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Biomedical subjects

John Marshall

Publications and source records attributed to John Marshall.

At least 19 recordsLinked to original sources

Mass spectrometry: uncovering the cancer proteome for diagnostics.

Despite impressive scientific achievements over the past few decades, cancer is still a leading cause of death. One of the major reasons is that most cancer patients are diagnosed with advanced disease. This is clearly illustrated with ovarian cancer in which the overall 5-year survival rates are only 20-30%. Conversely, when ovarian cancer is detected early (stage 1), the 5-year survival rate increases to 95%. Biomarkers, as tools for preclinical detection of cancer, have the potential to revolutionize the field of clinical diagnostics. The emerging field of clinical proteomics has found applications across a wide spectrum of cancer research. This chapter will focus on mass spectrometry as a proteomic technology implemented in three areas of cancer: diagnostics, tissue imaging, and biomarker discovery. Despite its power, it is also important to realize the preanalytical, analytical, and postanalytical limitations currently associated with this methodology. The ultimate endpoint of clinical proteomics is individualized therapy. It is essential that research groups, the industry, and physicians collaborate to conduct large prospective, multicenter clinical trials to validate and standardize this technology, for it to have real clinical impact.

Animals↗

The role of 12/15-lipoxygenase in the expression of interleukin-6 and tumor necrosis factor-alpha in macrophages.

12/15-lipoxygenase (12/15-LO) enzyme and products have been associated with inflammation and atherosclerosis. However, the mechanism of effects of the 12/15-LO products has not been fully clarified. To study the role of 12/15-LO in cytokine expression, experiments with direct additions of the12/15-LO products, 12(S)-hydroxyeicosa tetraenoic acid or 12(S)-hydroperoxyeicosa-5Z, 8Z, 10E, or 14Z-tetraenoic acid to macrophages were first carried out, and results showed that the 12/15-LO products stimulated mRNA and protein expression of IL-6 and TNF-alpha in a dose-dependent manner. In contrast, an inactive analogue of 12(S)-hydroxyeicosa tetraenoic acid had no effect. To further explore the role of endogenous 12/15-LO in cytokine expression, we used an in vitro and in vivo model to test the effect of 12/15-LO overexpression. The models included Plox-86 cells, a J774A.1 cell line that stably overexpresses leukocyte-type 12/15-LO and primary mouse peritoneal macrophages (MPMs) from 12/15-LO transgenic mice. The results showed a clear increase in IL-6 and TNF-alpha expression in Plox-86 cells and MPMs from 12/15-LO transgenic mice, compared with mock-transfected J774A.1 cells and MPMs from control C57BL6 mice. IL-1beta, IL-12, and monocyte chemoattractant protein (MCP)-1 mRNA were also increased in Plox-86 cells. These data clearly suggest a clear role of 12/15-LO pathway in cytokine production. We also demonstrated that signaling pathways including protein kinase C, p38 MAPK (p38), c-jun NH(2)-terminal kinase as well as nicotinamide adenine dinucleotide phosphate oxidase are important for 12-(S)-hydroxyeicosatetraenoic acid-induced increases in IL-6 and TNF-alpha gene expression. These results suggest a potentially important mechanism linking 12/15-LO activation to chronic inflammation and atherosclerosis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

Actinfilin is a Cul3 substrate adaptor, linking GluR6 kainate receptor subunits to the ubiquitin-proteasome pathway.

Kainate receptors have been implicated in excitotoxic neuronal death induced by diseases such as epilepsy and stroke. Actinfilin, a synaptic member of the BTB-Kelch protein family, is known to bind to the actin cytoskeleton. However, little is understood about its function at the synapse. Here, we report that actinfilin is able to bind to GluR6, a kainate-type glutamate receptor subunit, and target GluR6 for degradation. Like many members of its protein family, actinfilin acts as a substrate adaptor, binding Cullin 3 (Cul3) and linking GluR6 to the E3 ubiquitin-ligase complex. We map this interaction to the Kelch repeat domain of actinfilin and the GluR6 C terminus. Co-immunoprecipitation and immunofluorescence studies show that GluR6 is ubiquitinated, and that GluR6 levels are decreased by actinfilin overexpression but increased when actinfilin levels are reduced by specific RNA interference. Furthermore, actinfilin-Cul3 interactions appear to be important for regulating surface GluR6 expression. Synaptic GluR6 levels are elevated in mice with lowered neuronal Cul3 expression and when dominant-negative forms of Cul3 are transfected into hippocampal neurons. Together our data demonstrate that actinfilin acts as a scaffold, linking GluR6 to the Cul3 ubiquitin ligase to provide a novel mechanism for kainate receptor degradation.

