Epidemiological trends of imported infectious diseases in Japan: Analysis of imported 2-year infectious disease registry data

IntroductionThe epidemiology of infectious diseases in Japan remains undefined despite the increasing tourism. GeoSentinel, an epidemiological surveillance system for reporting imported infectious diseases, has only two participating facilities in Japan. Although the number of infectious diseases is reported by the National Institute of Infectious Diseases, there is no detailed clinical information about these cases. Therefore, we established J-RIDA (Japan Registry for Infectious Diseases from Abroad) to clarify the status of imported infectious diseases in Japan and provide detailed information.MethodsJ-RIDA was started as a registry of imported infectious diseases. Case registration began in October 2017. Between October 2017 and September 2019, 15 medical institutions participated in this clinical study. The registry collected information about the patient's age, sex, nationality, chief complaint, consultation date, date of onset, whether visit was made to a travel clinic before travel, blood test results (if samples were collected), travel history, and final diagnosis.ResultsOf the 3046 cases included in this study, 46.7% to Southeast Asia, 13.0% to Africa, 13.7% to East Asia, 11.5% to South Asia, 7.5% to Europe, 3.8% to Central and South America, 4.6% to North America, 3.9% to Oceania, and 2.8% to Central and west Asia. More than 85% of chief complaints were fever and general symptoms, gastrointestinal symptoms, respiratory symptoms, or dermatologic problems. The most common diseases were travelers’ diarrhea, animal bite, upper respiratory infection, influenza, and dengue fever.ConclusionsWe summarized two-year cases registered in Japan's imported infectious disease registry. These results will significantly contribute to the epidemiology in Japan.     

Improvement in physiological outcomes and health-related quality of life following cardiac rehabilitation in patients with acute myocardial infarction.

BACKGROUND: The present study examined the impact of an 8-week cardiac rehabilitation (CR) program on physiological outcomes and health-related quality of life (HRQOL) of patients with acute myocardial infarction (AMI). METHODS AND RESULTS: A total of 124 consecutive AMI patients were divided into a supervised outpatient CR group (n=82) and a non-CR group as a control (n=42). Peak oxygen uptake, handgrip strength, and knee extension muscular strength were used as physiological outcome measures. HRQOL outcomes were assessed by the Medical Outcome Study Short Form 36 (SF-36). CR group patients performed both aerobic exercise and moderate resistance training from 1 month (T1) to 3 months (T2) after AMI onset. Age, sex, body mass index, medications, and ejection fraction were similar in both groups. Significantly greater increases in overall physiological outcomes from T1 to T2 were measured in the CR group compared with those of the non-CR group. There were also significantly greater improvements in 4 of the 8 SF-36 health status subscales (physical functioning, role-physical, general health, and vitality) in the CR group compared with the non-CR group. CONCLUSIONS: Eight weeks of exercise training have specific effects on improvement in HRQOL and physiological outcomes in Japanese patients.     

Molecular basis of hereditary methaemoglobinaemia, types I and II: two novel mutations in the NADH-cytochrome b5 reductase gene

Hereditary methaemoglobinaemia, caused by deficiency of NADH-cytochrome b₅ reductase (b5R), has been classified into two types, an erythrocyte (type I) and a generalized (type II). We analysed the b5R gene of two Thai patients and found two novel mutations. The patient with type II was homozygous for a C-to-T substitution in codon 83 that changes Arg (CGA) to a stop codon (TGA), resulting in a truncated b5R without the catalytic portion. The patient with type I was homozygous for a C-to-T substitution in codon 178 causing replacement of Ala (GCG) with Val (GTG). To characterize effects of this missense mutation, we investigated enzymatic properties of mutant b5R (Ala 178 Val). Although the mutant enzyme showed normal catalytic activity, less stability and different spectra were observed. These results suggest that this substitution influenced enzyme stability due to the slight change of structure. In conclusion, the nonsense mutation led to type II because of malfunction of the truncated protein. On the other hand, the missense mutation caused type I, due to degradation of the unstable mutant enzyme with normal activities in patient's erythrocytes, because of the lack of compensation by new protein synthesis during the long life-span of erythrocytes.