Weight loss and improved metabolic outcomes amongst rural African American women in the Deep South: six-month outcomes from a community-based randomized trial.

BACKGROUND: Obesity is highly prevalent in African American women, especially those in the rural southern USA, resulting in persistent health disparities. OBJECTIVE: To test the effectiveness of an evidence-based behavioural weight loss intervention delivered by community health advisors to African American women in the rural south. DESIGN AND METHODS: Overweight or obese African American women (30-70 years) from eight counties in Mississippi and Alabama participated in a 24-month randomized controlled trial of an evidence-based behavioural weight loss programme augmented with community strategies to support healthy lifestyles (Weight Loss Plus, N = 154) compared to the weight loss programme alone (Weight Loss Only, N = 255). This study reports on 6-month outcomes on primary (weight change) and secondary (waist circumference, blood pressure, lipids, fasting blood glucose) outcomes, coinciding with the completion of the intensive weight loss phase. RESULTS: Weight Loss Only participants lost an average of 2.2 kg (P < 0.001). Weight Loss Plus participants lost an average of 3.2 kg (P < 0.001). The proportion of the total sample that lost at least 5% of their body weight was 27.1% with no difference between treatment groups. Similarly, we observed statistically significant reductions in blood pressure, waist circumference and triglycerides in each treatment group, with no statistical differences between groups. CONCLUSION: Trained lay health staff and volunteers from the rural southern USA were able to deliver a translation of a high-intensity behavioural intervention targeted to African American women, resulting in clinically meaningful weight loss and improvement in other metabolic outcomes in a significant proportion of participants.

Value and payment for oncology in the United States.

Rather than focus on reducing prices for innovative biopharmaceuticals, insurers in the United States are changing methods of payment for oncologists in order to moderate the growth in cancer drug expenditures. The desire is for a better pattern of utilization and expenditures without adversely affecting incentives for research and development. After an overview of the contemporary discussions of price and value, this paper describes three initiatives to influence the selection and management of oncology drugs. This includes initiatives to reduce the profit margins earned by oncologists as part of the purchasing of office-infused biopharmaceuticals; "episode-of-care" payments that bundle into a single fee the reimbursement for care management and specialty drugs; and payment methods that case rates for physician care management activities with cost-based reimbursement for the oncology drugs.

Mars: correlation of optical and radar observations.

A comparsion of recent photographic and radar data on Mars indicates a good positive correlation between dark areas and radar reflection peaks and also between cloudy "desert" areas and radar minima. The data may be taken as evidence that dark areas are, in general, relatively smooth whereas deserts are relatively rough.

Have tar and nicotine yields of cigarettes changed?

In official assays of the tar and nicotine yields of 12 popular brands of cigarettes, smoking machines took fewer puffs, on the average, in 1974 than in 1969. The decline in puffs appears to have been a major cause of the reported reductions in tar and nicotine yields during this period.

Mariner 9 television reconnaissance of Mars and its satellites: preliminary results.

At orbit insertion on 14 November 1971 the Martian surface was largely obscured by a dust haze with an extinction optical depth that ranged from near unity in the south polar region to probably greater than 2 over most of the planet. The only features clearly visible were the south polar cap, one dark, spot in Nix Olympica, and three dark spots in the Tharsis region. During the third week the atmosphere began to clear and surface visibility improved, but contrasts remained a fraction of their normal value. Each of the dark spots that apparently protrude through most of the dust-filled atmosphere has a crater or crater complex in its center. The craters are rimless and have featureless floors that, in the crater complexes, are at different levels. The largest crater within the southernmost spot is approximately 100 kilometers wide. The craters apparently were formed by subsidence and resemble terrestrial calderas. The south polar cap has a regular margin, suggsting very flat topography. Two craters outside the cap have frost on their floors; an apparent crater rim within the cap is frost free, indicating preferentia loss of frost from elevated ground. If this is so then the curvilinear streaks, which were frost covered in 1969 and are now clear of frost, may be low-relief ridges. Closeup pictures of Phobos and Deimos show that Phobos is about 25 +/-5 by 21 +/-1 kilometers and Deimos is about 13.5 +/- 2 by 12.0 +/-0.5 kilometers. Both have irregular shapes and are highly cratered, with some craters showing raised rims. The satellites are dark objects with geometric albedos of 0.05.

