Molecular species of sialic acids released by mild acid hydrolysis from mucins of bovine small and large intestine were characterized by two dimensional thin layer chromatography and gas chromatography-mass spectrometry. The small and large intestinal mucins contained both N-acetyl- and N-glycolylneuraminic acid. Although O-acetylated derivatives were not detectable in the small intestinal mucin, 9-O-acetyl-N-glycolylneuraminic acid was demonstrated in the large intestinal mucin by thin-layer chromatography and its structure was confirmed by mass spectrometry. Moreover, the presence of three kinds of O-acetyl-N-acetylneuraminic acid and five kinds of O-acetyl-N glycolylneuraminic acid in the large intestinal mucin was suggested by thin layer chromatography and mass chromatograph y. The limited distribution of O-acetylated neuraminic acids suggests that their derivatives are only produced in the mucous glands of the large intestine.

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Some of the relatively easily measurable and possibly hypertension-associated parameters were evaluated in thirty normotensive young subjects divided into the PHT (either parent hypertensive) group and the PNT (both parents normotensive) group. In subjects of the PHT group, the platelet aggregating sensitivity to the arachidonic acid and the ratio of total cholesterol to HDL cholesterol were significantly (p<0.05) increased while urinary kallikrein excretion was decreased without simultaneously significant elevation of blood pressure. The enhanced platelet aggregating sensitivity to the arachidonic acid and the increased ratio of total cholesterol to HDL cholesterol suggest that subjects with a positive family history of hypertension might have a greater tendency to atherosclerosis and could contribute to the development of essential hypertension. Decreased urinary kallikrein excretion suggests that the vasodepressive activity of the kallikrein-kinin system might be inhibited in subjects with a positive family history of hypertension.

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For a fuller understanding of the fascial relationships of the visceral organs and their vessels, a general scheme is presented. According to this scheme, there are four basic layers internal as well as external to the trunk musculature. In the abdomen, the internal layers (numbered outwards) consist of (1) the peritoneum, (2) the deep layer of the subperitoneal fascia, (3) the superficial layer of the subperitoneal fascia and (4) the transversalis fascia, while the external layers (numbered inwards) comprise (1) the skin, (2) the superficial layer of the subcutaneous fascia, (3) the deep layer of the subcutaneous facia and (4) the investing layer of the abdominal fascia. Each interfascial space between layers 2 and 3 gives passage to the main vessels and nerves and will be referred to as the “neurovascular corridor.” By the addition of some slight modifications to the basic scheme, the fascial relatonships of some organs is illustrated. Photographs of dissections, substantiating the schemes are also included. The schemes and dissections together demonstrate three points: (1) The mammary gland to be situated within the neurovascular corridor, external to the thorax, (2) That the layers of the renal fascia, comprising layers 2 and 3, continue into the pelvic cavity to form the fascia around the ureter and urinary bladder, (3) An outline arrangement of the vascular sheath in the pelvis.

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The effects of fluoroacetate on the ameloblasts were studied in the rat incisor. Fluoroacetate is an inhibitor of tricarboxylic acid cycle and accumulation of citrate occurred in the animal tissues due to fluoroacetate administration. In the present study, fluoroacetate injection caused severe morphologic changes in the ameloblasts. The most prominent change was observed in the mitochondria. Reduction of the mitochondrial matrix density was the earliest change followed by varying degrees of matrix swelling. Loss of the matrix granules and disintegration of the cristae were also observed. The difference in the mitochondrial activities in regard to the citrate metabolism was found between the matrix formation stage and the maturation stage in the ameloblasts. Extensive dilatation of the rough-surfaced endoplasmic reticulum and grossly enlarged vacuoles were found mainly in the early maturation stage at 12 and 24 hours after the fluoroacetate administration. These abnormally large vacuoles seemed to be caused by the water stored within the endoplasmic reticulum cisternae. Accumulation of plasma citrate and decrease of ionized calcium concentration in the whole blood were observed in the fluoroacetate treated group. These findings suggest that fluoroacetate may cause the lowering of the function of the ameloblasts through the suppression of cell energy production and that both the secretion of the matrix and the calcification of the enamel may be inhibited.

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The membrane potential s and isometric tension of canine ventricular muscle fibers in the K+-free, Ca2+-rich solution developing oscillatory afterpotentials (OAPs) were recorded simultaneously. The OAPs were always accompanied by aftercontractions (ACs). Both activities appeared with almost a similar frequency and timing. The amplitude of the OAPs, ACs and twitch tension were dependent on the basic cycle length of the train as well as on the number of impulses. The manner of this dependence was similar in the OAPs and ACs but showed a slight difference in the twitch tension. The increase in the [Ca2+]0 and the application of isoproterenol caused augmentation of the OAPs during the application. By washing out the drug, the OAPs and ACs quickly recovered to the control level but the twitch tension did not. The application of 2 mM K+ or Rb+ quickly and reversibly abolished the OAPs and ACs with a marked suppression of the twitch tension. One mM of caffeine eliminated the oscillations of both the membrane potentials and tension. The wash-out of caffeine brought about a transient increase in the OAPs and ACs. Two or five mM of procaine caused a complete elimination of the OAPs and ACs. These results suggest that the OAPs are formed by a process related to the cyclic release of Ca2+ from the sarcoplasmic reticulum.

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