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Biomedical subjects

J R Wright

Publications and source records attributed to J R Wright.

At least 37 records · Page 2Linked to original sources
PubMed2001

Hyperopic laser in situ keratomileusis to treat overcorrected myopic LASIK.

PURPOSE: To evaluate the safety and efficacy of hyperopic laser in situ keratomileusis (LASIK) in treating hyperopia caused by overcorrected myopic LASIK and to evaluate a new technique to place the hyperopic treatment after lifting the initial myopic flap. SETTING: Open-access outpatient excimer laser surgical facility. METHODS: A retrospective analysis was performed of 54 eyes in 47 patients who had spherical hyperopic LASIK by 21 surgeons for the treatment of significant hyperopia after overcorrected LASIK for myopia. In 42 eyes, the initial LASIK flaps were lifted and in 12 eyes, new flaps were cut. The mean age of the 25 men (53%) and 22 women (47%) was 48.2 years +/- 8.4 (SD). Outcome measures included refractive error, uncorrected visual acuity (UCVA), best spectacle-corrected visual acuity (BSCVA), and complications. The mean follow-up was 2.97 months. RESULTS: In eyes in which postoperative emmetropia was attempted (n = 45), the mean spherical equivalent improved from +1.21 +/- 0.49 diopters (D) preoperatively to -0.38 +/- 0.50 D postoperatively (P <.001). The mean UCVA improved from 20/38.6 +/- 16.3 to 20/27.4 +/- 9.4 (P <.001). At the last follow-up, 69% of eyes were within +/-0.5 D and 96% were within +/-1.0 D of emmetropia; 42% had a UCVA of 20/20 and 96% had a UCVA of 20/40 or better. No eyes lost 2 or more lines of BSCVA. No vision-threatening complications occurred. Results in patients who had initial flaps lifted and those who had new flaps cut were statistically indistinguishable. On average, achieved hyperopic corrections were 18% greater than intended. CONCLUSION: Hyperopic LASIK was safe, predictable, and effective in the treatment of hyperopia caused by overcorrected myopic LASIK. Results were similar whether the original flap was lifted or a new one was cut.

Cornea↗
PubMed2001

Clinicopathological correlation in biopsy-proven atherosclerotic nephropathy: implications for renal functional outcome in atherosclerotic renovascular disease.

BACKGROUND: Atherosclerotic renovascular disease (ARVD) is commonly associated with renal failure. It is now recognized that intrarenal damage, (ischaemic or atherosclerotic nephropathy) is a major contributor to the renal impairment in these patients. In this study the impact of histological changes upon renal functional outcome was investigated in patients with atherosclerotic nephropathy. METHODS: The Hope Hospital renal biopsy database (1985-1998) was interrogated for patients with histology compatible with atherosclerotic nephropathy. Case-note review enabled the assessment of several clinical parameters and outcomes, including change in creatinine clearance per year (DeltaCrCl (ml/min/year)), blood pressure control, dialysis need, and death. Renal parenchymal damage was analysed by morphometric analysis (of interstitial fibrosis and glomerulosclerosis) and a semi-quantitative chronic damage score (score 0-3 (normal-severe) for each of glomerulosclerosis, interstitial fibrosis, tubular atrophy, and arteriolar hyalinosis; maximum=12). Patients were stratified into two groups who had either deteriorating (group 1) or stable (group 2) renal function during follow-up. RESULTS: Twenty-five patients (age 64.7+/-10.5, range 43-83 years; 17 male, eight female) were identified. Sixteen patients had undergone angiography; two had significant (>50%) renal artery stenosis. Mean follow-up was 25.6+/-14.8 (range 5-50) months. Group 1 patients had DeltaCrCl -7.4+/-6.8 ml/min/year, n=14 and group 2 patients had DeltaCrCl 4.8+/-7.0 ml/min/year, n=11. Four patients in group 1 developed end-stage renal disease and five patients died (three in group 1 and two in group 2). At study entry, group 1 patients had worse renal function (CrCl 27.6+/-17.6 vs 36.0+/-33.9, NS), greater proteinuria (1.2 vs 0.5 g/24 h, NS), and higher systolic blood pressure (167.1+/-30.8 mmHg vs 150.6+/-37.8, NS) compared with group 2 patients. Group 1 patients showed more glomerulosclerosis (51.6 vs 24.9%, P:<0.01), greater proportional interstitial volume (44.9 vs 33.9%, P:<0.02), and higher overall chronic damage score (P:<0.05) than those in group 2. There was a significant correlation between renal functional outcome and chronic damage score, glomerulosclerosis and proportional interstitial volume for the entire patient cohort. CONCLUSION: In patients with atherosclerotic nephropathy the severity of histopathological damage is an important determinant and predictor of renal functional outcome.