ArcR modulates biofilm formation in the dental plaque colonizer Streptococcus gordonii.

Biofilm formation and cell-cell sensing by the pioneer dental plaque colonizer Streptococcus gordonii are dependent upon arginine. This study aimed to identify genetic factors linking arginine-dependent responses and biofilm formation in S. gordonii. Isogenic mutants disrupted in genes required for the biosynthesis or catabolism of arginine, or for arginine-dependent gene regulation, were screened for their ability to form biofilms in a static culture model. Biofilm formation by a knockout mutant of arcR, encoding an arginine-dependent regulator of transcription, was reduced to < 50% that of the wild-type whereas other strains were unaffected. Complementation of S. gordonii ∆arcR with a plasmid-borne copy of arcR restored the ability to develop biofilms. By DNA microarray analysis, 25 genes were differentially regulated in S. gordonii ∆arcR compared with wild-type under arginine-replete conditions including eight genes encoding components of phosphotransferase systems for sugar uptake. By contrast, disruption of argR or ahrC genes, which encode paralogous arginine-dependent regulators, each resulted in significant changes in the expression of more than 100 genes. Disruption of a gene encoding a putative extracellular protein that was strongly regulated in S. gordonii ∆arcR had a minor impact on biofilm formation. We hypothesize that genes regulated by ArcR form a critical pathway linking arginine sensing to biofilm formation in S. gordonii. Further elucidation of this pathway may provide new targets for the control of dental plaque formation by inhibiting biofilm formation by a key pioneer colonizer of tooth surfaces.

A silicon-based, sequential coat-and-etch process to fabricate nearly perfect substrate surfaces.

For many thin-film applications substrate imperfections such as particles, pits, scratches, and general roughness, can nucleate film defects which can severely detract from the coating's performance. Previously we developed a coat-and-etch process, termed the ion beam thin film planarization process, to planarize substrate particles up to approximately 70 nm in diameter. The process relied on normal incidence etching; however, such a process induces defects nucleated by substrate pits to grow much larger. We have since developed a coat-and-etch process to planarize approximately 70 nm deep by 70 nm wide substrate pits; it relies on etching at an off-normal incidence angle, i.e., an angle of approximately 470 degrees from the substrate normal. However, a disadvantage of this pit smoothing process is that it induces defects nucleated by substrate particles to grow larger. Combining elements from both processes we have been able to develop a silicon-based, coat-and-etch process to successfully planarize approximately 70 nm substrate particles and pits simultaneously to at or below 1 nm in height; this value is important for applications such as extreme ultraviolet lithography (EUVL) masks. The coat-and-etch process has an added ability to significantly reduce high-spatial frequency roughness, rendering a nearly perfect substrate surface.

Homozygous deletion and frequent allelic loss of chromosome 8p22 loci in human prostate cancer.

Allelic loss studies have been instrumental in identifying tumor suppressor gene loci in a variety of cancers. In this study we analyzed prostate cancer specimens from 52 patients for allelic loss using 8 polymorphic probes for the short arm of chromosome 8. Overall, 32 of 51 (63%) informative tumors showed loss of at least one locus on chromosome 8p. The most frequently deleted region is observed at chromosome 8p22-8p21.2. Loss of one allele is identified in 14 of 23 (61%) tumors at D8S163, in 15 of 32 (47%) tumors at lipoprotein lipase, and in 20 of 29 (69%) tumors at MSR, all on 8p22. Loss of one allele is identified in 16 of 27 (59%) tumors at D8S220 at 8p21.3-8p21.2. In addition to frequent loss of one allele at the MSR locus, one metastatic prostate cancer sample demonstrated homozygous deletion of MSR sequences. Loci telomeric and centromeric to this region are largely retained. A chromosome 8p deletion map is constructed and defines the smallest region of overlap to a 14-cM interval at 8p22 between D8S163 and lipoprotein lipase, flanking the MSR locus. Evidence of chromosome 8q multiplication at locus D8S39 was detected in 5 of 32 (16%) tumors, all of which demonstrated loss with at least one probe on chromosome 8p. This study extends the previous finding of frequent loss of chromosome 8p in prostate cancer by defining a common region of loss of heterozygosity at 8p22 and a homozygous deletion of the MSR locus contained within this region. This is the first homozygous deletion identified in the genome of a human prostate cancer and the highest rate of loss yet reported on chromosome 8p in cancer. These results strongly suggest the presence of a tumor suppressor gene in this region which is frequently inactivated in prostate cancer.