Animals↗

Clinical implications of the mechanism of epidermal growth factor receptor inhibitors.

Novel therapeutic agents that target the epidermal growth factor receptor (EGFR) constitute an important addition to the therapeutic armamentarium for the treatment of metastatic disease. EGFR-targeted agents currently approved by the U.S. Food and Drug Administration include cetuximab, a monoclonal antibody for the treatment of colorectal cancer; and the small-molecule EGFR tyrosine kinase inhibitor (TKI) erlotinib for the treatment of nonsmall cell lung cancer (NSCLC) and pancreatic cancer. Approval of the TKI gefitinib for NSCLC recently was withdrawn. Although both classes of anti-EGFR agents target the same receptor, substantial distinctions regarding their mechanism significantly affect dosing requirements, toxicity profiles, and their use as combination agents.

Antibodies, Monoclonal↗

Insulin-like growth factor-1 modulation of CaV1.3 calcium channels depends on Ca2+ release from IP3-sensitive stores and calcium/calmodulin kinase II phosphorylation of the alpha1 subunit EF hand.

In neurons, L-type calcium channels (CaV1.2 and CaV1.3) regulate an extensive range of functions. However, the roles of CaV1.3-containing L channels, which are physiologically and pharmacologically distinct from the better understood CaV1.2 channels, are only beginning to be determined. We find that CaV1.3 channels are modulated by the insulin-like growth factor-1/receptor tyrosine kinase (IGF-1/RTK) through a signaling pathway that involves phospholipase C, calcium release from IP3-sensitive internal stores, and calcium/calmodulin kinase II. In addition, we find that the IGF-1-induced modulation requires phosphorylation of a specific serine residue, S1486, in the EF hand motif of the CaV1.3 subunit. This modulation alters CaV1.3 activity, causing a left shift in the current-voltage relationship and strongly potentiating peak currents at hyperpolarized membrane potentials. We also find that CaV1.3 channels and their RTK-dependent potentiation contribute to the regulation of the survival-promoting transcription factor cAMP response element-binding protein (CREB): in both cortical and hippocampal neurons, depolarization and IGF-1 rapidly increase phospho-CREB levels in a manner that requires CaV1.3 activity and the S1486 phosphorylation site to achieve a full effect. Although the full effects of CaV1.3 channels remain to be determined, their preferential localization to dendritic shafts and spine heads coupled with their ability to activate at relatively hyperpolarized and even subthreshold potentials suggests that CaV1.3 activity may subserve different cellular functions from CaV1.2 and, in particular, may be important in transducing signals initiated by excitatory neurotransmission.

Animals↗

CaMKII-independent effects of KN93 and its inactive analog KN92: reversible inhibition of L-type calcium channels.

Widely regarded as a specific and potent inhibitor of CaM kinases, especially CaMKII, KN93 has long been used to investigate the possible roles of CaMKII in a wide range of biological functions and systems, such as cultured cells, primary neurons, and brain slices. However, here we present evidence showing that KN93 and its structural analog KN92, which does not inhibit CaMKII, exert an unexpected, reversible, and specific reduction of currents of L-type calcium channels (CaV1.3 and CaV1.2), as compared to N-type calcium channels (CaV2.2). This effect is dependent not only on incubation time, but also on the dose of KN93 or KN92. Moreover, the effect appears to be independent of endocytosis, exocytosis, and proteasome activity. Washout and return to normal media rescues the L channel currents. Conversely, the structurally unrelated CaMKII inhibitor, AIP, fails to mimic the KN93/KN92 effect on L channel currents. Together, our data suggest that, in addition to inhibiting CaMKII, KN93 also affects CaV1.3 and CaV1.2 calcium channels in a CaMKII-independent manner.

Benzylamines↗

Phase I study of liposome-encapsulated c-raf antisense oligodeoxyribonucleotide infusion in combination with radiation therapy in patients with advanced malignancies.

