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Biomedical subjects

A Imai

Publications and source records attributed to A Imai.

At least 253 records · Page 14Linked to original sources
PubMed1982

[Comparative study on cefmetazole and cefazolin in the treatment of suppurative otitis media].

Cefmetazole (CMZ) was compared to cefazolin (CEZ) for efficacy and safety in the treatment of suppurative otitis media (including acute otitis media and chronic otitis media in acute aggravating stage) under well controlled clinical trials. The therapeutic effects were analyzed statistically in 172 patients (82 administered CMZ, 90 administered CEZ). The adverse reactions were also analyzed statistically in 199 patients (CMZ 99, CEZ 100) in whom the judgement was possible. 1. The efficacy rate of CMZ (72.3% for good to excellent response) was assessed by physicians in charge to be similar to that of CEZ (59.3%). This was the same being assessed by the committee, too (CMZ 64.6%, CEZ 56.7%). 2. When patients were classified into 2 groups (acute otitis media, chronic otitis media in acute aggravating stage) with respect to diagnosis, statistically significant difference in clinical efficacy assessed by physicians in charge was observed in the cases with chronic otitis media (CMZ, CEZ). In addition, the improvements of flares on the drum membrane and the mucous membrane of eardrum were significantly better in the CMZ group than in the CEZ group. 3. Bacteriologically, 16 cases (19.8%) of S. aureus were resistant to CEZ, while only 1 case (1.2%) to CMZ. CMZ was judged to be effective in 5 of the 6 cases in which CEZ-resistant strains were detected. 4. Side effects were found in 2 cases (2.0%) treated with CMZ: one complained of retching and abdominal pain and the other developed skin eruption. On the other hand, only 1 case (1.0%) developed skin eruption in the CEZ group. These results suggest that CMZ is a new antibiotic agent which is highly valuable in the treatment of suppurative otitis media.

Adolescent↗
PubMed1982

Evidence for predominance of phospholipase A2 in release of arachidonic acid in thrombin-activated platelets: phosphatidylinositol-specific phospholipase C may play a minor role in arachidonate liberation.

Human platelets prelabeled with [3H]glycerol exhibited a trasient increase in radioactivity (1.5-fold gain) in 1,2-diacylglycerol when they were exposed to thrombin. An alteration in radioactivity in monoacylglycerol which is derived from diacylglycerol by diacylglycerol lipase, however, was not observed during the whole period of incubation with thrombin. Lysophosphatidylcholine and lysophosphatidylethanolamine gained radioactivity. By contrast, the level of lysophosphatidylinositol plus lysophosphatidylserine did not show any change. When the effects of thrombin on platelet lipids were examined for [3H]arachidonate-labeled platelets, thrombin-activation induced a 15-fold increase in radioactivity in 1,2-diacylglycerol, a subsequent decrease of which was accompanied by accumulation of radioactivity in phosphatidic acid. There was a concurrent release of free arachidonic acid. These findings, taken together with phospholipid alteration analyzed by phosphorus assay upon thrombin-activation, indicate evidence than newly produced diacyglycerol in thrombin-activated platelets may be immediately converted to phophatidic acid by a diacylglycerol kinase rather than metabolized to monoacylglycerol or arachidonic acid by diacylglycerol lipase, and also that arachidonic acid would be mainly released from phosphatidylcholine and phosphatidylethanolamine by a phospholipase A2 activity.

Arachidonic Acid↗
PubMed1982

The significance of measurements of lipid peroxide and a newly-discovered amidase in inflammation.

Inflammation is a biological defence mechanism against noxious stimuli. Over-strong and oversuppressed inflammatory responses both lead to tissue damage and delay of tissue repair. Determination of inflammatory responses on the basis of chemical mediators, however, only informs about the degree of these responses themselves. It cannot show whether these responses are over-strong or oversuppressed. We have developed a prototype standard for safe judgement of the appropriateness of inflammatory responses: measurements of lipid peroxide (a product of tissue damage) and a newly-discovered amidase (related to wound healing).

Amidohydrolases↗
PubMed1979

The occurrence of calicivirus in infants with acute gastroenteritis.

Calicivirus was detected in 8 (1.2%) of 647 hospitalized patients during a survey of acute gastroenteritis in infants and young children, conducted between December 1974 and September 1977. Morphologically calicivirus was approximately 30 nm in diameter with an easily recognizable staining "star of David" configuration. Its buoyant density in cesium chloride was 1.38-1.40 gm/ml. The serologic response to calicivirus by immune electron microscopy (IEM) was demonstrated only in paired sera from patients who shed the virus in their stools. The results suggest that calicivirus might be a cause of acute gastroenteritis in infants and young children.

Acute Disease↗
PubMed1978

Human rotavirus infection in infants and young children with intussusception.

Human rotavirus was detected by electron microscopy in 11 of 30 infants and young children with intussusception (37% of subjects under study). Serologic complement fixation tests revealed evidence of infection with the rotavirus in 70% of the patients examined who eliminated the rotavirus in their stools. These results indicate that human rotavirus, in addition to adenovirus, may be an infectious agent causing intussusception in infants and young children.

Adenoviruses, Human↗
PubMed1978

A long-term survey of rotavirus infection in Japanese children with acute gastroenteritis.

Human rotavirus was detected by electron microscopic examination of the stools of 320 (63%) of 506 infants and young children hospitalized with acute gastroenteritis between December 1974 and March 1977. Serologic responses to infection with the rotavirus were revealed by the complement-fixation test in 130 (70%) of 185 patients examined. During the study period three epidemics of human rotavirus infection occurred during the winter months. The peak incidences occurred in January 1975 (88% of patients positive by serologic analysis or electron microscopy of stools), January 1976 (92%), and February 1977 (96%). Rotavirus was detected in the stools of 288 (79%) of 365 patients tested during the cooler months (December to March) and 35 (25%) of 141 during the rest of the year. In the summer (June to August), rotavirus infection occurred rarely. The frequency of human rotavirus infection was highest among patients aged six to 11 months. These results indicate that human rotavirus can be regarded as a major etiologic agent of acute gastroenteritis in infants and young children, of which wintertime epidemics are common in Japan.

Acute Disease↗
PubMed1977

Reovirus-like agent in acute epidemic gastroenteritis in Japanese infants: fecal shedding and serologic response.

The reovirus-like agent, sometimes referred to as duovirus or rotavirus, was visualized by electron microscopy in stool extracts from Japanese infants and young children with acute epidemic gastroenteritis. The virus particles measured 70 nm in diameter and had double-shelled capsids. One hundred ten (89%) of 124 patients with the gastroenteritis had such virus particles in stools obtained during the acute phase. The virus particles were excreted in the stools usually during the first eight days of illness. Agglutination of virus particles by antibody present in convalescent-phase sera was demonstrated by immune electron microscopy. Complement-fixing antibody was detected as early as day 3 of illness, and antibody titers peaked during the second and third weeks of the disease. The antibody appearing in the acute and early convalescent phases was sensitive to 2-mercaptoethanol. Antibody resistant to 2-mercaptoethanol was produced approximately 10 days after the onset of the symptoms. The serologic evidence suggests that a primary infection with the reovirus-like agent was responsible for the clinical attack of acute gastroenteritis.

Acute Disease↗