Chromosome 5 suppresses tumorigenicity of PC3 prostate cancer cells: correlation with re-expression of alpha-catenin and restoration of E-cadherin function.

Considerable evidence now exists to support an important role for the E-cadherin-mediated cell-cell adhesion pathway as a suppressor of the invasive phenotype in adenocarcinoma cells. Previous studies have found that this pathway is frequently aberrant in prostate cancers, particularly those that are likely to metastasize. In this study, we report on the effects of re-establishment of this pathway in a prostate cancer cell line, PC-3, in which this adhesion system is dysfunctional by virtue of a deletion of the gene that codes for alpha-catenin, an E-cadherin-associated protein necessary for normal E-cadherin function. Re-expression of alpha-catenin was accomplished either by transfection of PC-3 cells with a copy of the alpha-catenin cDNA under the control of a heterologous promoter or by microcell-mediated transfer of chromosome 5, which contains the alpha-catenin gene and its normal regulatory elements. In both cases, re-expression of alpha-catenin is associated with a similar, dramatic alteration in cell morphology, whereby extensive cell-cell contact is observed. In the case of transfection of the cDNA, this expression is only transient, because the transfected cells either cease to proliferate or, more commonly, revert to the parental phenotype with concomitant cessation of alpha-catenin expression. In contrast, cells containing one or more copies of microcell-transferred chromosome 5 express alpha-catenin in a stable manner and continue to proliferate. Upon injection into nude mice, these latter cells are no longer tumorigenic, or form only slowly growing tumors with greatly extended doubling times when compared to the parental PC-3 cells. During passage in culture, clones that contain only one transferred copy of chromosome 5 reproducibly revert to the parental phenotype. This reversion is associated with loss of the chromosome 5 region containing the alpha-catenin gene and consequent loss of alpha-catenin expression, as well as re-emergence of tumorigenicity. Transfer of chromosome 5 into prostate cancer cells that are E-cadherin negative does not result in either morphological transformation or suppression of tumorigenicity, suggesting that these effects of alpha-catenin expression are dependent upon concomitant expression of E-cadherin. These data demonstrate the tumor suppressive ability of chromosome 5 in the PC-3 prostate cancer cells and suggest that re-expression of alpha-catenin with resultant restoration of E-cadherin function plays a critical role in this process.

Cadherin-6, a cell adhesion molecule specifically expressed in the proximal renal tubule and renal cell carcinoma.

Cadherins are a family of calcium-dependent, cell-cell adhesion molecules that play an important morphoregulatory role in a wide variety of tissues. Alterations in cadherin function have been implicated in tumor progression in a number of adenocarcinomas. Despite the increasing number of new cadherins identified, little is known about cadherins in normal renal tissue and renal carcinomas. A novel cadherin transcript, cadherin-6, was recently described to be present in renal cancer cell lines and fetal kidney, but no data on protein expression nor tissue localization has been reported. In this study, we demonstrate that the expression of cadherin-6 is restricted to the proximal tubule epithelium. This finding is critical because these cells give rise to the majority of neoplasms of this organ. Furthermore we demonstrate typical cadherin features of cadherin-6, including cytoplasmic binding to alpha- and beta-catenin. We present data of cadherin-6 expression in a series of 32 primary renal cell cancers. Cadherin-6 expression tended to vary with histology in these samples. Whereas the majority of renal cell cancers with histology-associated poor prognosis (i.e., high grade clear cell carcinomas and sarcomatoid renal tumors) show aberrant expression of cadherin-6, in tumors with a favorable prognosis (i.e., low grade clear cell carcinomas and papillary cancers), normal cadherin-6 expression was predominant. Overall, these findings demonstrate specific expression of cadherin-6 in the proximal renal tubules in normal human kidney and suggest that alterations of cadherin-6 expression are associated with progression of renal cell carcinoma.

An uncertain role for p53 gene alterations in human prostate cancers.

