Interdecadal changes in the community, population and individual levels of the fish fauna of an extensively modified estuary.

This study examined inter-period changes over two to three decades in the fish fauna of an urbanized estuary experiencing rapid population growth and a drying climate (Swan-Canning Estuary, Western Australia). Responses were compared at the fish community level (species composition; 1978-2009 in the shallows and 1993-2009 in deeper waters) and at the population and individual levels of an estuarine indicator species, black bream Acanthopagrus butcheri (biomass-abundance and per capita mass at age, respectively; 1993-2009). All three levels showed distinct shifts from earlier to later periods, but their patterns, sensitivity and breadth differed. Community composition changed markedly in the shallows of the lower-middle estuary between the late 1970s and all later periods and moderately between more disparate periods from 1995 to 2009. Several species trends could be linked to the increasing salinity of the estuary or declining dissolved oxygen levels in its middle-upper reaches. Community changes were, however, small or insignificant in the shallow and deeper waters of the upper estuary and deeper waters of the middle estuary, where environmental perturbations are often most pronounced. This may reflect the resilience of the limited suite of species that typify those reaches and thus their lack of sensitivity in reflecting longer-term change at the coarser level of mean abundance. One such species, the selected indicator, A. butcheri, did, however, show marked temporal changes at both the population and individual levels. Biomass decreased markedly in deeper waters while increasing in the shallows from earlier to later periods, presumably reflecting an onshore movement of fish, and per capita body mass in the 2+, 3+ and 4+ year classes fell steadily over time. Such changes probably indicate deteriorating habitat quality in the deeper waters. The study outcomes provide support for a multifaceted approach to the biomonitoring of estuaries using fishes and highlight the need for complementary monitoring of relevant stressors to better disentangle cause-effect pathways.

Ocular herpes simplex virus reactivation in mice latently infected with latency-associated transcript mutants.

A mouse model for ocular reactivation of herpes simplex virus type 1 (HSV-1) was modified and used to study the effect of strain difference on the frequency of ocular HSV reactivation. Outbred male NIH white mice were immunized with 1.0 ml of anti-HSV serum with a neutralizing titer of 1:400 24 hr before infection and bilaterally infected at 10(5) plaque-forming units/eye with one of three HSV-1 strains: 17 Syn+, LAT+ (XC-20), or LAT- (X10-13). Latency-associated transcripts (LAT) are produced by strain 17 Syn+ and LAT+ but not by LAT-. The primary infection was monitored by ocular swabbing for HSV. Reactivation was induced by intravenous (i.v.) injection of cyclophosphamide (5 mg) followed 24 hr later by i.v. dexamethasone (0.2 mg). These drugs significantly reduced the white cell count between 0 and 6 days post-administration. The eyes were swabbed for 7 consecutive days to monitor reactivation, and HSV-1 reactivation was induced at the following frequencies in individual eyes: 17 Syn+ (32.5%), LAT+ (18.5%), and LAT- (2.5%) (P less than or equal to 0.002). Co-culture of trigeminal ganglia was done, and random isolates were checked to ascertain their identity. The HSV was recovered from individual trigeminal ganglia at the following frequencies: 17 Syn+ (83%), LAT+ (100%), and LAT- (67%) (P less than or equal to 0.091). These results confirm that the mouse can be used as a reactivation model for ocular HSV infection and that the presence of LAT facilitates reactivation in vivo in the mouse.

Vitrectomy in endophthalmitis. Results of study using vitrectomy, intraocular antibiotics, or a combination of both.

A rabbit model of endophthalmitis was produced by inoculating Staphylococcus epidermidis and S aureus into the vitreous cavity. Elimination of microorganisms was compared using intravitreal administration of 0.1 mg of gentamicin alone, vitrectomy alone, and a combination of gentamicin and vitrectomy. In the case of S. epidermidis treated 24 hours after inoculation, all untreated eyes were culture-positive at one week, eyes treated with gentamicin alone or intravitreal gentamicin in combination with vitrectomy were all culture-negative, and vitrectomy alone rendered half of the eyes culture-negative. In the case of S aureus, eyes not treated by vitrectomy alone were all culture-positive at one week. Eyes treated with intravitreal gentamicin 25 to 31 hours after infection were culture-negative for S aireus in 33% at one week, while eyes treated with combined vitrectomy plus intraocular gentamicin were culture-negative in 83% of cases. When treatment was delayed 40 to 49 hours after inoculation of S aureus, intravitreal rendered 50% culture-negative at one week, while vitrectomy combined with intravitreal gentamicin eliminated the infection in 100% of eyes.