PURPOSE: Raf proteins are key elements of growth-related cellular signaling pathways and are a component of cancer cell resistance to radiation therapy. Antisense oligonucleotides to c-raf-1 permit highly selective inhibition of the gene product and offer a strategy for sensitizing cancer cells to radiation therapy. In this dose escalation study, we evaluated the safety of combined liposomal formulation of raf antisense oligonucleotide (LErafAON) and radiation therapy in patients with advanced malignancies. EXPERIMENTAL DESIGN: Patients with advanced solid tumors were treated with LErafAON in a phase I dose escalation study while receiving palliative radiation therapy. Drug-related and radiation-related toxicities were monitored. Pharmacokinetics and expression of c-raf-1 mRNA and Raf-1 protein were determined in peripheral blood mononuclear cells. RESULTS: Seventeen patients with palliative indications for radiation therapy were entered into this study. Thirteen patients received daily infusions of LErafAON and four received twice-weekly infusions. Radiation therapy was delivered in daily 300-cGy fractions over 2 weeks. Patients tolerated radiation, and no unexpected radiation-related side effects were observed. Drug-related reactions (grade > or =2), such as back pain, chills, dyspnea, fatigue, fever, flushing, and hypertension, were observed in most patients and were managed by premedication with corticosteroids and antihistamines. Serious adverse events occurred in five patients, including acute infusion-related symptoms, abnormal liver function tests, hypoxia, dehydration, diarrhea, esophagitis, fever, hypokalemia, pharyngitis, and tachypnea. Twelve of 17 patients were evaluable for tumor response at completion of treatment; four showed partial response, four showed stable disease, and four experienced progressive disease. The intact rafAON was detected in plasma for 30 minutes to several hours. Six patients with partial response or stable disease were evaluable for c-raf-1 mRNA and/or Raf-1 protein expression. Inhibition of c-raf-1 mRNA was observed in three of five patients. Raf-1 protein was inhibited in four of five patients. CONCLUSION: This is the first report of the combined modality treatment using antisense oligonucleotides with radiation therapy in patients with advanced cancer. A dose of 2.0 mg/kg of LErafAON administered twice weekly is tolerated with premedication and does not enhance radiation toxicity in patients. The observation of dose-dependent, infusion-related reactions has led to further modification of the liposomal composition for use in future clinical trials.

Abdominal Pain↗

A gradient of acute gastroenteritis was characterized, to assess risk of long-term health sequelae after drinking bacterial-contaminated water.

OBJECTIVE: A municipal water system became contaminated with Escherichia coli O157:H7 and Campylobacter spp. Beginning 2 years after an outbreak, all residents from the region were invited to participate in a cohort study assessing the risk of long-term sequelae. We aimed to develop a method to grade the accuracy and severity of self-reported acute symptoms. STUDY DESIGN AND SETTING: We corroborated participant survey responses with health records at the time of the outbreak. Of the 4,135 participants, 1,388 were asymptomatic during the outbreak, 1,752 had symptoms of acute self-limited gastroenteritis that could neither be confirmed nor refuted by prior health records, and 995 had symptoms that necessitated medical attention (and thus were confirmed by prior health records). RESULTS: The gradient related to the severity of acute symptoms. Compared to those with unconfirmed gastroenteritis, participants with confirmed gastroenteritis were more likely to describe fever, bloody diarrhea, and prolonged diarrhea (all P < .03). The gradient also correlated with long-term plausible outcomes, including chronic gastrointestinal symptoms, chronic symptoms of arthritis or depression, and the avoidance of municipal water ingestion after the outbreak (P for trend consistently < .03). Conversely, for the outcome of chronic tinnitus, an association was neither expected nor observed (P for trend = .26). CONCLUSION: We successfully characterized a gradient to be used in future primary analyses assessing the risk of long-term health sequelae after an outbreak.

Acute Disease↗

AAV8-mediated expression of glucocerebrosidase ameliorates the storage pathology in the visceral organs of a mouse model of Gaucher disease.

