@article{gift_english_nadelstein_weigt_gilger_2009, title={Comparison of capsular opacification and refractive status after placement of three different intraocular lens implants following phacoemulsification and aspiration of cataracts in dogs}, volume={12}, ISSN={1463-5216 1463-5224}, url={http://dx.doi.org/10.1111/j.1463-5224.2009.00667.x}, DOI={10.1111/j.1463-5224.2009.00667.x}, abstractNote={OBJECTIVE To evaluate the effect of lens design and biomaterial on formation of posterior capsular opacification (PCO) and refractive correction. Animals studied Sixty dogs undergoing bilateral phacoemulsification for mature or diabetic cataracts. PROCEDURES One randomly selected eye received a rounded edge 41D polymethyl-methacrylate (PMMA) intraocular replacement lens (IOL) and the contralateral eye received either a squared edge 41D hydrophilic acrylic IOL (n = 35) or a squared edge 40D hydrophobic acrylic IOL (n = 25). At the (mean = 79 day) reexamination period, PCO was graded using direct slit-lamp observation and by masked observer evaluation of digital images of the IOLs. Streak retinoscopy and B-mode ultrasound were performed at this period. RESULTS The PCO score via direct slit-lamp was significantly lower for the hydrophilic acrylic IOL when compared to the PMMA IOL. Masked observer evaluation of digital images revealed that the acrylic IOLs had lower but generally not statistically significant PCO scores than the PMMA IOLs. Streak retinoscopy showed that the PMMA IOL was significantly closer to emmetropia (+0.44 D) when compared to either the hydrophilic acrylic (+0.96 D) or the hydrophobic acrylic (+1.2 D) IOLs. B-mode ultrasonography revealed the center of the hydrophilic acrylic IOL is 0.31 mm closer to the retina and the center of the hydrophobic acrylic IOL is 0.63 mm further from the retina when compared to the center of the PMMA to retina distance. CONCLUSIONS Square edged foldable acrylic IOLs show a predisposition towards generating slightly less PCO than round edged PMMA IOLs in the early postoperative period, however, both acrylic IOLs had greater persistent hyperopia than the PMMA IOLs.}, number={1}, journal={Veterinary Ophthalmology}, publisher={Wiley}, author={Gift, Barrett W. and English, Robert V. and Nadelstein, Brad and Weigt, Anne K. and Gilger, Brian C.}, year={2009}, month={Jan}, pages={13–21} } @article{ghosh_engelsberg_english_petters_2007, title={Long-term neuroretinal full-thickness transplants in a large animal model of severe retinitis pigmentosa}, volume={245}, ISSN={["1435-702X"]}, DOI={10.1007/s00417-006-0437-9}, abstractNote={The purpose of this study was to explore neuroretinal transplantation in a large animal model of severe retinitis pigmentosa and to establish graft development, long-term survival, graft-host integration, and effects on the host retina. Rhodopsin transgenic pigs, aged 6 months, received in one eye a fetal full-thickness neuroretinal sheet in the subretinal space by means of vitrectomy and retinotomy. Six months postoperatively, eyes were studied in the light microscope and with immunohistochemical markers. Full-field electroretinography (ERG) was performed at 4 and 6 months. Laminated grafts with well-organized photoreceptors, rod bipolar cells, and Müller cells were found in five of six eyes. Neuronal connections between graft and host retina were not seen. In the five eyes containing a graft, the number of surviving rods in the host retina was significantly higher compared with unoperated eyes. The ERG did not reveal any significant difference in b-wave amplitude between operated and control eyes, but the cone-derived response in operated eyes increased significantly from 4 to 6 months while the rod response in control eyes decreased significantly. Fetal full-thickness neuroretina can be transplanted safely to an eye with severe retinal degeneration. In their major part, the transplants develop a normal laminated morphology and survive for at least 6 months. Graft and host retinal neurons do not form connections. Retinal function in the host is reduced initially by the surgical trauma, but the presence of a well-laminated graft counteracts this effect and rescues rods from degeneration.}, number={6}, journal={GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY}, author={Ghosh, Fredrik and Engelsberg, Karl and English, Robert V. and Petters, Robert M.