Early Days of Pressure Denaturation Studies of Proteins.

The denaturation of protein by pressure has been generally well known since the findings of the perfect coagulation of egg white by a pressure of 7,000 atm within 30 min by Bridgman (J Biol Chem 19:511-512, 1914), and Kiyama and Yanagimoto (Rev Phys Chem Jpn 21:41-43, 1951) confirmed that the coagulation occurs above 3,880 kg cm(-2). Grant et al. (Science 94:616, 1941) and Suzuki and Kitamura (Abstracts of 30th annual meeting of Japanese Biochemical Society, 1957) found that SH groups are detected at the compressed sample of ovalbumin. On the other hand, Johnson and Campbell (J Cell Comp Physiol 26:43-49, 1945), Tongur (Kolloid Zhur 11:274-279, 1949; Biokhimiya 17:495-503, 1952) and Suzuki et al. (Mem Res Inst Sci Eng Ritsumeikan Univ 3:1-4, 1958) reported that the thermal denaturation of proteins is retarded in a few examples by the low pressure of about 1,000 atm. Before 1960, the studies of denaturation under high pressure were, however, rare and almost qualitative compared with those by heat, acid, urea and so on, so that there was no theory for the influence of hydrostatic pressure on the mechanism of denaturation. Here I review how I started experiments and analysis on pressure denaturation of proteins in early days of 1950s and 1960s in my laboratory and others.

A proposal of subcategorization of bacterial prostatitis: NIH category I and II diseases can be further subcategorized on analysis by therapeutic and immunological procedures.

AIM: We propose preliminarily that acute (category I of the NIH consensus definition) and chronic prostatitis (category II) can be subcategorized into primary and recurrent diseases based on the precise analysis of the clinical course and the immunological parameters in prostatic secretions of our cases. METHODS: Five patients with stone-free, acute febrile prostatitis and nine patients with acute episodes of afebrile urinary infection were included. The expressed prostatic secretions (EPS) were collected soon after the acute illnesses subsided after medication administration and they were examined microscopically, bacteriologically, and serologically. First-line medications were cefem antibiotics with conventional doses for febrile cases and low doses for afebrile cases. They were administered for at least 2 weeks. Second-line conventional medication with sulfamethoxazole-trimethoprim or levofloxacin was given only to the patients in whom remaining prostatic infections were revealed. RESULTS: The first-line medications were successful in all patients and they promptly became asymptomatic in 1 week. All the EPS were infected except for two afebrile cases. Prostatic infections were eradicated by second-line conventional medications. In a patient with afebrile prostatitis whose EPS were free of macrophages and immunoglobulin (Ig)M, the eradication of prostatic pathogens was achieved without second-line antibacterial medication. CONCLUSIONS: Bacterial prostatitis could be classified into primary and recurrent chronic infections in each of the febrile (category I) and afebrile (category II) illnesses. A cefem regimen in varying doses was a clue for differential diagnosis as it did not affect the pathogens in the prostatic ducts or acini unless heavy urine reflux occurred in the ductal draining systems. Macrophages and immunoglobulins, especially IgM, in the EPS were useful immunological parameters to differentiate primary and recurrent infections of the prostate. Fluoroquinolones or sulfamethoxazole-trimethoprim should not be employed in acute urinary infections in male patients until the confirmation of prostatic infection to avoid injudicious use of them, which might cause an increasing prevalence of resistant uropathogens in the community. The evacuation of the prostate by repetitive massage seemed to be effective to enhance the prompt eradication of pathogens from the prostatic tissue and to keep patients asymptomatic throughout the course of the disease by preventing tissue pressure elevation.