The author compared the whole course of blood coagulation in the cases of beriberi and jaundice with that of a normal person and obtained results as follow. In case of beriberi, the time duration of the first, the beginning and the active phase inclined to decrease and the mean-value of the hardness decreased in the beginning and increased in the completing, but showed no difference in the active. In case of jaundice, the time duration of the first and the beginning showed prolongation, but that of the active was shortened a little. The mean-value of the hardness increased in the beginning and the completing, but decreased in the active.

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1) The writer's observations plainly show that alkali metal compounds are externally photoelectrically active as against other authors' reports to the present time. 2) Potassium bromide clearly shows external photoelectric effect even by the visible rays longer than 5600Å; potassium chloride, sodium chloride, potassium cyanide, sodium ferrocyanide, sodium bromide and sodium sulphate by ultraviolet rays longer than 3150Å; potassium iodide, potassium ferrocyanide, ammonium chloride and sodium carbonate by ultraviolet rays longer than 2500Å; kalium oxalicum neutrale by visible rays longer than 4300Å; and sodium hydroxide, natriokalium tartaricum, sodium hyposulphite, potassium carbonate, potassium nitrate, sodium citrate, sodium phosphate, potassium sulphate, anhydrous iodic acid and potassium bichromate by ultraviolet rays longer than 2000Å. 3) The threshold wave lengths of halogen compounds and cyanide are relatively long amongst alkali metal compounds. 4) The photoelectric effect of potassium carbonate is very much weaker than that of other alkali metal compounds. 5) Thoroughly dry potassium nitrate is also photoelectrically active no less so than when it is slightly wet.

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The author studied the change of skin temperature of the human extremity with a thermo-junction when the venous return current was obstructed by the pressure of cuff. The temperature drops after the obstruction and rises after the release of pressure, and generally it recovers in 8-13 minutes to the temperature before pressure. At this experiment, in several cases the temperature after the release of pressure rose rather higher than that before pressure, the author believes that this fact must be caused by the so-called "reactive hyperaemia". In arteriosclerotic patients the temperature drop was slight and the recovery of temperature after the release of pressure was delayed compared with normal persons.

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