Inactivation of the p53 gene has been implicated in prostate cancer progression. To determine the role of p53 inactivation in the progression of clinical prostatic carcinomas, we assessed 67 tumors derived from patients with clinically localized disease for chromosome 17p and p53 gene allelic loss, p53 gene mutations using single-strand conformational polymorphism and direct sequencing, and p53 protein expression using immunohistochemical staining. Of 55 informative tumors, 10 demonstrated loss of 17p or the p53 gene; however, only a single tumor had a mutation in its remaining p53 allele. Significant p53 overexpression was observed in 2 of 38 tumors, and 9 others had faint staining of a few nuclei ( < 1%). p53 overexpression occurred in no informative tumor with allelic loss or mutation. In a 1-7-year follow-up, positive immunohistochemical staining did not confer an increased risk of recurrence (risk of recurrence, 0.86, P = 0.78), whereas allelic loss of chromosome 17p appeared to be highly correlated with recurrence (risk of recurrence, 3.7, P = 0.003). In an unrelated group of 42 patients with metastatic prostate cancer, p53 overexpression was found in 26 tumors (62%), and 15(36%) had high grade staining. Neither the presence nor the degree of expression correlated with time to progression or time to death. This series suggests that p53 gene inactivation is rare in primary prostatic tumors, not essential to the development of prostate cancer metastases, and of limited use as a prognostic marker in patients with primary or metastatic disease. Another gene or genes on chromosome 17p may be involved in prostate cancer progression.

Macromolecular assemblage of aminoacyl-tRNA synthetases: quantitative analysis of protein-protein interactions and mechanism of complex assembly.

The structure of the mammalian multi-synthetase complex was investigated in vitro using qualitative and quantitative approaches. This macromolecular assemblage comprises the bifunctional glutamyl-prolyl-tRNA synthetase, the seven monospecific isoleucyl, leucyl, methionyl, glutaminyl, lysyl, arginyl and aspartyl-tRNA synthetases, and the three auxiliary p43, p38 and p18 proteins. The scaffold p38 protein was expressed in Escherichia coli and purified to homogeneity as a His-tagged protein. The different components of the complex were shown to associate in vitro with p38 immobilized on Ni(2+)-coated plates. Interactions between peripheral enzymes and p38 are referred to as central interactions, as opposed to lateral interactions between peripheral enzymes. Kinetic parameters of the interactions were determined by the means of a biosensor-based approach. The two dimeric proteins LysRS and AspRS were found to tightly bind to p38, with a K(d) value of 0.3 and 4.7 nM, respectively. These interactions involved the catalytic core of the enzymes. By contrast, binding of ArgRS or GlnRS to p38 was much weaker (>5 microM). ArgRS and p43, two peripheral components, were shown to interact with moderate affinity (K(d)=93 nM). Since all the components of the complex are tightly associated within this particle, lateral interactions were believed to contribute to the stabilization of this assemblage. Using an in vitro binding assay, concomitant association of several components of the complex on immobilized p38 could be demonstrated, and revealed the involvement of synergistic effects for association of weakly interacting proteins. Taking into account the possible synergy between central and lateral contributions, a sub-complex containing p38, p43, ArgRS and GlnRS was reconstituted in vitro. These data provide compelling evidence for an ordered and concerted mechanism of complex assembly.

Macromolecular assemblage of aminoacyl-tRNA synthetases: identification of protein-protein interactions and characterization of a core protein.

In eukaryotes, from fly to human, nine aminoacyl-tRNA synthetases contribute a multienzyme complex of defined and conserved structural organization. This ubiquitous multiprotein assemblage comprises a unique bifunctional aminoacyl-tRNA synthetase, glutamyl-prolyl-tRNA synthetase, as well as the monospecific isoleucyl, leucyl, glutaminyl, methionyl, lysyl, arginyl, and aspartyl-tRNA synthetases. Three auxiliary proteins of apparent molecular masses of 18, 38 and 43 kDa are invariably associated with the nine tRNA synthetase components of the complex. As part of an inquiry into the molecular and functional organization of this macromolecular assembly, we isolated the cDNA encoding the p38 non-synthetase component and determined its function. The 320 amino acid residue encoded protein has been shown to have no homolog in yeast, bacteria and archaea, according to the examination of the complete genomic sequences available. The p38 protein is a moderately hydrophobic protein, displays a putative leucine-zipper motif, and shares a sequence pattern with protein domains that are involved in protein-protein interactions. We used the yeast two-hybrid system to register protein connections between components of the complex. We performed an exhaustive search of interactive proteins, involving 10 of the 11 components of the complex. Twenty-one protein pairs have been unambiguously identified, leading to a global view of the topological arrangement of the subunits of the multisynthetase complex. In particular, p38 was found to associate with itself to form a dimer, but also with p43, with the class I tRNA synthetases ArgRS and GlnRS, with the class II synthetases AspRS and LysRS, and with the bifunctional GluProRS. We generated a series of deletion mutants to localize the regions of p38 mediating the identified interactions. Mapping the interactive domains in p38 showed the specific association of p38 with its different protein partners. These findings suggest that p38, for which no homologous protein has been identified to date in organisms devoid of multisynthetase complexes, plays a pivotal role for the assembly of the subunits of the eukaryotic tRNA synthetase complex.