}, year={2007}, month={Jun}, pages={835–846} } @article{hess_english_hegarty_brown_breitschwerdt_2006, title={Experimental Ehrlichia canis infection in the dog does not cause immunosuppression}, volume={109}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2005.07.027}, abstractNote={A carrier state develops in some Ehrlichia canis-infected dogs due to ineffective host defenses. The subsequent development of immune-mediated diseases or opportunistic infections in chronic ehrlichiosis suggests dysregulation of immunity; however, the immunobiology of this infection has not been well characterized. In this study, eight dogs were infected with E. canis, and changes in seroreactivity, serum immunoglobulin (Ig) concentrations, peripheral blood T cell subsets, lymphocyte blastogenesis (LBT), and lymphokine-activated killer (LAK) activity were evaluated over 4 months. Infection, which was documented by seroconversion, polymerase chain reaction, and blood culture, caused self-limiting fever and thrombocytopenia. Infected dogs developed an anti-E. canis antibody response but were not immune to re-infection. Serum IgM, IgG, and IgA concentrations were unaffected by E. canis. The percentage of circulating CD4+ T cells was similar in uninfected and infected dogs at all points. Infected dogs developed a CD8+ lymphocytosis 6 weeks after inoculation that subsequently subsided, despite organism persistence. Functional defects of cell-mediated immunity, measured as suppression of LAK activity or mitogen-driven LBT, were not observed. These results suggest that immune responses are not grossly impaired in young dogs during the first several months following experimental E. canis infection.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Hess, PR and English, RV and Hegarty, BC and Brown, GD and Breitschwerdt, EB}, year={2006}, month={Jan}, pages={117–125} } @article{hendrix_rohrbach_bochsler_english_2004, title={Comparison of histologic lesions of endophthalmitis induced by Blastomyces dermatitidis in untreated and treated dogs: 36 cases (1986-2001)}, volume={224}, ISSN={["0003-1488"]}, DOI={10.2460/javma.2004.224.1317}, abstractNote={OBJECTIVE To compare prevalence of organisms and histologic changes in eyes from dogs with blastomycosis that were either untreated or undergoing treatment with itraconazole. DESIGN Retrospective study. ANIMALS 36 dogs with endophthalmitis associated with blastomycosis. PROCEDURE Signalment, results of ophthalmic examination, and duration of treatment with itraconazole were extracted from medical records. Histologic sections from eyes were examined for prevalence and viability (ie, budding) of fungal organisms. A scoring system was devised to assess the degree of inflammation. RESULTS Clinically, all eyes were blind and had signs of severe endophthalmitis. Histologically, the type and degree of inflammation and prevalence of Blastomyces dermatitidis were not significantly different between dogs treated with itraconazole and untreated dogs or among groups of dogs treated for different time periods (4 to 14, 15 to 28, or 29 to 72 days). Replication of the organisms in vascular tissues as well as avascular spaces in the eyes was similar in treated and untreated dogs. Lens rupture was seen in 12 of 29 (41%) eyes. CONCLUSIONS AND CLINICAL RELEVANCE Persistence of inflammation in eyes of dogs with naturally occurring blastomycosis is likely attributable to the continued presence of B. dermatitidis, regardless of the duration of treatment with itraconazole. Lens capsule rupture, a common and previously unreported histologic finding, may contribute to cataract formation and continued inflammation.}, number={8}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Hendrix, DVH and Rohrbach, BW and Bochsler, PN and English, RV}, year={2004}, month={Apr}, pages={1317–1322} } @article{butterworth_english_jordan_tompkins_2001, title={Distribution of immune cells in the female reproductive tract in uninfected and FIV infected cats}, volume={83}, ISSN={["0165-2427"]}, DOI={10.1016/S0165-2427(01)00371-3}, abstractNote={Cell-free and cell-associated FIV effectively cross the mucosa of the feline female reproductive tract. To identify possible cellular targets of FIV and to characterize changes in mucosal immunity after infection, we examined the types and numbers of immune cells residing in the reproductive tracts of control and intravaginally FIV-infected cats. Sections of the vestibule, vagina, cervix, uterus, and ovaries, were examined by immunohistochemistry for CD4+ and CD8+ T lymphocytes, CD22+ B lymphocytes, CD1a+ dendritic cells, and CD14+ macrophages. The reproductive tract of uninfected cats contained substantial numbers of CD8+ T lymphocytes, CD4+ T lymphocytes and macrophages, as well as moderate numbers of CD1a+ dendritic cells, and few B lymphocytes. The most prominent change between FIV- and FIV+ cats was a marked decrease in the concentration of CD4+ T lymphocytes resulting in inverted CD4+:CD8+ ratios throughout the reproductive tract of infected cats. There was also a trend towards increasing numbers of CD1a+ dendritic cells in the intravaginally-infected FIV+ cats, and decreasing numbers of macrophages and CD22+ B lymphocytes. This study indicates that similar to the peripheral immune system, FIV infection is associated with CD4+ cell loss and reduced CD4+:CD8+ ratios in the female reproductive mucosal tissue.