Adult↗
PubMed2001

Surfactant proteins a and d and pulmonary host defense.

The lung collectins, SP-A and SP-D, are important components of the innate immune response to microbial challenge and participate in other aspects of immune and inflammatory regulation within the lung. Both proteins bind to surface structures expressed by a wide variety of microorganisms and have the capacity to modulate multiple leukocyte functions, including the enhanced internalization and killing of certain microorganisms in vitro. In addition, transgenic mice with deficiencies in SP-A and SP-D show defective or altered responses to challenge with bacterial, fungal, and viral microorganisms and to bacterial lipopolysaccharides in vivo. Thus collectins could play particularly important roles in settings of inadequate or impaired specific immunity, and acquired alterations in the levels of active collectins within the airspaces and distal airways may increase susceptibility to infection.

Animals↗
PubMed2001

Enhanced clearance of surfactant protein D during LPS-induced acute inflammation in rat lung.

Pulmonary surfactant participates in the regulation of alveolar compliance and lung host defense. Surfactant homeostasis is regulated through a combination of synthesis, secretion, clearance, recycling, and degradation of surfactant components. The extracellular pool size of surfactant protein (SP) D fluctuates significantly during acute inflammation. We hypothesized that changes in SP-D levels are due, in part, to altered clearance of SP-D. Clearance pathways in rats were assessed with fluorescently labeled SP-D that was instilled into control lungs or lungs that had been treated with lipopolysaccharide (LPS) 16 h earlier. SP-D clearance from lavage into lung tissue was time dependent from 5 min to 1 h and 1.7-fold greater in LPS-treated lungs than in control lungs. Analysis of cells isolated by enzymatic digestion of lung tissue revealed differences in the SP-D-positive cell population between groups. LPS-treated lungs had 28.1-fold more SP-D-positive tissue-associated neutrophils and 193.6-fold greater SP-D association with those neutrophils compared with control lungs. These data suggest that clearance of SP-D into lung tissue is increased during inflammation and that tissue-associated neutrophils significantly contribute to this process.

Acute Disease↗
PubMed2001

Lung surfactant and reactive oxygen-nitrogen species: antimicrobial activity and host-pathogen interactions.

Surfactant protein (SP) A and SP-D are members of the collectin superfamily. They are widely distributed within the lung, are capable of antigen recognition, and can discern self versus nonself. SPs recognize bacteria, fungi, and viruses by binding mannose and N-acetylglucosamine residues on microbial cell walls. SP-A has been shown to stimulate the respiratory burst as well as nitric oxide synthase expression by alveolar macrophages. Although nitric oxide (NO.) is a well-recognized microbicidal product of macrophages, the mechanism(s) by which NO. contributes to host defense remains undefined. The purpose of this symposium was to present current research pertaining to the specific role of SPs and reactive oxygen-nitrogen species in innate immunity. The symposium focused on the mechanisms of NO*-mediated toxicity for bacterial, human, and animal models of SP-A- and NO.-mediated pathogen killing, microbial defense mechanisms against reactive oxygen-nitrogen species, specific examples and signaling pathways involved in the SP-A-mediated killing of pulmonary pathogens, the structure and binding of SP-A and SP-D to bacterial targets, and the immunoregulatory functions of SP-A.

Animals↗
PubMed2001

Surfactant protein D enhances bacterial antigen presentation by bone marrow-derived dendritic cells.

Surfactant protein (SP) D functions as a soluble pattern recognition molecule to mediate the clearance of pathogens by phagocytes in the innate immune response. We hypothesize that SP-D may also interact with dendritic cells, the most potent antigen presenting cell, to enhance uptake and presentation of bacterial antigens. Using mouse bone marrow-derived dendritic cells, we show that SP-D binds to immature dendritic cells in a dose-, carbohydrate-, and calcium-dependent manner, whereas SP-D binding to mature dendritic cells is reduced. SP-D also binds to Escherichia coli HB101 and enhances its association with dendritic cells. Additionally, SP-D enhances the antigen presentation of an ovalbumin fusion protein expressed in E. coli HB101 to ovalbumin-specific major histocompatibility complex class II T cell hybridomas. The enhancement of antigen presentation by SP-D is dose dependent and is not shared by other collectin-like proteins tested. These studies demonstrate that SP-D augments antigen presentation by dendritic cells and suggest that innate immune molecules such as SP-D may help initiate an adaptive immune response for the purpose of resolving an infection.