Evaluation of French Guiana traditional antimalarial remedies.

In order to evaluate the antimalarial potential of traditional remedies used in French Guiana, 35 remedies were prepared in their traditional form and screened for blood schizonticidal activity in vitro on Plasmodium falciparum chloroquine re4sistant strain (W2). Some of these extracts were screened in vivo against Plasmodium yoelii rodent malaria. Ferriprotoporphyrin inhibition test was also performed. Four remedies, widely used among the population as preventives, were able to inhibit more than 50% of the parasite growth in vivo at around 100 mg/kg: Irlbachia alata (Gentiananceae), Picrolemma pseudocoffea (Simaroubaceae), Quassia amara (Simaroubaceae), Tinospora crispa (Menispermaceae) and Zanthoxylum rhoifolium (Rutaceae). Five remedies displayed an IC50 in vitro < 10 microg/ml: Picrolemma pseudocoffea, Pseudoxandra cuspidata (Annonaceae) and Quassia amara leaves and stem, together with a multi-ingredient recipe. Two remedies were more active than a Cinchona preparation on the ferriprotoporphyrin inhibition test: Picrolemma pseudocoffea and Quassia amara. We also showed that a traditional preventive remedy, made from Geissospermum argenteum bark macerated in rum, was able to impair the intrahepatic cycle of the parasite. For the first time, traditional remedies from French Guiana have been directly tested on malarial pharmacological assays and some have been shown to be active.

Efficacy of topical aciclovir for the treatment of feline herpetic keratitis: results of a prospective clinical trial and data from in vitro investigations.

This study aimed to evaluate the efficacy of topical ophthalmic aciclovir applied five times daily as a treatment for feline herpesvirus type 1 (FHV-1) keratitis in a group of cats in a first-opinion practice setting. Cats with ocular signs indicative of FHV-1 or Chlamydophila species infection, predominantly conjunctivitis and keratitis, were tested for FHV-1 antigen using an immunofluorescent technique on air-dried conjunctival swabs. They were first treated with topical chlortetracycline with efficacy against Chlamydophila species and then, in cases positive for FHV-1, with topical aciclovir. The time to recovery was determined and illustrated using a Kaplan-Meier plot. Three cats were infected with Chlamydophila species and showed a median time to recovery of 14 days (95 per cent confidence interval [CI] 10 to 18 days), while 30 cats infected with FHV-1 showed a median time to recovery of 12 days (95 per cent CI 10 to 14 days). The drug dose at which 50 per cent plaque reduction (ED50) occurred in a standard plaque reduction assay was determined in an in vitro study. This showed a mean (SD) ED50 of aciclovir of 25 (3.5) mg/ml compared with 0.4 (0.05) mg/ml for trifluorothymidine, a drug known to be efficacious against FHV-1. The study shows that even though aciclovir is generally considered to lack efficacy against ocular FHV-1 infection, when used frequently it can have a beneficial effect in FHV-1 conjunctivitis and keratitis.

Can postmenopausal hormone replacement improve plasma lipids in women with diabetes? The Atherosclerosis Risk in Communities Study Investigators.

