizures, and it was characterized pathologically by cellular losses and shrinkage as well as vesiculations of cytoplasmic membranous structures in the cerebellum. The double heterozygote was shown to have both pathologic characteristics seen in each homozygote, and also showed shrinkage of Purkinje cells and vesiculation of the endoplasmic reticulum and Golgi apparatus. These clinical and pathological findings supported the genetic data suggesting that la and tg constitute an allele.

Alleles↗
PubMed1974

Adenylate cyclase from Brevibacterium liquefaciens. III. In situ regulation of adenylate cyclase by pyruvate.

In the presence of DL-alanine intracellular cyclic AMP in nonproliferating cells of Brevibacterium liquefaciens increased rapidly to the maximum level of approximately 180 muM, and extracellular cyclic AMP increased to 100 muM within 4 hr at 25 degrees . Adenylate cyclase (EC 4.6.1.1) induction was not observed during this incubation. The concentration of pyruvate in the total culture increased concomitantly with that of cyclic AMP and reached approximately 20 mM after 4 hr of incubation. Since the activity of cyclic nucleotide phosphodiesterase is extremely low in this bacterium, the accumulation of cyclic AMP with DL-alanine appeared to be due to the activation of adenylate cyclase by pyruvate. D-alanine was more effective than L-alanine in producing pyruvate, and a high activity of D-alanine oxidation was detected in the cell lysate of B. liquefaciens.Thus, adenylate cyclase in this bacterium appeared to be regulated in vivo by pyruvate which was formed, in this case, predominantly from D-alanine through the action of D-aminoacid oxidase (EC 1.4.3.3). Pyruvate, added extracellularly, also caused a rapid accumulation of intracellular cyclic AMP. Glucose did not change the level of cyclic AMP significantly. It also did not affect the intracellular accumulation of cyclic AMP with DL-alanine.

Adenylyl Cyclases↗