BACKGROUND: Gaucher disease is the most common of the lysosomal storage disorders. The primary manifestation is the accumulation of glucosylceramide (GL-1) in the macrophages of liver and spleen (Gaucher cells), due to a deficiency in the lysosomal hydrolase glucocerebrosidase (GC). A Gaucher mouse model (D409V/null) exhibiting reduced GC activity and accumulation of GL-1 was used to evaluate adeno-associated viral (AAV)-mediated gene therapy. METHODS: A recombinant AAV8 serotype vector bearing human GC (hGC) was administered intravenously to the mice. The levels of hGC in blood and tissues were determined, as were the effects of gene transfer on the levels of GL-1. Histopathological evaluation was performed on liver, spleen and lungs. RESULTS: Vector administration to pre-symptomatic Gaucher mice resulted in sustained hepatic secretion of hGC at levels that prevented GL-1 accumulation and the appearance of Gaucher cells in the liver, spleen and lungs. AAV administration to older mice with established disease resulted in normalization of GL-1 levels in the spleen and liver and partially reduced that in the lung. Analysis of the bronchoalveolar lavage fluid (BALF) from treated mice showed significant correction of the abnormal cellularity and cell differentials. No antibodies to the expressed hGC were detected following a challenge with recombinant enzyme suggesting the animals were tolerized to human enzyme. CONCLUSIONS: These data demonstrate the effectiveness of AAV-mediated gene therapy at preventing and correcting the biochemical and pathological abnormalities in a Gaucher mouse model, and thus support the continued consideration of this vector as an alternative approach to treating Gaucher disease.

Animals↗

Objective measurement of intraocular lens movement and dioptric change with a focus shift accommodating intraocular lens.

PURPOSE: To objectively measure the shift and refractive change of the 1CU accommodating intraocular lens (IOL) (HumanOptics) and compare them to that of a monofocal AcrySof MA30 IOL (Alcon Laboratories) in the fellow eye. SETTING: Ophthalmology Department, St. Thomas' Hospital, London, United Kingdom. METHODS: Thirty patients who had bilateral cataract surgery 18 to 24 months previously with a 1CU IOL prospectively randomly allocated to 1 eye and an AcrySof MA30 monofocal IOL to the other eye were examined. Distance correction, near vision, reading fluency, near point, and defocus to minus spheres were measured. Intraocular lens shift to an accommodative stimulus following instillation of pilocarpine 4% was measured with the ACMaster. Refractive change between distance and near was measured with the Tracey wavefront analyzer. RESULTS: Of the original 30 patients recruited, complete measurements could only be obtained for 20. There was no significant difference in near visual function with either IOL. A small anterior movement of the 1CU was seen with accommodation 0.010 mm +/- 0.028 (SD). After pilocarpine 4% instillation, a forward movement of 0.220 +/- 0.169 mm was seen with the 1CU compared to a backward movement of 0.028 +/- 0.095 with the MA30. There was no significant correlation between distance corrected near visual acuity and IOL movement. No change in spherical equivalent between distance and near was seen on wavefront analysis of either IOL. CONCLUSIONS: Small forward movement of the 1CU IOL was seen with accommodation and increased following pilocarpine, compared to the posterior movement of the MA30 IOL. The amount of the IOL shift was not sufficient to provide useful near vision, but the difference suggests that the engineering concept behind the 1CU IOL is valid.

Accommodation, Ocular↗

Topography-guided customized laser-assisted subepithelial keratectomy for the treatment of postkeratoplasty astigmatism.