Animals↗
PubMed2001

Overview of progeny-test programs of artificial-insemination organizations in the United States.

Characteristics of progeny-test (PT) programs of artificial insemination (AI) organizations in the United States were examined for changes since 1960. Mean number of bulls that were progeny tested annually by major AI organizations during the mid 1990s was 11 for Ayrshires, 24 for Brown Swiss, 21 for Guernseys, 1261 for Holsteins, 112 for Jerseys, and 3 for Milking Shorthorns. Mean parent age at progeny-test (PT) bull birth decreased except for Milking Shorthorns; mean age of maternal grandsire at bull birth decreased for Holsteins and Jerseys but increased for other breeds. For Holsteins, mean ancestor ages at PT bull birth were 85 mo for sires, 47 mo for dams, and 136 mo for maternal grandsires during the mid 1990s. Percentage of PT bulls that resulted from embryo transfer increased to 78% for Brown Swiss and 80% for Holsteins by 1999. Inbreeding in PT bulls increased over time and ranged from 3.8% for Brown Swiss to 6.4% for Jerseys (5.6% for Holsteins) during the mid 1990s. Mean numbers of daughters and herds per PT bull generally declined except for Holsteins, which increased during the early 1990s to 61 daughters and 44 herds. Mean number of states in which PT daughters are located increased; for Holstein PT bulls during 1994, 22% of daughters were in California, 13% in Wisconsin, 12% in New York, and 10% in Pennsylvania and Minnesota. Percentage of first-lactation cows that were PT daughters increased and ranged from 6% for Milking Shorthorns to 22% for Ayrshires (14% for Holsteins) during 1998. Percentage of PT daughters that were registered declined and was 19% for Holsteins and around 80% for other breeds.

Age Factors↗
PubMed2001

Accuracy of recorded birth and calving dates of dairy cattle in the United States.

Frequencies of births that were reported for specific days of the month were documented for US dairy cattle born since 1987 by birth year, herd size, and registry status and compared with calving frequencies for those dates. Because birth dates are expected to be random and uniformly distributed throughout each month, percentages of births on individual dates were expected to be equal (3.3% for d 1 to d 28, 3.2% for d 29, 3.0% for d 30, and 1.9% for d 31). However, percentages of reported birth dates for d 1, 2, 10, 15, and 20 were higher than expected. The percentage of reported births for d 1 was highest (5.3%) of all days of the month regardless of herd size or registry status. The nonuniform distribution of birth dates within month indicated that a substantial number of birth dates were unknown and that estimated birth dates had been reported. About one-third of the birth dates recorded on d 1 appeared to have been estimated, or altered to gain an advantage in cattle shows. The highest frequencies for birth dates on d 1 (5.9 to 7.4%) were found for registered cows during months that initiated age groupings for dairy shows (March, June, September, and December). Birth dates for some registered cows were intentionally misreported as confirmed by comparison of birth dates of individual cows with calving dates of their dams. Reported calving dates appeared to be more accurate than reported births; the inflated frequency of recorded calvings on d 1 was only about 30% as large as the inflated frequency of recorded births. Because cow age is determined by birth date, proper reporting of birth dates is important to ensure the accuracy of standardized yield and fitness records and the genetic evaluations that are based on those records. When animals' recorded birth dates and their dams' calving dates differ, more credence should be given to the latter to improve accuracy.

Age Distribution↗
PubMed2000

Salivary agglutinin, which binds Streptococcus mutans and Helicobacter pylori, is the lung scavenger receptor cysteine-rich protein gp-340.

