After pretreatment with the selective monoamine oxidase B inhibitor, (-)-deprenyl, in doses sufficient for complete inhibition of the platelet enzyme, 4 normal and 6 parkinsoniam volunteers (2 receiving levodopa and 2 levodopa plus carbidopa) suffered no adverse pressor reaction ('cheese effect') after challenge with oral tyramine in amounts considerably greater than those likely to be encountered in a normal diet. Nor did the levodopa-deprenyl combination itself result in a pressor response. Normal human intestinal mucosa was shown predominantly to contain the deprenyl-insensitive A form of the enzyme, which presumably degraded administered tyramine in the deprenyl-treated volunteers; even those receiving the drug for prolonged periods manifested no 'cheese effect', suggesting that the A form remained uninhibited. Intestinal monoamine oxidase A was able to oxidise dopamine, whereas in human platelet or striatum the amine is a monoamine oxidase B substrate. Like tyramine, oral phenylethylamine challenge with amounts greater than those known to be present in a normal diet similarly gave rise to no adverse reaction in (-)-deprenyl-treated subjects; the reasons for this remain to be determined.

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Actions of salbutamol, disodium cromoglycate, and placebo administered as aerosols in acute asthma 725Resistance to DSCG in acute asthma is greater therefore, than to salbutamol. However, clinical observation suggests that resistance to beta-2 stimulants does also increase with severity of the attack. It would appear probable that only when severity exceeds the point at which measurements can be made with a peak flow meter does resistance to salbutamol become pronounced. Although placebo effects are greater in the attack than between attacks, again no information is available about attacks severe enough to prevent measurement using a peak flow meter. pipette into a capillary tube (for this technique blood pH capillary tubes cut to the same length as standard glass capillary tubes were used). They were sealed at one end by a flame and centrifuged for 15 minutes at 12 000 g, using a haematocrit centrifuge (Hawksley, London).After centrifugation the tubes were removed immediately and placed vertically. The length of the fat layer at the top and that of the solid layer at the bottom was measured with vernier callipers to the nearest 0 05 mm. Stool fat content was expressed as a percentage (steatocrit) of the total length of the solid column in the tube (that is fat layer + solid layer) (Fig. 1). The steatocrit was measured in duplicate. The stool fat content was also measured by Sobel's method2 which requires 3 g of stool.

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Sixteen patients with oral isoniazid, pyrazinamide, rifampin, and intramuscular streptomycin for tuberculous meningitis were studied. The concentrations of isoniazid, pyrazinamide, rifampin, and streptomycin in cerebrospinal fluid (CSF) obtained 3 hours after administration were 2.40, 34.78, 0.29, and 3.78 micrograms/ml, respectively. The CSF concentrations of isoniazid and pyrazinamide were well above the minimum inhibitory concentration for Mycobacterium tuberculosis. Concentrations of rifampin and streptomycin were above the minimal inhibitory concentration initially but declined below the minimal inhibitory concentration at later times. The CSF penetration of isoniazid, pyrazinamide, rifampin, and streptomycin was about 89%, 91%, 5%, and 20%, respectively. In eight patients who received antituberculous drugs in combination with steroids, the mean CSF and serum concentrations, as well as CSF/serum ratios at various intervals of treatment, were not statistically different (p greater than 0.05) from those of the eight patients who did not receive steroids.

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An extensive outbreak of acute hemorrhagic conjunctivitis (AHC) occurred from September to December 1974 in Thailand. At least 29 patients with polio-like motor paralysis that complicated AHC were hospitalized in Bangkok. Paired or triplicate samples of serum from 16 patients were tested for neutralizing antibody to enterovirus type 70 (EV70). A significant rise in titer of antibody was found for two patients, and the other 14 had neutralizing antibody titers ranging from 1:8 to 1:512 without an increasf larger than or equal to 1:16, a level which is considered to be diagnostically significant. Neutralizing antibody to EV70 was detected in 19S fractions of nine sera examined, but neutralizing antibody to three types of poliovirus was confined to 7S fractions. EV70 was isolated from one of seven stool specimens collected on day 37 after the onset of AHC and none of 10 samples of cerebrospinal fluid. These results and additional clinical and epidemiologic findings gave further support to the hypothesis that EV70 infection can cause polio-like motor paralysis as a complication of AHC.