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Articles by H Sano
Total Records ( 2 ) for H Sano
  H Sano

The aim of the study was to investigate trends in the incidence of blindness and the association with laser photocoagulation in patients with type 1 diabetes in Japan.


Patients diagnosed between 1965 and 1979 aged under 18 years old were studied. The status of blindness and laser photocoagulation was identified as of 1 January 1995. To examine the time trend, we divided the cohort into two groups: 285 patients diagnosed between 1965 and 1969 (65–69 cohort) and 769 patients diagnosed between 1975 and 1979 (75–79 cohort). Survival analysis was performed using the Kaplan–Meier method. Cox proportional hazard models were used to assess the demographic characteristics.


Blindness developed in 60 subjects in the 65–69 cohort and 15 subjects in the 75–79 cohort. The incidence of blindness in the 75–79 cohort was significantly lower than that in the 65–69 cohort (p<0.0001). In spite of no change in the use of laser photocoagulation in the 75–79 cohort compared with the 65–69 cohort, the hazard ratio for the blindness in those who received laser photocoagulation in the 75–79 cohort decreased significantly to 0.55 (p<0.01) compared with those in the 65–69 cohort when adjusted for the age of onset, sex, and time of diagnosis.


The incidence of blindness decreased significantly for the subjects diagnosed more recently. The change in quality and the earlier introduction of laser photocoagulation might have contributed to the decreased incidence of blindness observed over time.

  M Kuroda Morimoto , H Tanaka , N Hayashi , M Nakahira , Y Imai , M Imamura , K Yasuda , S Yumikura Futatsugi , K Matsui , T Nakashima , K Sugimura , H Tsutsui , H Sano and K. Nakanishi

We previously reported that intranasal challenge with ovalbumin (OVA) plus IL-18 induces airway hyperresponsiveness (AHR) and eosinophilic airway inflammation in mice with OVA-specific Th1 cells. These two conditions can be prevented by neutralizing anti-IFN- and anti-IL-13 antibodies, respectively. The mice develop AHR and eosinophilic airway inflammation after challenge with OVA plus LPS instead of IL-18 and endogenous IL-18 is known to be involved. In contrast, IL-18 does not facilitate these changes in mice possessing OVA-specific Th2 cells. Here, we investigated whether IL-18 is involved in the development of asthma in mice immunized and challenged with bacterial proteins. Upon intranasal exposure to protein A (SpA) derived from Staphylococcus aureus, mice immunized with SpA exhibited AHR and peribronchial eosinophilic inflammation if IFN- or IL-13 were present, respectively. The CD4+ T cells from draining lymph nodes (DLNs) of the SpA-immunized and -challenged mice produced a robust IFN- and IL-13 in response to immobilized anti-CD3 antibodies. Treatment with neutralizing anti-IL-18 antibodies prevented asthmatic inflammation concomitant with their impaired potential to express IFN- and IL-13. Furthermore, naive mice that received the CD4+ T cells from DLNs of SpA-immunized mice developed airway inflammation depending upon the presence of IL-18. Immunodeficient mice that received human PBMCs, which had been stimulated with SpA in vitro, developed dense peribronchial accumulation of human CD4+ T cells upon SpA challenge. Neutralizing anti-human IL-18 antibodies protected against this airway inflammation. These results suggest the importance of IL-18 for the development of asthmatic inflammation associated with airway exposure to bacterial proteins.

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