Salivary agglutinin is a high molecular mass component of human saliva that binds Streptococcus mutans, an oral bacterium implicated in dental caries. To study its protein sequence, we isolated the agglutinin from human parotid saliva. After trypsin digestion, a portion was analyzed by matrix-assisted laser/desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS), which gave the molecular mass of 14 unique peptides. The remainder of the digest was subjected to high performance liquid chromatography, and the separated peptides were analyzed by MALDI-TOF/post-source decay; the spectra gave the sequences of five peptides. The molecular mass and peptide sequence information showed that salivary agglutinin peptides were identical to sequences in lung (lavage) gp-340, a member of the scavenger receptor cysteine-rich protein family. Immunoblotting with antibodies that specifically recognized either lung gp-340 or the agglutinin confirmed that the salivary agglutinin was gp-340. Immunoblotting with an antibody specific to the sialyl Le(x) carbohydrate epitope detected expression on the salivary but not the lung glycoprotein, possible evidence of different glycoforms. The salivary agglutinin also interacted with Helicobacter pylori, implicated in gastritis and peptic ulcer disease, Streptococcus agalactiae, implicated in neonatal meningitis, and several oral commensal streptococci. These results identify the salivary agglutinin as gp-340 and suggest it binds bacteria that are important determinants of either the oral ecology or systemic diseases.

Agglutinins↗
PubMed2000

Pleuropulmonary blastoma: A case report documenting transition from type I (cystic) to type III (solid).

BACKGROUND: Pleuropulmonary blastoma is a rare, aggressive neoplasm that typically occurs in young children. It has been classified as type I, II, or III on the basis of the cystic versus solid nature of the lesion as well as the histologic appearance. Although it has been speculated that type I lesions may have a tendency to progress into type III lesions, no such case has been reported to date. METHODS: A case of type I pleuropulmonary blastoma in a girl age 2 years 9 months was found in our departmental archive. This case, originally diagnosed as a hamartoma over 20 years ago, predated the description of this pathologic entity. Over a 3-year period, the patient underwent excisions of a primary tumor and 3 subsequent recurrences, thus allowing us to follow the natural history of this neoplasm. RESULTS: The primary tumor was a large, multicystic mass (roughly 90% cystic by volume) with benign histologic appearance except for occasional foci with bland, embryonal rhabdomyosarcomatous features. In subsequent recurrences, the resected specimens became increasingly solid and had an anaplastic, multiphasic mesenchymal pattern. CONCLUSIONS: The course of the patient described here represents the first case in which transition from type I (cystic) to type III (solid) was documented.

Cell Transformation, Neoplastic↗
PubMed2000

Expression of nm23 antimetastatic gene product in head and neck squamous cell carcinoma.

The nm23 gene has been implicated as a suppressor gene involved in the control of the metastatic process of malignant cells. Reduced levels of nm23 gene product have been found in tumor cells with high metastatic potential such as several types of rodent tumors and human breast, colorectal, and lung carcinoma. This pilot study examines the expression of the nm23 gene product compared with nodal status in 70 consecutive patients with squamous cell carcinomas of the head and neck. Immunohistochemical staining was carried out on these tumor tissues with a monoclonal antibody to nm23-H1 peptide sequence. The tissues were scored from 0 to 2 by 2 independent observers. Reduced immunoreactivity, grades 0 and 1, was observed in 30 patients with positive nodal status (N = 34, 88%). Strong immunoreactivity, grade 2, was observed in 20 patients with negative nodal status (N = 36, 56%). Reduced expression of nm23 gene product was observed in patients with positive lymph node metastasis (P = 0. 0006, chi(2)). However, no significant differences in survival of these groups based on nm23 expression could be shown with the Kaplan-Meier analysis. This initial finding in the difference of nm23 gene product expression in patients with differing lymph node status is exciting but must be further validated with future studies.

Carcinoma, Squamous Cell↗
PubMed2000

Surfactant protein A prevents silica-mediated toxicity to rat alveolar macrophages.

Silicosis is a serious occupational lung disease associated with irreversible pulmonary fibrosis. The interaction between inhaled crystalline silica and the alveolar macrophage (AM) is thought to be a key event in the development of silicosis and fibrosis. Silica can cause direct injury to AMs and can induce AMs to release various inflammatory mediators. Acute silicosis is also characterized by a marked elevation in surfactant apoprotein A (SP-A); however, the role of SP-A in silicosis is unknown. We investigated whether SP-A directly affects the response of AMs to silica. In this study, the degree of silica toxicity to cultured rat AMs as assessed by a (51)Cr cytotoxicity assay was shown to be dependent on the time of exposure and the concentration and size of the silica particles. Silica directly injured rat AMs as evidenced by a cytotoxic index of 32.9 +/- 2.5, whereas the addition of rat SP-A (5 microg/ml) significantly reduced the cytotoxic index to 16.6 +/- 1.2 (P < 0. 001). This effect was reversed when SP-A was incubated with either polyclonal rabbit anti-rat SP-A antibody or D-mannose. These data indicate that SP-A mitigates the effect of silica on AM viability, and this effect may involve the carbohydrate recognition domain of SP-A. The elevation of SP-A in acute silicosis may serve as a normal host response to prevent lung cell injury after exposure to silica.