OBJECTIVE: to evaluate the association of postmenopausal hormone replacement with plasma lipids in diabetic women. RESEARCH DESIGN AND METHODS: Cross-sectional data from a multiracial population study were used to evaluate the relationship of hormone replacement status with plasma lipids in diabetic (n = 694) versus nondiabetic (n = 5,321) postmenopausal women. RESULTS: Although diabetic women who currently used hormone replacement had higher adjusted mean HDL cholesterol levels than those who did not (56.9 vs. 53.6 mg/dl), they had proportionately lower hormone-related increases in HDL, HDL2, and HDL3 cholesterol than did nondiabetic women (HDL cholesterol 64.9 [current users] vs. 55.7 mg/dl [those who never used hormones]). There was a trend toward greater triglyceride values with hormone replacement in diabetic women (156.6 [current users] vs. 125.4 mg/dl [those who never used hormones]) than in nondiabetic women (143.3 [current users] vs. 123.7 mg/dl [those who never used hormones]). LDL cholesterol and apolipoprotein B levels were lower and apolipoprotein A-I levels were higher with hormone replacement, to a similar degree in diabetic and nondiabetic women. CONCLUSIONS: Diabetic women appear to have a blunted response to the HDL-raising effects of estrogen and an exaggerated hypertriglyceridemic response. This may result in attenuated cardioprotection from postmenopausal hormone replacement therapy and potentially an increased risk of acute pancreatitis from hypertriglyceridemia. The risks and benefits of postmenopausal hormone replacement need to be carefully weighed in diabetic women.

Regulation of the synthesis of human chorionic gonadotrophin by 5-bromo-2'-deoxyuridine and dibutyryl cyclic AMP in trophoblastic and nontrophoblastic tumor cells.

Synthesis of hCG and its alpha subunit (hCG-alpha) by trophoblastic tumor cell lines (JEG-3, Reid, and BeWo) and by nontrophoblastic tumor cell lines [ChaGo and three HeLa lines (HeLa CCL2, HeLa S3, and HeLa 65)] was studied. cAMP, dibutyryl cAMP, and 8-bromo-cAMP induced, but 5-bromo-2'-deoxyuridine inhibited, the synthesis of hCG-alpha and hCG in trophoblastic tumor cells, Addition of 5-bromo-2'-deoxyuridine partially blocked the induction by dibutyryl cAMP in these cells. The synthesis of hCG-alpha and hCG in nontrophoblastic tumor cells was stimulated by dibutyryl cAMP. cAMP and 8-bromo-cAMP, however, did not affect the synthesis of hCG-alpha, although the synthesis of hCG was enhanced. 5-Bromo-2'-deoxyuridine induced hCG-alpha synthesis but did not affect hCG synthesis in nontrophoblastic tumor cells. In HeLa S3 and HeLa 65 cells, the amount of hCG-alpha and hCG produced in the presence of dibutyryl cAMP and 5-bromo-2'-deoxyuridine together was greater than the total hormone produced by each inducer separately. Our data indicate that the regulation of the production of hCG-alpha and hCG differs in trophoblastic and nontrophoblastic tumors.

Cytochalasin B potentiates epinephrine's outflow facility-increasing effect.

Total outflow facility was determined in both eyes of cynomolgus monkeys by two-level constant pressure perfusion. After a baseline measurement, one eye of the experimental animal received intracameral cytochalasin B (CB); the other eye received vehicle without CB. Twenty minutes later both eyes received intracameral epinephrine (EPI), and 30 min later the outflow facility was again determined. Doses of CB and EPI which were subthreshold when given singly produced significant facility increases when given concurrently. Subthreshold doses of CB given concurrently with a maximal dose of EPI produced significantly larger facility increases than a maximal dose of EPI given alone. A maximal dose of CB produced a larger facility increase than a maximal dose of EPI. Maximal doses of CB and EPI given concurrently produced a larger facility increase than did a maximal dose of EPI alone and had about the same effect as a maximal CB dose given alone. Since CB's facility-increasing effect is likely due to "disruption" of actin filaments in the endothelial cells of the trabecular meshwork and Schlemm's canal and since CB potentiates the facility-increasing effect of EPI, EPI may also act by "disrupting" actin filaments and consequently altering endothelial cell shape.

Superior cervical ganglionectomy in monkeys: surgical technique.

Seven cynomolgus monkeys underwent a histologically confirmed left superior cervical ganglionectomy (SCGx). Unilateral ocular sympathetic denervation persisting for at least 2 yr was confirmed by ipsilateral ptosis, miosis, supersensitivity of pupillary dilation to topical phenylephrine, and profound pupillary hyporesponsiveness to topical hydroxyamphetamine. Intraocular pressure 8-9 and 23-27 months postoperatively were identical in the denervated and contralateral control eyes. This model should facilitate studies of aqueous humor physiology and pharmacology.