Further observations on the diagnosis cause, and treatment of endophthalmitis.

In our study of 54 suspected cases of endophthalmitis, vitreous aspiration was more sensitive in making a culture-proven diagnosis than anterior chamber paracentesis; Staphylococcus epidermidis was a more common cause of endophthalmitis than previously appreciated; and intraocular antibiotics in the recommended dosage are reasonably safe clinically and add a new dimension to the treatment of endophthalmitis.

Corneal aberrations and visual performance after radial keratotomy.

BACKGROUND: Refractive surgery and videokeratography have allowed us to study the effects on visual performance of relatively large changes in corneal aberration structure induced by surgical changes in corneal shape. METHODS: We quantified in one eye of nine normal and 23 radial keratotomy patients, the area under the log contrast sensitivity function (AULCSF) and corneal first surface wavefront variance for two artificial pupil sizes (3 and 7 mm). Contrast sensitivity was measured with sine-wave gratings at six spacial frequencies. Wavefront variance was derived from videokeratographs using Zernike polynomials. RESULTS: For normals eyes there were no significant changes over time. For eyes that had radial keratotomy, there were significant pupil size-dependent changes. For the 3 mm pupil, there were significant surgery-induced changes in the corneal wavefront variance which became large (approximately 30 times preoperative values) at 7 mm. Significant correlated changes in AULCSF for the 7 mm pupil but not for the 3 mm pupil occurred immediately following surgery and remained. CONCLUSIONS: Radial keratotomy, like photorefractive keratectomy, shifts the distribution of aberrations from third order dominance (coma-like aberrations) to fourth order dominance (spherical-like aberrations). Radial keratotomy-induced aberrations and loss in contrast sensitivity are reduced with increasing clear zone diameter. Radial keratotomy induces an increase in the optical aberrations of the eye and the increase for large pupils (7 mm) but not small (3 mm) is correlated to a decrease in contrast sensitivity.

Kinetic studies of immobilized alpha-chymotrypsin in apolar solvents.

The mechanism of alpha-chymotrypsin action has been probed by extending studies of native chymotrypsin to immobilized chymotrypsin, where the organic content of the solution can be raised to much higher levels and thus one can explicitly look at the role of water. When one does this, one finds that water only appears in the deacylation reaction. The premise that one can go from native chymotrypsin (souble) to immobilized chymotrypsin (insoluble) has been tested by several criteria. It has been found in many instances that the two are identical: in absolute rate, in pKa. They are, however, not identical to one another in binding, due to differences in diffusion, which is to be expected. Thus, mechanistically immobilized and native chymotrypsin are identical to one another and the use of immobilized chymotrypsin can be used to specify the mechanism even more: it must proceed through two tetrahedral intermediates and two acyl-enzyme intermediates.

Further observations on the diagnosis, etiology, and treatment of endophthalmitis.

This report of 54 suspected cases of endophthalmitis emphasizes the following findings: 1. That vitreous aspiration is more sensitive in making a culture proven diagnosis than anterior chamber paracentesis. 2. That Staphylococcus epidermidis is a much more common cause of endophthalmitis than previously apprediated. 3. That intraocular antibiotics in the recommended dosage, are reasonably safe clinically and add a new dimension to the treatment of endophthalmitis.

Comparison of serological and bacteriological methods in the confirmation of plague infections.