PURPOSE: To assess topography-assisted corneal wavefront excimer laser surface ablation for the correction of ametropia and irregular astigmatism after keratoplasty. SETTING: Department of Ophthalmology, St. Thomas' Hospital, London, United Kingdom. METHODS: In this pilot study, 15 patients (16 eyes) who were intolerant of spectacle and contact lens correction due to astigmatic anisometropia after keratoplasty (15 penetrating and 1 lamellar) had topography-assisted customized excimer laser treatments. Corneal topographic data using a Keratron Scout, Placido disk system allowed for preoperative analysis of wavefront anomalies of the anterior corneal surface from which a customized excimer laser correction of both lower-order aberrations (LOAs) and higher-order aberrations (HOAs) was prepared (ORK software) for treatment with a Schwind Esiris flying-spot laser. All eyes had laser-assisted subepithelial keratectomy (LASEK) using 15% alcohol with a 20-second to 30-second application. Four eyes received an application of mitomycin-C (MMC) 0.2 mg/mL for 1 minute after stromal ablation. RESULTS: The mean preoperative spherical equivalent (SE) was -3.50 diopters (D) +/- 3.97 (SD) (range +1.625 to -9.25 D). The preoperative cylindrical error was -7.2 D (range -2.75 to -13.5 D). The programmed laser correction was -3.14 D (range +1.62 to -9 D) with a maximum attempted cylindrical correction of -7 D. Adherent LASEK epithelial flaps along suture lines and the graft-host junction were noted in 9 eyes (56%), although it was possible to obtain and replace a partial flap. A follow-up of 18 months was achieved in all eyes. At the final follow-up visit, the mean postoperative SE was -1.08 +/- 1.85 D (range +3 to -4.78 D) (P<.01, F<.01). Ten eyes (62.5%) were within +/-1 D of the intended correction. The mean postoperative cylindrical error was -2.72 D (range -0.5 to -6.5 D) (P<.001), with vector analysis demonstrating a mean 6.23 D correction. Analysis of HOAs using a 6.0 mm pupil size demonstrated a significant reduction of higher-order root mean square (RMS) (P<.002), trefoil (P<.005), and 4th-order spherical aberration (P<.02) at 18 months compared with preoperative values. Uncorrected visual acuity improved in all eyes (P<.0001). Best spectacle-corrected visual acuity was unchanged or improved in 13 eyes (81%) and worse in 2 eyes by 1 line; 1 eye lost 3 lines due to an increase in preexisting cataract. In eyes that did not receive MMC, corneal haze (grade II to IV) was encountered in 3 eyes (27%). One eye required phototherapeutic keratectomy with MMC application at 12 months. Of the 4 eyes treated with MMC, 1 had trace haze and 3 had no detectable haze. There were no reported cases of epithelial instability, ectasia, or graft rejection. CONCLUSIONS: Topography-assisted customized LASEK was effective in the correction of postkeratoplasty astigmatism. A significant improvement of both LOAs and HOAs was obtained with good refractive stability for over 18 months. Iatrogenic haze typically occurred but appeared to be minimized with adjunctive use of intraoperative MMC.

Adult↗

Cellular effects of mitomycin-C on human corneas after photorefractive keratectomy.

PURPOSE: To investigate the effects of mitomycin-C (MMC) on epithelial and keratocyte cell kinetics after photorefractive keratectomy (PRK) using an in vitro human cornea model. SETTING: Department of Academic Ophthalmology, Rayne Institute, St. Thomas' Hospital, London, United Kingdom. METHODS: Twenty-four human eye-bank corneas were placed in a specially designed acrylic corneal holder and cultured using the air-interface organ culture technique for up to 4 weeks. The corneas were divided into 3 groups. Group 1 consisted of 8 human corneas that had -9.00 diopter (D) myopic PRK without MMC application. Group 2 consisted of 8 corneas that had -9.00 D PRK with MMC (0.2 microg/mL) application for 1 minute on the stromal surface after ablation. Group 3 consisted of 8 corneas that had -9.00 D PRK with 2-minute exposure to MMC (0.2 microg/mL). Temporal events in epithelial and keratocyte cell kinetics were evaluated using digital imaging, confocal microscopy, and light microscopy. RESULTS: Epithelial latency was significantly delayed with MMC application in Groups 2 and 3 (P<.001). Epithelial migration was delayed in Group 3 (2-minute exposure) compared to migration in Group 2 (P<.04), with a consequent delay in epithelial closure (P<.001). Group 3 corneas had poorly differentiated epithelium that was significantly thinner than in Groups 1 and 2 (P<.0001). A significant delay in keratocyte regeneration occurred after MMC application (P<.0005). At 4 weeks, the anterior stromal cell density was significantly lower in Group 3 than Group 2 (P<.001). There were no significant differences in the mid- and posterior stromal keratocyte density between the groups. CONCLUSIONS: Results suggest that epithelial healing after MMC is characterized by prolonged latency and decreased migration rate dependent on exposure time. Mitomycin C application did not result in increased loss of keratocytes, but it significantly delayed keratocyte repopulation in the anterior stroma. The use of MMC 0.2 microg/mL for 1 minute resulted in optimum modulation of healing characterized by reduced keratocyte activation with normal epithelial differentiation.