Animals↗
PubMed2000

Binding and uptake of surfactant protein D by freshly isolated rat alveolar type II cells.

Alveolar type II cells secrete, internalize, and recycle pulmonary surfactant, a lipid and protein complex that increases alveolar compliance and participates in pulmonary host defense. Surfactant protein (SP) D, a collagenous C-type lectin, has recently been described as a modulator of surfactant homeostasis. Mice lacking SP-D accumulate surfactant in their alveoli and type II cell lamellar bodies, organelles adapted for recycling and secretion of surfactant. The goal of current study was to characterize the interaction of SP-D with rat type II cells. Type II cells bound SP-D in a concentration-, time-, temperature-, and calcium-dependent manner. However, SP-D binding did not alter type II cell surfactant lipid uptake. Type II cells internalized SP-D into lamellar bodies and degraded a fraction of the SP-D pool. Our results also indicated that SP-D binding sites on type II cells may differ from those on alveolar macrophages. We conclude that, in vitro, type II cells bind and recycle SP-D to lamellar bodies, but SP-D may not directly modulate surfactant uptake by type II cells.

Animals↗
PubMed2000

Surfactant-associated protein A inhibits LPS-induced cytokine and nitric oxide production in vivo.

The role of surfactant-associated protein (SP) A in the mediation of pulmonary responses to bacterial lipopolysaccharide (LPS) was assessed in vivo with SP-A gene-targeted [SP-deficient; SP-A(-/-)] and wild-type [SP-A(+/+)] mice. Concentrations of tumor necrosis factor (TNF)-alpha, macrophage inflammatory protein-2, and nitric oxide were determined in recovered bronchoalveolar lavage fluid after intratracheal administration of LPS. SP-A(-/-) mice produced significantly more TNF-alpha and nitric oxide than SP-A(+/+) mice after LPS treatment. Intratracheal administration of human SP-A (1 mg/kg) to SP-A(-/-) mice restored regulation of TNF-alpha, macrophage inflammatory protein-2, and nitric oxide production to that of SP-A(+/+) mice. Other markers of lung injury including bronchoalveolar fluid protein, phospholipid content, and neutrophil numbers were not influenced by SP-A. Data from experiments designed to test possible mechanisms of SP-A-mediated suppression suggest that neither binding of LPS by SP-A nor enhanced LPS clearance are the primary means of inhibition. Our data and others suggest that SP-A acts directly on immune cells to suppress LPS-induced inflammation. These results demonstrate that endogenous or exogenous SP-A inhibits pulmonary LPS-induced cytokine and nitric oxide production in vivo.

Animals↗
PubMed2000

Incorporation of biotinylated SP-A into rat lung surfactant layer, type II cells, and clara cells.

The goal of this study was to compare the functions of Clara and type II cells during alveolar clearance and recycling of surfactant protein (SP) A, a secretory product of both cell types. We examined the incorporation of instilled biotinylated SP-A (bSP-A) into rat lung type II and Clara cells as a measure of clearance and recycling of the protein. Ultrastructural localization of bSP-A was accomplished by an electron-microscopic immunogold technique at 7, 30, and 120 min after intratracheal instillation. Localization of bSP-A was quantitatively evaluated within extracellular surfactant components (lipid-rich forms: myelin figures, vesicles, and tubular myelin; and lipid-poor hypophase) and in compartments of type II and Clara cells. bSP-A was incorporated into myelinic and vesicular forms of extracellular surfactant, but tubular myelin and hypophase had little bSP-A. Lamellar bodies of type II cells demonstrated a significant time-dependent increase in their incorporation of bSP-A. There was a concentration of bSP-A in the secretory granules and mitochondria of Clara cells, but no Clara cell compartment showed a pattern of time-dependent change in immunolabeling. Our immunolabeling data demonstrated a time-dependent movement of exogenous SP-A from extracellular components into type II cells and their secretory granules. Clara cells did not demonstrate a time-dependent incorporation of bSP-A into their secretory granules during the period of this study. If Clara cells recycle SP-A, they must reach a steady state very quickly or very slowly.

Animals↗