A recent, defined outbreak of bubonic plague in a remote area of the central highlands of Viet-Nam provided an opportunity to undertake studies of antibody production during the course of infections with Pasteurella pestis (Yersinia pestis). The haemagglutination (HA) test of Chen & Meyer, modified to a microtechnique, was used in studies of patients with clinical plague, and in studies of unvaccinated, asymptomatic contacts of plague patients.HA antibody was demonstrated in the sera of nearly 45% of the unvaccinated, asymptomatic contacts of plague patients, and a large proportion of these exhibited 4-fold or greater rises in titre during the outbreak. In 6 of the 16 clinical plague cases, the diagnosis could not be confirmed by bacteriological methods; however, 5 of the 6 exhibited HA antibody in sera collected on admission or in second sera collected 9-14 days later or in both. Of the 5 with positive sera, 4 had very mild clinical illnesses (pestis minor). These findings were in sharp contrast to those among the 8 surviving, bacteriologically confirmed cases, most of whom had clinically very severe illnesses. Only 1 of the 8 had demonstrable plague HA antibody in acute and early convalescent sera; however, all of the latter on whom follow-up studies could be obtained exhibited HA antibody in sera collected 1-1(1/2) months later.These findings indicate that natural active immunization with P. pestis was occurring during the outbreak, and further, that developing immunity from earlier subclinical infections may have accounted for amelioration of clinical signs and symptoms, as well as for failure to isolate P. pestis in patients with pestis minor.HA tests may be particularly useful in confirming the diagnosis of plague if employed with sera collected 3-6 weeks after the onset of illness. The HA test would appear also to provide a highly reliable tool in surveys for plague in areas of unknown endemicity.

Further evidence of exclusion of linkage between type II autosomal dominant retinitis pigmentosa (ADRP) and D3S47 on 3q.

Linkage of the anonymous DNA marker D3S47 (CRI-C17) and autosomal dominant retinitis pigmentosa (ADRP) was tested in a large, extended family with type II (late onset) ADRP. D3S47 has been shown previously to be tightly linked to the RP locus in one family with type I (early onset) ADRP (McWilliams et al., 1989, Genomics 5: 619-622). Linkage between ADRP type II and D3S47 has recently been excluded in a single family (Ingelhearn et al., 1990, Genomics 6: 168-173). Results of our linkage analysis clearly establish that type II ADRP in our family is unlinked to D3S47. These findings support the hypothesis that type II ADRP is genetically distinct from type I ADRP.

Linkage mapping of autosomal dominant retinitis pigmentosa (RP1) to the pericentric region of human chromosome 8.

Linkage mapping in a large, seven-generation family with type 2 autosomal dominant retinitis pigmentosa (ADRP) demonstrates linkage between the disease locus (RP1) and DNA markers on the short arm of human chromosome 8. Five markers were most informative for mapping ADRP in this family using two-point linkage analysis. The markers, their maximum lod scores, and recombination distances were ANK1 (ankyrin)--2.0 at 16%; D8S5 (TL11)--5.3 at 17%; D8S87 [a(CA)n repeat]--7.2 at 14%; LPL (lipoprotein lipase)--1.5 at 26%; and PLAT (plasminigen activator, tissue)--10.6 at 7%. Multipoint linkage analysis, using a simplified pedigree structure for the family (which contains 192 individuals and two inbreeding loops), gave a maximum lod score of 12.2 for RP1 at a distance 8.1 cM proximal to PLAT in the pericentric region of the chromosome. Based on linkage data from the CEPH (Paris) reference families and physical mapping information from a somatic cell hybrid panel of chromosome 8 fragments, the most likely order for four of these five loci and the diseases locus is 8pter-LPL-D8S5-D8S87-PLAT-RP1. (The precise location of ANK1 relative to PLAT in this map is not established). The most likely location for RP1 is in the pericentric region of the chromosome. Recently, several families with ADRP with tight linkage to the rhodopsin locus at 3q21-q24 were reported and a number of specific rhodopsin mutations in families with ADRP have since been reported. In other ADRP families, including the one in this study, linkage to rhodopsin has been excluded. Thus mutations at two different loci, at least, have been shown to cause ADRP. There is no remarkable clinical disparity in the expression of disease caused by these different loci.