Alkylating Agents↗

Effects of ablation diameter on long-term refractive stability and corneal transparency after photorefractive keratectomy.

OBJECTIVE: To evaluate the effects of ablation diameter on long-term refractive stability and corneal transparency after photorefractive keratectomy (PRK). DESIGN: Long-term, prospective, follow-up study. PARTICIPANTS: One hundred twenty-three eyes treated between 1990 and 1993 at one institution as part of a number of ethical committee-approved clinical studies underwent long-term follow-up at 10 to 12 years after PRK. INTERVENTION: Photorefractive keratectomy was performed using the Summit Technology UV 200 and OmniMed Excimer lasers with either 4.0-mm (n = 36), 5.0-mm (n = 47), or 6.0-mm (n = 40) optical zones and either -3.0-diopters (D) or -6.0-D myopic spherical corrections, based on the original Munnerlyn algorithms. MAIN OUTCOME MEASURES: Refractive stability, refractive predictability, best spectacle-corrected visual acuity, and corneal haze. RESULTS: Refractive outcome at 1 and 10 to 12 years of follow-up was better with 6.0-mm treatments, especially for -6.0-D corrections (P>0.001). The early hyperopic shift was significantly reduced with 6.0-mm zones, with less regression between 1 and 6 months, compared with 5.0- and 4.00-mm PRK, especially for -6.0-D corrections (P<0.001). The postoperative refraction remained stable between 1 and 10 to 12 years in all groups. Objective measurements of haze were less with 6.0-mm compared with 4.0- and 5.0-mm treatments (P<0.001). Night vision problems were significantly less with 6.0-mm PRK (P<0.01). There was no evidence of progressive hyperopic shift, corneal ectasia, or late onset of corneal haze in any of the eyes during the follow-up period. CONCLUSIONS: Refractive stability was maintained between 1 year and 10 to 12 years after PRK with 4.0-, 5.0-, and 6.0-mm optical zones. A significant linear trend was observed in terms of refractive predictability, early hyperopic shift, regression, corneal transparency, and night haloes with better outcomes in PRK with a larger ablation zone. None of the eyes had sight-threatening complications such as ectasia or late-onset corneal haze during the follow-up.

Cornea↗

Optimum use of biologics and role of maintenance therapy in colon cancer.

The current standard of care for the treatment of metastatic colorectal cancer involves at least six different regimens, and with the advent of new therapies, including biologic therapies, patients are projected to live beyond an average of 2 years. Data suggest a synergy between the biologics, which are in their infancy in terms of utilization, and they are being tested in the adjuvant setting in stage II and stage III disease. Ongoing and future trials will determine how best to incorporate these medicines into combination chemotherapy and determine if these medicines (or others) will have a role in maintenance chemotherapy for patients with metastatic colon cancer. However, the concept of incorporating maintenance therapy for colon cancer is clearly not established. Maintenance therapy has a requirement for less toxicity than current front-line therapies, and over the coming years, new agents will become available that maintain response and improve quality of life. Clinical trials involving novel agents as maintenance therapy are needed.

Antineoplastic Combined Chemotherapy Protocols↗

Age-related maculopathy and the impact of blue light hazard.

