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Some infants with hypertrophic pyloric stenosis (HPS) have responded to oral atropine treatment. To achieve sufficient effect of atropine, it must be administered intravenously (i.v.). Therefore, with ultrasonography, we studied the changes in the pyloric muscle in HPS during and after intravenous administration of atropine. Twenty-three infants were studied. Atropine sulfate was initially administered at a dose of 0.04 mg/kg day i.v., and the dose was increased by 0.01 mg/kg/day until vomiting ceased. When vomiting ceased after administration of intravenous atropine sulfate, the infants received oral atropine sulfate at twice the effective intravenous dose; this was continued for 2 weeks. Ultrasonography was repeated until pyloric muscles normalized. Twenty-two infants were free from vomiting after 1-8 days of intravenous atropine sulfate (dosages of 0.04-0.11 mg/kg/day). In 21 infants, weight gain continued after atropine treatment even though no change in thickness of the pyloric muscles was demonstrated ultrasonographically. Only 2 infants required pyloromyotomy because of prolonged treatment or a mistake in underdosing of oral atropine. All of the 21 infants who recovered after intravenous atropine without surgery had normalization of pyloric muscle caliber, as shown by ultrasonography 4-12 months after treatment. Atropine is an effective medicine for HPS. Regression of pyloric thickening after vomiting has been controlled implies that pyloric muscle hypertrophy could be worsened by the spasm that occurs in HPS.

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Practical catalysts that work at a low temperature for selective catalytic reduction of NO x using NH3 (NH3–SCR) have been required to treat NO x at the outlet temperature in boiler systems (100–150 °C). In this paper, we report bulk vanadium oxide catalysts that show NH3–SCR activity at a low temperature below 150 °C. Defective bulk vanadium oxide (V­(V)+V­(IV)) catalysts were synthesized by the calcination of vanadium­(IV)-oxalate at 270 °C (1–4 h). The reaction rate per mol of surface vanadium atom of the catalyst calcined at 270 °C for 2 h (V 270-2, 6.4 × 10–2 molNO molV –1 s–1) was 10–14 times faster than those of conventional 1–9 wt % V2O5/TiO2 (4.5 × 10–3–6.1 × 10–3 molNO molV –1 s–1), indicating that bulk vanadium oxide is more favorable for NH3–SCR and V­(IV) species enhance the activity. The NH3–SCR of V 270-2 is driven by the Lewis acid mechanism, which proceeds faster than the Brønsted acid mechanism.

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