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Butterworth, JL and English, RV and Jordan, HL and Tompkins, MB}, year={2001}, month={Nov}, pages={37–51} } @article{betton_healy_english_bunch_1999, title={Atypical limbal melanoma in a cat}, volume={13}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(1999)013<0379:ALMIAC>2.3.CO;2}, number={4}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Betton, A and Healy, LN and English, RV and Bunch, SE}, year={1999}, pages={379–381} } @article{meeker_azuma_bragg_english_tompkins_1999, title={Microglial proliferation in cortical neural cultures exposed to feline immunodeficiency virus}, volume={101}, ISSN={["0165-5728"]}, DOI={10.1016/S0165-5728(99)00126-5}, abstractNote={Microglia are thought to play an important role in neurodegenerative changes due to infection with human or animal immunodeficiency viruses. Using feline immunodeficiency virus and cat neural cultures, we observed a dramatic increase in the accumulation of microglia from a basal rate of 5-7% day(-1) to 25-126% day(-1). Both live virus and heat-inactivated virus induced proliferation. Negligible proliferation was seen in purified microglial cultures. Conditioned medium from astrocytes or mixed neural cultures treated with feline immunodeficiency virus stimulated the proliferation of purified microglia. Disease progression may be facilitated by early non-infectious interactions of lentiviruses with neural tissue that promote the activation and proliferation of microglia.}, number={1}, journal={JOURNAL OF NEUROIMMUNOLOGY}, author={Meeker, RB and Azuma, Y and Bragg, DC and English, RV and Tompkins, M}, year={1999}, month={Nov}, pages={15–26} } @article{bragg_meeker_duff_english_tompkins_1999, title={Neurotoxicity of FIV and FIV envelope protein in feline cortical cultures}, volume={816}, ISSN={["0006-8993"]}, DOI={10.1016/S0006-8993(98)01177-9}, abstractNote={The neurotoxic effects of the feline immunodeficiency virus (FIV) and FIV envelope proteins were measured in primary cultures of feline cortical neurons. Envelope protein from the FIV-PPR strain promoted neuronal swelling and death, whereas envelope protein from the FIV-34TF10 isolate produced intermediate or negligible toxicity. No effect was observed in control cultures treated with envelope protein from the Epstein–Barr virus. A concentration–effect curve showed that FIV-PPR protein produced maximal toxicity at 200 pM protein and decreased toxicity at higher concentrations, which is consistent with previous reports of the HIV-1 surface glycoprotein, gp120. These effects required the presence of low concentrations of glutamate. Using the natural host cells as targets, the effects of envelope protein and infectious virions were directly compared. All of the toxic activity could be attributed to non-infectious interactions between the viral envelope and target cells. Addition of 1 μM tetrodotoxin failed to block the effects of FIV-PPR in the presence of 20 μM glutamate. Toxicity would appear to involve two steps in which the envelope protein first sensitizes neurons through non-synaptic interactions (TTX insensitive) thereby setting the stage for enhanced synaptic activation via glutamate receptors (TTX sensitive).}, number={2}, journal={BRAIN RESEARCH}, author={Bragg, DC and Meeker, RB and Duff, BA and English, RV and Tompkins, MB}, year={1999}, month={Jan}, pages={431–437} } @article{jordan_howard_bucci_butterworth_english_kennedy-stoskopf_tompkins_tompkins_1998, title={Horizontal transmission of feline immunodeficiency virus with semen from seropositive cats}, volume={41}, DOI={10.1016/s0165-0378(98)00070-9}, abstractNote={The AIDS virus of cat species, feline immunodeficiency virus (FIV), has been used extensively as an animal model of HIV-1 infection. This felid lentivirus shares many molecular and biochemical traits with HIV-1 and causes similar immunologic and clinical perturbations, most notably CD4+ cell loss, impaired cell-mediated immunity and increased susceptibility to opportunistic pathogens. Previous reports have shown that FIV is transmitted horizontally by biting and vertically in utero and through nursing. Our objective was to determine whether FIV could be venereally transmitted in domestic cats. In the first experiment, susceptibility of the female reproductive tract to mucosal transmission of the FIV isolate, NCSU1, was demonstrated via intravaginal inoculation with infected cultured cells. We