1. Compressed air above 5 atm. lessens the CO2 output, and lowers the body temperature in mice, rats, and young rabbits.

2. Oxygen at and above 1 atm. has the same effect. It is a sign of oxygen poisoning.

3. Compressed air at 10 atm. is more damaging–at least to small animals—than oxygen at 2 atm.

4. Compressed air increases the loss of body heat both because it is a better conductor, and because it is saturated with moisture.

5. The saturation of the air with moisture in caissons does not prevent evaporation from the body because the skin temperature is above that of the air. The wet air by damping fur or clothes increases loss of heat.

6. Highly compressed air may possibly interfere with the diffusion of CO2 from the alveolar air, and may, owing to increased friction, hinder the passage of air in and out of the air-tubes.

7. The nitrogen output in dogs is not altered in any noteworthy degree by exposure for six hours to 8 atm. air.

8. Inflammation and consolidation of the lungs is produced by exposure to 8 atm. air for over 24 hours. 1½ atm. of pure oxygen has a similar effect. The higher the oxygen tension the more rapidly does the inflammation ensure, e.g. 6 atm. O2 produces marked congestion in 2 hours.

9. It does not seem likely that inflammation of the lungs should be produced in the pressures and times of exposure usual in caissons.

10. Excised frog's hearts, muscles, and nerves are not rapidly poisoned by even 50 atm. O2. A heart will beat more than an hour exposed to this pressure. The vagus nerve endings appear to be paralysed by such exposure, while inhibition can be obtained by stimulating the crescent. The thin sartorius muscle is much more easily affected than the gastrocnemius, and soon gives a curve like a fatigue curve.

11. All animals investigated, vertebrates and invertebrates, are instantly convulsed and killed by exposure to 50 atm. O2.

12. Convulsions are frequently produced in vertebrates by exposure to 4—5 atm. O2, while exposure to 6—25 atm. O2 produces dyspnoea and coma, and the convulsive stage does not usually appear. Cleaning movements, salivation, gaping, jerky deep respiration, are symptoms which precede the convulsions, and coma soon follows them.

13. We have not observed convulsions with air pressures up to 12 atm. Salivation, dyspnoea, and coma are the symptoms.

14. The blood-gases increase in compressed air or oxygen according to Dalton's law, but the process of complete saturation of blood and tissues takes some time.

15. The circulation is unaffected mechanically by compressed air.

16. The cause of caisson-sickness is the escape of gas bubbles in the blood vessels and tissue fluids on decompression. An animal exposed for 4 hours to 8 atm. air and quickly decompressed is like an opened bottle of soda-water. The fluids of the body generally effervesce.

17. The effervescence can be studied in the circulation of the frog's web or bat's wing, the animals being enclosed in a suitable chamber. It takes a little time for the bubbles to grow to an appreciable size.

18. Recompression causes the bubbles to go into solution, and if applied quickly enough the circulation recommences.

19. The bubbles after rapid decompression can be seen post-mortem in the blood vessels, in the heart, retinae, aqueous humour, connective tissue spaces, etc. The alimentary canal is blown out with gas. The bubbles produce cyst-like cavities in solid organs, e.g. in the central nervous system, the liver. The cells are compressed round these cysts.

20. In the case of oxygen an animal may recover after an extraordinary amount of this gas has been set free by rapid decompression. The nerve cells are not killed by the oxygen bubbles, and the animals are convulsed and exhibit hyper-reflex-excitability.

21. The varying symptoms of caisson-sickness are due to the varying seat of the air emboli.

22. Young men escape caisson-sickness owing to the elasticity of their tissues, and greater facility for collateral pathways of circulation.

23. Animals can be safely exposed to 8 atm. of air for 4 hours if 2 hours be spent in gradual decompression. Such exposure can be safely repeated three times a week.

24. By the choice of suitable men, and proper regulation of the period of compression and decompression, caisson and diver's sickness can be avoided.

The task with which I have been honoured—of reporting upon the action of English Public Health Authorities in regard to tuberculosis—can, I believe, be best fulfilled (a) by a review of the history of the mortality from tuberculosis in England since 1837, when vital statistics first became available, (b) by a statement of the factors which have been instrumental in causing the reduction in the mortality from tuberculosis shown in these statistics, and an attempt at weighing their relative importance, (c) by a description of the more direct measures taken in England to diminish the prevalence of tuberculosis, and (d) by a forecast of the lines on which preventive measures against this disease are likely to be extended.

Of all British colonies New Zealand is the one that most closely resembles Great Britain in size, in situation, and in climate. And the inhabitants of the two countries are of practically the same race. The vital statistics of New Zealand are therefore eminently suitable for comparison with those of Great Britain. In the present paper comparison has been restricted to the birth-rates and death-rates, and in this limited survey several points of interest present themselves.

The Select Committee of the House of Commons which was first appointed on April 16th, 1902, and subsequently re-appointed with certain changes in its constitution, for the purpose of inquiring into the Ventilation of the House, instructed the author to make for their information a number of analyses of the air in the Debating Chamber and many other parts of the House. In this communication only the methods used and the results obtained in the case of the Debating Chamber will be referred to. The Committee reported to the House on the 28th July last, and its report, which is published by H.M.'s Stationary Office (No. 283), should be consulted for particulars of its conclusions and recommendations in regard to the ventilation of the House.

The investigations described in the present paper were undertaken during the summer of 1902, at the request of the Select Committee on the Ventilation of the House of Commons.

The above heading sufficiently indicates a difficulty which has doubtless often occurred to those who have studied the subject of the agency of Anopheles in the causation of malaria. In some cases this difficulty has seemed so formidable that disbelief in any such agency has been boldly professed. The following observations, most of which I owe to the kindness of Dr Gould, who succeeded me at Acre in Palestine, will help to explain the occurrence of malaria at places where there would seem to be little or no breeding-ground for Anopheles, and prolonged observation by residents has not revealed the presence of the perfect insect.