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S Yamoto

Publications and source records attributed to S Yamoto.

6 recordsLinked to original sources

Sequence-defined dimer block synthesis from unprotected nucleoside.

mediates to synthesize the oligodeoxynucleotides have been synthesize otected nucleoside using morpholinophosphorditetrazolide. From these sequence-defined oligodeoxynucleotides were also synthesized. The gen is composed of following steps; a) reaction of 5'-O-protected nucleo orpholinophosphorditetrazolide (phosphitilation), b) reaction of the nucleoside phosphoramidite with the second nucleoside (condensation), ueous oxidation with t-BuOOH (oxidation). RE 1/hlp F2/cmt F3/ext F4/can F5/nxt F6/ins F7/up F8/dwn F9/fin

Indicators and Reagents

An approach to DNA fragment synthesis from unprotected nucleoside.

Oligodeoxynucleotides have been synthesized from unprotected nucleoside by use of morpholinophosphordichloridite as a phosphorylating reagent. This procedure consists of three (in situ) steps; the reaction of 5'-O-protected deoxynucleotide with morpholinophosphordichloridite, the reaction of the resulting on active mononucleotide derivative with the second nucleoside, non-aqueous oxidation, and then removal of amino moiety at phosphate diester linkage.

Base Sequence

A rapid synthesis of a DNA fragment using an unprotected nucleoside and a phosphine derivative.

A rapid synthesis of DNA fragment from unprotected nucleoside and phosphine derivative, morpholinophosphordichloridite, has been studied, demonstrating a d(T-T) and its amino-phosphonate derivative syntheses. A high selectivity of this reagent eliminates the protection of nucleoside hydroxyl groups. The P-N bond in the resulting dinucleoside phosphite can readily be converted to a phosphite triester with alcohol and to the corresponding aminophosphonate by a non-aqueous oxidation with m-chlorobenzoic acid. The P-N bond in the phosphate link is very stable and so provides a protection for the phosphoryl group which has many potential uses. Deprotection can be achieved by a simple treatment with NH2OH.

DNA

The role of macrophages in demyelination in experimental allergic neuritis.

The role of macrophages and serum factors in demyelination in experimental allergic neuritis (EAN) was examined by a simple in vitro method. Cultivated rabbit peritoneal macrophages, preincubated with serum obtained from rabbit EAN produced by sensitization with bovine spinal nerve roots, could agglutinate and phagocytize purified bovine or rabbit peripheral nerve myelin. Sera from normal animals or from controls given adjuvant alone could not. Adhesion and phagocytosis were inhibited if EAN sera were absorbed with peripheral nerve myelin. Rabbit red blood cells were not phagocytized by macrophages exposed to EAN serum. Concomitant to these observations, three lysosomal acid hydrolases: acid proteinase, acid phosphatase and beta-glucuronidase, were assayed with respect to their topographical and chronological distribution. In the group examined at clinical onset, increases in the specific activities were 1.5-3.0-fold in the spinal roots and 1.0-1.5-fold in the sciatic nerves compared with control. The degree of increase in total activities per whole root or sciatic nerve was much higher for specific activities. The topographical distribution of the increase closely corresponded to the histological distribution of EAN lesions. These observations suggested that the increased lysosomal activity originated from lysosomal-rich infiltrating cells. These observations strongly indicated the significant role of macrophages activated by EAN serum in the demyelination of EAN.

Acid Phosphatase

[Neurogenic hypernatremia caused by a teratoma on the supraoptic region (author's transl)].

This is a case report involving a 9 year old girl with a teratoma that infaced mainly the bilateral hypothalamus. The girl was observed for 14 months after partial surgical removal. During that time she showed aphagia, adipsia, hypopituitarism, and visual and psychiatric disturbances. Severe hypernatremia also was present, even though large amounts of 5% glucose solution without salt were given I.V. Food and water were given by nasal gastric gavage and later gavage via gastric fistula, but the hypernatremia remained unchanged. When pitressin or spironolacton (anti-aldosterone) were administered, remarkable effect on the hypernatremia couldn't be found. Upon autopsy it was discovered that the bilateral hypothalamus, left subthalamus and ventral part of the thalamus were invaded by teratoma. Comparing many similar clinical reports and manifestations of hypothalamic lesions in experimental animals, it is reasonable to assume that the mechanisms of hypernatremia were caused by the disturbances of ADH secretion, thirst centre and osmoreceptor in the hypothalamus.

Aldosterone