next identified virus in electroejaculates from asymptomatic, chronically FIV-NCSU1-infected, adult males. A fragment of FIV gag provirus DNA was detected by nested polymerase chain reaction (PCR) in nonfractionated seminal cells and in swim-up sperm preparations. Additionally, replication-competent virus was isolated from cell-free seminal plasma and seminal cells by co-cultivation with a feline CD4+ T-cell line. In the third study, queens were artificially inseminated via an intrauterine laparoscopic technique with electroejaculates from FIV-NCSU1-infected males. Of six inseminations carried out with fresh semen, three resulted in infection of queens. Lastly, immunohistochemical studies identified potential virus target cell populations in normal female reproductive tissues. In conclusion, these experiments indicate that FIV infection in domestic cats may provide a unique small animal model of sexual transmission of HIV-1.}, number={1-2}, journal={Journal of Reproductive Immunology}, author={Jordan, H. L. and Howard, J. G. and Bucci, J. G. and Butterworth, J. L. and English, R. and Kennedy-Stoskopf, S. and Tompkins, M. B. and Tompkins, W. A.}, year={1998}, pages={341–357} } @article{bucci_english_jordan_childers_tompkins_tompkins_1998, title={Mucosally transmitted feline immunodeficiency virus induces a CD8(+) antiviral response that correlates with reduction of cell-associated virus}, volume={177}, ISSN={["0022-1899"]}, DOI={10.1086/513822}, abstractNote={Intravaginal inoculation of cats with feline immunodeficiency virus (FIV) results in acute systemic infection accompanied by a strong CD8+ immune response that inhibits viral replication. CD8+ anti-FIV activity, revealed by increased FIV replication in peripheral blood mononuclear cells (PBMC) depleted of CD8+ lymphocytes, was detected by 6 weeks after inoculation and correlated with reduced PBMC-associated virus at 12, 16, and 32 weeks after inoculation. Some cats with strong CD8+ anti-FIV activity during acute infection did not seroconvert and yielded no evidence of FIV infection at later times. These data suggest that CD8+ immunity may play a major role in eliminating virus during primary transmucosal FIV infection and may down-regulate viral replication during asymptomatic infection.}, number={1}, journal={JOURNAL OF INFECTIOUS DISEASES}, author={Bucci, JG and English, RV and Jordan, HL and Childers, TA and Tompkins, MB and Tompkins, WAF}, year={1998}, month={Jan}, pages={18–25} } @article{bucci_gebhard_childers_english_tompkins_tompkins_1998, title={The CD8(+) cell phenotype mediating antiviral activity in feline immunodeficiency virus-infected cats is characterized by reduced surface expression of the CD8 beta chain}, volume={178}, ISSN={["0022-1899"]}, DOI={10.1086/515699}, abstractNote={The acute stage of feline immunodeficiency virus (FIV) infection is characterized by a CD8+ anti-FIV response that parallels the appearance of a CD8+ subpopulation with reduced expression of the beta chain (CD8 alpha + beta lo). The relationship between the CD8 alpha + beta lo phenotype and CD8+ anti-FIV activity was examined. Flow cytometric analysis of peripheral blood mononuclear cells with anti-CD8 beta chain monoclonal antibody 117 revealed that the CD8 alpha + beta lo phenotype expanded throughout the asymptomatic infection, constituting 80%-90% of the CD8 beta + cells in long-term-infected cats. Purified CD8 alpha + beta hi and CD8 alpha + beta lo subpopulations were analyzed for anti-FIV activity in an acute infection assay. Anti-FIV activity resided principally in the CD8 alpha + beta lo population and was demonstrated in acute FIV infections, as well as in long-term asymptomatic infections. These data suggest that a unique CD8 alpha + beta lo anti-FIV phenotype arises early in infection and may play a major role in eliminating virus and maintaining the asymptomatic infection.}, number={4}, journal={JOURNAL OF INFECTIOUS DISEASES}, author={Bucci, JG and Gebhard, DH and Childers, TA and English, RV and Tompkins, MB and Tompkins, WAF}, year={1998}, month={Oct}, pages={968–977} } @article{english_1993, title={Feline immunodeficiency virus}, volume={14}, number={4}, journal={Veterinary Technician}, author={English, R. V.}, year={1993}, pages={213} } @article{english_johnson_gebhard_tompkins_1993, title={In vivo lymphocyte tropism of feline immunodeficiency virus}, volume={67}, number={9}, journal={Journal of Virology}, author={English, R. V. and Johnson, C. M. and Gebhard, D. H. and Tompkins, M. B.}, year={1993}, pages={5175} } @article{english_1992, title={Regulation of intraocular immune responses}, volume={2}, number={1}, journal={Veterinary and Comparative Ophthalmology}, author={English, R. V.}, year={1992}, pages={41} }