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Seasonal variations in environmental conditions lead to changing infectious disease epidemic risks at different times of year. The probability that early cases initiate a major epidemic depends on the season in which the pathogen enters the population. The instantaneous epidemic risk (IER) can be tracked. This quantity is straightforward to calculate, and corresponds to the probability of a major epidemic starting from a single case introduced at time t=t0, assuming that environmental conditions remain identical from that time onwards (i.e. for all t≥t0). However, the threat when a pathogen enters the population in fact depends on changes in environmental conditions occurring within the timescale of the initial phase of the outbreak. For that reason, we compare the IER with a different metric: the case epidemic risk (CER). The CER corresponds to the probability of a major epidemic starting from a single case entering the population at time t=t0, accounting for changes in environmental conditions after that time. We show how the IER and CER can be calculated using different epidemiological models (the stochastic Susceptible-Infectious-Removed model and a stochastic host-vector model that is parameterised using temperature data for Miami) in which transmission parameter values vary temporally. While the IER is always easy to calculate numerically, the adaptable method we provide for calculating the CER for the host-vector model can also be applied easily and solved using widely available software tools. In line with previous research, we demonstrate that, if a pathogen is likely to either invade the population or fade out on a fast timescale compared to changes in environmental conditions, the IER closely matches the CER. However, if this is not the case, the IER and the CER can be significantly different, and so the CER should be used. This demonstrates the need to consider future changes in environmental conditions carefully when assessing the risk posed by emerging pathogens.

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Two Japanese sisters with persistent uveitis showed significant increased levels of urinary beta-2 microglobulin. A percutaneous renal biopsy performed in the younger sister revealed tubulointerstitial nephritis (TIN) with helper/inducer T cell infiltrates. Also, abnormal 67-gallium accumulation in the kidneys, suggesting TIN, was observed in the other one at the same time. Although patients with the syndrome of tubulointerstitial nephritis and uveitis (TINU) have been reported to date, its occurrence in siblings has rarely been seen. Both of them shared same human leukocyte antigen (HLA) DR6, suggesting the potential association between HLA-DR6 and TINU.

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PURPOSE: To understand the effect of the error in corneal refractive power on the optically calculated axial length (AXO) and the postoperative predicted refraction (Q'gl) calculated from the aphakic refraction (Qaph). METHOD: We used the Gullstrand's schematic eye, in which the intraocular lens (+20 D) was inserted at a depth of 5 mm, and calculated Qaph and postoperative refraction (Qgl) geometrically when the corneal radius of the anterior surface (Rfc) changed from 7 mm to 9 mm. AXO was calculated using the calculation formula from a previous report, and then Q'gl was calculated from the AXO and the true axial length (AXT) using the theoretical calculation formula (regarding the fictitious corneal refractive index as 1.3315). RESULTS: When the measured corneal radius of the anterior surface (K) was equal to Rfc, the error of the AXO was largest (AXO/AXT = 101.512) when K was 9 mm. The error in power prediction (Qgl-Q'gl) of the AXT was 7.7 times larger than that of AXO. CONCLUSION: If K is exact, AXO is useful to predict the intraocular lens depth because the error of AXO is small. The error in power prediction of AXO is smaller than that of AXT.

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PURPOSE: Postoperative refraction was calculated using aphakic refraction measured with intraoperative retinoscopy, and its clinical usefulness was investigated statistically. OBJECTS AND METHODS: We studied 115 eyes of 89 patients, 28 males and 61 females aged 35 to 90 years, who had received intracapsular insertion of an intraocular lens. To decrease the error in measuring, retinoscopy was performed after the attachment of a hard contact lens of +15 D to the patient's cornea, with the exclusion of high myopia. We modified the Haigis calculation and used it to predict the postoperative refraction. RESULTS: The refraction could be measured in 112 eyes. The mean error between the actual and the predicted (actual minus predicted) in 112 eyes was 0.40 +/- 1.05 (mean +/- standard deviation) D. The mean error calculated using the SRK-II method, the Binkhorst method, and the Holladay method was -0.09 +/- 1.13 D, -0.58 +/- 1.00 D, and -0.44 +/- 1.00 D, respectively. The mean error of the average of these three formulas and our method was 0.15 +/- 0.82 D, -0.09 +/- 0.83 D, and -0.02 +/- 0.82 D, respectively. CONCLUSION: Our method seemed to have the same accuracy as other calculation formulas. By using our method together with other formulas, the postoperative refraction could be predicted more accurately.

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Patients with central serous chorioretinopathy noticed that a part of the visual field became light for a few seconds when half of the visual field was covered in front of the eye. We devised a stenopeic flicker test (s-f test) to elicit this phenomenon continuously, and evaluated the clinical usefulness. We examined 17 eyes with central serous chorioretinopathy using the s-f test and Amsler grid test. Retinal abnormality was detected in 17 of 17 eyes with the s-f test and 14 of 17 eyes with the Amsler grid test. In detecting the extent of the retinal detachment on fluorescein angiograms, the s-f test (p < 0.0001, r = 0.842) was more precise than the Amsler grid test (p < 0.0003, r = 0.506). These results suggest that the s-f test is useful to detect retinal abnormality and to grasp the extest of the retinal detachment in central serous chorioretinopathy.

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Using the serum-soft agar technic of Staphylococcus epidermidis typing, an epidemiologic study of pollution with S. epidermidis in the tuberculosis and pediatric wards of a hospital was conducted. Specimen samples were taken from 334 locations, including beds, bedspreads, pillows, doors and window knobs, chairs, tables, and incubators of premature infants. These were cultured on Staphylococcus 110 medium and the strains identified as S. epidermidis were obtained. Of the strains from both patients' rooms and the nurses' station in the tuberculosis ward a considerable number were of serotype 53, suggesting an interrelationship of this organism and these locations. In the rooms of newborns and premature infants in the pediatric ward, 55.5% of the strains of S. epidermidis isolated were of the serotype 53/408, indicating a high degree of pollution of these environments with these serotype strains.

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Of 91 compact-type strains of Staphylococcus aureus in regular serum soft agar (SSA), 82 converted diffuse-type growth in serum soft agar (pH adjusted to 6.0). With the addition of four different rabbit anticapsular sera (anti-type A, B, C, and D sera) in low pH (6.0) SSA, 21 strains of S. aureus showed compact-type colonial morphologies. Eleven, one, and one strains of S. aureus reacted singly with rabbit anticapsular sera types A, B, and C, respectively, and no strain reacted with rabbit anticapsular type D. Eight of the e strains reacted with both rabbit anticapsular sera types A and B. When the ability to absorb the converting activities of the antisera (changes of colonial morphologies of anticapsular sera in SSA) was quantitatively tested, 7- to 27-fold of these organisms were capable of absorbing the activities compared with the Smith diffuse organisms. These results suggest that even unencapsulated S. aureus strains are capable of producing capsular substance, although the capability is quantitatively different from strain to strain.

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