[Leukomycin resistance of staphylococci].
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Biomedical subjects
Publications and source records attributed to M Kono.
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We examined critical duration for visual acuity in eyes with central serous retinopathy (CSR), macular edema (ME) and glaucoma. Critical duration for visual acuity is the minimum period of time to perceive the acuity chart of his best. Visual acuity was measured at several limited exposure durations and the results were then compared with that of normal eyes. The acuity target was a single Landolt ring. The size, direction, and exposure duration of the target were computer controlled. The mean critical duration for visual acuity of the CSR and ME groups was 1.78 s and 2.69 s. These were significantly longer than that of the normal group (0.62 s). The critical duration of the glaucoma group was 0.42 s, which was not significantly prolonged. Critical duration for the increment or static threshold was measured for the purpose of comparison, and no significant differences were found between the diseased eyes (the CSR and ME groups) and the normal eyes, although the thresholds were significantly higher in the diseased eyes. Next, fixation movements which occurred during visual acuity testing were observed in order to investigate their role in acuity testing. In both normal and ME eyes the frequency and amplitude of microsaccades were smaller while the visual acity chart was shown. This suggests that microsaccades play no positive role in the reading of acuity charts, and that they bear little relation to the phenomenon of critical duration for visual acuity. From these results we hypothesized that in the CSR and ME groups the X-type ganglion cells send incomplete information to the central neural system. Thus, a longer time is required to obtain complete information before responding. Furthermore, one glaucoma case suggested that in diseased eyes in which mainly the Y-cell systems are damaged, temporal specificity in visual acuity for shorter exposure duration may reveal different response patterns.
To prevent embolization of necrotic renal vein tumor after transcatheter embolization of a left renal cell carcinoma, we placed a suprarenal Bird's nest inferior vena cava filter. The patient tolerated the procedure well and had extensive tumor infarction including the tumor thrombus on 6-month follow-up computed tomography.
Successful treatment was achieved for a patient with superior mesenteric artery thromboembolism concomitant with bilateral renal artery thromboembolism. Thrombi of the three vessels were lysed simultaneously with a three-catheter technique using short-term, high-dose urokinase followed by overnight infusion with low-dose urokinase.
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Tetracycline-resistance (TCr) plasmid pTP-5 (4.46 kb) from Staphylococcus aureus was cleaved with HindIII into three fragments: A (2.35 kb), B (1.57 kb) and C (0.54 kb). A deletion plasmid (3.92 kb) lacking HindIII-C fragment was obtained, and was designated pNS1. This plasmid retained the TCr phenotype and the ability to replicate autonomously in Bacillus subtilis. A restriction endonuclease cleavage map of pNS1 was constructed. Attempts to construct smaller plasmids by digesting pNS1 with BAL31 nuclease led to production of a set of deletion derivatives whose molecular sizes range from 3.75 to 2.77 kb. Through analyses of these derivatives, the regions essential for autonomous replication and expression of TCr were deduced.
Heparin inhibited haemagglutination by porcine reproductive and respiratory syndrome virus (PRRSV) and by Aujesky's disease virus, but failed to inhibit haemagglutination by parainfluenza virus type 3. The minimal inhibitory concentration of heparin required to inhibit 8 HA U of PRRSV haemagglutinin ranged from 0.1 to 1 U ml-1. Mouse erythrocytes failed to combine with the haemagglutination inhibitory factor of heparin. However, mouse erythrocytes treated with heparinase had greatly reduced agglutinability by PRRSV. The formation of a haemagglutinin-heparin complex could be observed by sedimenting heparin with the haemagglutinin. All these findings suggest that a heparin-like molecule on the surface of mouse erythrocytes serves as the virus-cell receptor.
The visual pigment from the ultraviolet (UV) cone photoreceptor of the tiger salamander has been cloned, expressed, and characterized. The cDNA contains a full-length open reading frame encoding 347 amino acids. The phylogenetic analysis indicates that the highest sequence homology is to the visual pigments in the S group. The UV opsin was tagged at the carboxy-terminus with the sequence for the 1D4 epitope. This fusion opsin was expressed in COS-1 cells, regenerated with 11-cis retinal (A1) and immuno-purified, yielding a pigment with an absorbance maximum (lambdamax) of 356 nm which is blue shifted from the absorption of retinal itself. The transducin activation assay demonstrated that this pigment is able to activate rod transducin in a light-dependent manner. Regeneration with 11-cis 3,4-dehydroretinal (A2) yielded a pigment with a lambdamax of 360 nm, only 4 nm red shifted from that of the A1 pigment, while bovine rhodopsin generated with A2 showed a 16-nm red shift from the corresponding A1 pigment. These results demonstrate that the trend for a shorter wavelength pigment to have a smaller shift of lambdamax between the A1 and A2 pigments also fits UV pigments. We hypothesize that the small red shift with A2 could be due to a twist in the chromophore that essentially isolates the ring double bond(s) from conjugation with the rest of the polyene chain.
PURPOSE: Surprisingly, an important characteristic of astigmatism has been overlooked by ophthalmic and clinical scientists. Apparently, refractive astigmatism is due largely to a form of high spatial frequency image distortion. METHODS: Characteristic astigmatic image distortion can be minimized or eliminated by using a low-pass spatial filter (here, a ground glass plate was employed for this purpose). The ground glass is placed a short distance in front of a visual acuity chart, or it may be used with other tests, such as vernier acuity. RESULTS: This test has been performed by us on large numbers of patients and test subjects. A clinician can try this test for himself/herself. Place a +2.00 D.C. (any axis) lens in front of the eye; the usual distortions will be observed. Locate the ground glass plate as described. The usual distortions associated with the conoid of Stürm will not be visible or will be virtually eliminated, although some image blur will remain. CONCLUSIONS: This technique has significance, e.g., in visual screening programs in developing nations, or in assessing patients with media disorders prior to ophthalmic surgery.