The pathogenesis of age-related maculopathy (ARM), the most common cause of visual loss after the age of 60 years, is indeed a complicated scenario that involves a variety of hereditary and environmental factors. The pathological cellular and molecular events underlying retinal photochemical light damage, including photoreceptor apoptosis, have been analysed in experimental animal models. Studies of age-related alterations of the retina and photoreceptors, the accumulation of lipofuscin in retinal pigment epithelium (RPE) cells, and the formation of drusen have greatly contributed to our knowledge. A new concept of an inflammatory response to drusen has emerged, suggesting immunogenic and systemic reactions in Bruch's membrane and the subretinal space. Oxidative stress and free radical damage also impact on the photoreceptors and RPE cells in the ageing eye. Based on the photoelectric effect, a fundamental concept in quantum physics, the consequences of high-energy irradiation have been analysed in animal models and cell culture. Short-wavelength radiation (rhodopsin spectrum), and the blue light hazard (excitation peak 440 nm), have been shown to have a major impact on photoreceptor and RPE function, inducing photochemical damage and apoptotic cell death. Following cataract surgery, there is a dramatic change in ocular transmittance. In aphakic or pseudophakic eyes (with clear intraocular lenses), high-energy (blue) and ultraviolet-A radiation strikes the retina. Epidemiological data indicate a significantly increased 5-year incidence of late ARM in non-phakic eyes compared with phakic eyes. In recent years, putative prophylactic measures against ARM have emerged. The implantation of 'yellow' intraocular lenses (IOLs) that absorb high-energy blue radiation is, from a theoretical point of view, the most rational approach, and, from a practical point of view, is easy to accomplish. With increasing age, RPE cells accumulate lipofuscin (chromophore A2E). It is noteworthy that the yellow IOL not only protects A2E-laden human RPE cells from blue light (peak 430 nm) damage, but also alleviates the detrimental effects of green (peak 550 nm) and white light. A prophylactic treatment using antioxidants is aimed at counteracting oxidative stress and free radical cellular damage. The Age-Related Eye Disease Study (AREDS), a randomized clinical trial, showed a significantly lower incidence of late ARM in a cohort of patients with drusen maculopathy treated with high doses of antioxidants than in a placebo group. In recent years, considerable progress in retinal research has been achieved, creating a platform for the search for new prophylactic and therapeutic measures to alleviate or prevent photoreceptor and RPE degeneration in ARM.

Animals↗

Human scleral hydraulic conductivity: age-related changes, topographical variation, and potential scleral outflow facility.

PURPOSE: To measure the specific hydraulic conductivity (K) of human sclera over a range of ages, to assess topographical variation, and to provide a theoretical estimate of potential scleral outflow facility. METHODS: Human donor sclera (n = 18; mean age 56.7 +/- 25.9 years; range 4-89) was clamped in a modified Ussing chamber connected to a water column set at 15.7 mm Hg. Column descent was measured over 24 hours at 20 degrees C with a digital micrometer. Scleral thickness of glutaraldehyde-fixed specimens was measured by light microscopy, taking the mean of 15 measurements per donor. Topographical variation in hydraulic conductivity (HC) was determined in an additional 10 donor eyes (mean age, 54.1 +/- 26.4 years; range 12-89), comparing anterior, equatorial, and posterior sclera. The potential transscleral outflow facility was calculated by multiplying HC by total scleral surface area and adjusting water viscosity to core body temperature. RESULTS: Mean K +/- 1SD in adults (>18 years) was 5.85 +/- 3.89 x 10(-18) m(2). K tended to be higher in pediatric donors, but there was no statistically significant age-related change. However, when all data sets were combined (n = 28), HC showed a significant decline with age. There was no significant topographical variation in HC. The potential transscleral outflow facility was 0.33 microL.min(-1).mm Hg(-1). CONCLUSIONS: Quantifying HC may help refine ocular pharmacotherapy, as transscleral water movement increases intraocular drug elimination and impedes transscleral drug delivery. The potential scleral outflow is two to three times higher than that which occurs in vivo; hence, medical or surgical interventions that fully exploit this pathway have considerable capacity to lower intraocular pressure.

Adolescent↗

A randomized controlled trial of laparoscopic nissen fundoplication versus proton pump inhibitors for treatment of patients with chronic gastroesophageal reflux disease: One-year follow-up.

A randomized controlled trial conducted in patients with gastroesophageal reflux disease compared optimized medical therapy using proton pump inhibitor (n = 52) with laparoscopic Nissen fundoplication (n = 52). Patients were monitored for 1 year. The primary end point was frequency of gastroesophageal reflux dis-ease symptoms. Surgical patients had improved symptoms, pH control, and overall quality of life health index after surgery at 1 year compared with the medical group. The overall gastroesophageal reflux disease symptom score at 1 year was unchanged in the medical patients, but improved in the surgical patients. Fourteen patients in the medical arm experienced symptom relapse requiring titration of the proton pump inhibitor dose, but 6 had satisfactory symptom remission. No surgical patients required additional treatment for symptom control. Patients controlled on long-term proton pump inhibitor therapy for chronic gastroesophageal reflux disease are excellent surgical candidates and should experience improved symptom control after surgery at 1 year.

Adult↗