Comparison of near heterophoria tests under varying conditions on an adult sample

PURPOSE: This study compared the near phoria measurement using the Bernell muscle balance card with and without prism neutralization, using both trial frame and phoropter correction, and compared with the conventional Maddox rod method. METHODS: Forty young normal Chinese adults had their near phoria measured with trial frame correction using the conventional muscle balance card method (method 1). Any deviation was compensated with a prism bar as an alternative approach (method 2). The conventional Maddox rod method (method 3) was also carried out for comparison. These three methods were repeated with phoropter correction and considered as methods 4, 5 and 6. RESULTS: The phorias obtained from these six methods were not significantly different from each other (repeated measures anova, p > 0.05). More than half of the subjects were exophoric. Although the difference in phoria was not significant, phoria measurement using phoropter correction yielded a greater coefficient of variation. CONCLUSIONS: Near phoria measurement using the muscle balance card conducted with trial frame correction was less variable, and was also more natural and similar to a real reading situation. The use of prism for compensation did not affect the phoria results. Exophoria seems to be more common than esophoria in young Chinese adults.     

Correction of genetic diabetes insipidus by adult hypothalamic grafts

Brattleboro rats manifest chronic diabetes insipidus as a result of the genetic deficiency of hypothalamic vasopressin. When basal hypothalamic tissue derived from adult F344 rats was implanted as cell suspensions or tissue blocks in the supraoptic regions of these animals, concentration of urine together with reduced urine output and water intake was observed in some animals. Histologic examination of the grafted brains from the responding animals revealed neuronal cells at the implant sites and vasopressin-staining fibers in the median eminence. This study demonstrates the feasibility of the grafting of adult cerebral tissues to correct a genetic hormonal deficiency.     

Evidence for distinct binding sites in the cumene hydroperoxide-dependent metabolism of benzo[a]pyrene catalyzed by cytochrome P-450

A few constitutive cytochrome P-450 isozymes in male rat liver microsomes catalyzed the metabolism of benzo[a]pyrene (BP) in cumene hydroperoxide (CHP)-dependent reactions, which produced predominantly 3-hydroxyBP and BP quinones. This process varied with the concentration of CHP. At 0.05 mM CHP, 3-hydroxyBP was the major metabolite. An increase in CHP concentration reduced 3-hydroxyBP formation but increased the level of BP quinones. This change in metabolic profile was reversed by preincubation with pyrene. Pyrene selectively inhibited quinone formation and enhanced 3-hydroxyBP formation. Naphthalene, phenanthrene and benz[a]anthracene nonspecifically inhibited total metabolism. BP binding to microsomal protein correlated with quinone formation, suggesting a common precursor reactive intermediate. BP metabolism by female rat liver microsomes also depended on CHP concentration but was much less effective than that in the male. With females, quinones were the major metabolites at all CHP concentrations, and their formation was again modulated by pyrene. These data indicate that two distinct binding sites are responsible for the formation of 3-hydroxyBP and BP quinones.     

An update of treatment options for neovascular age-related macular degeneration.

OBJECTIVES: To review the role of conventional and new treatment modalities in the management of neovascular age-related macular degeneration. DATA SOURCES AND EXTRACTION: Literature search of Medline till March 2007, using the key words/terms 'treatment' and 'age-related macular degeneration' to retrieve relevant original papers and review articles. DATA SYNTHESIS: Age-related macular degeneration is the leading cause of irreversible visual loss in the elderly in developed countries. Neovascular age-related macular degeneration has a relentless course and the consequent visual loss is debilitating. Successful treatment has always been a challenge due to poor understanding of its pathogenesis. Laser photocoagulation and photodynamic therapy with verteporfin are the standard conventional treatments. However, these approaches do not prevent disease recurrence and repeated treatments are required. Recent advances in understanding the molecular pathway for the angiogenesis of neovascular age-related macular degeneration enables exploration of new treatment approaches. Antiangiogenic therapy with anti-vascular endothelial growth factor agents, such as pegaptanib and ranibizumab, have recently been approved for clinical practice. Other antiangiogenic agents include bevacizumab, triamcinolone, and anecortave are also being evaluated in clinical trials. Additional treatment modalities include transpupillary thermotherapy and surgical intervention. CONCLUSIONS: Regarding patients with neovascular age-related macular degeneration, increased understanding in its pathogenesis coupled with rapid development in instrumental technology and new/emerging medications greatly expands available treatment options. Despite these various therapeutic options, current treatment is mainly directed at achieving visual stabilisation. Restoration of vision with newer agents is limited and not possible in every patient. Thus, early recognition and treatment to arrest the progression of neovascular age-related macular degeneration is the preferred means of attaining the best visual outcome.     

Surgical treatment of lymph nodes with metastatic melanoma from unknown primary site

To determine the prognosis of patients with lymph node metastases from an unknown primary melanoma, we retrospectively reviewed the clinicopathologic features of 188 such patients treated from 1971 through 1986 and compared their records with those of patients with clinical stage II melanoma with known primary lesions. Patients with lymph node metastases from an unknown primary melanoma represented 4.6% of all patients with melanoma treated during that period. The five- and ten-year survival rates were 42% and 40%, respectively (median, 37 months). When stratified by number of tumor-containing lymph nodes, there was no significant difference in survival between patients with an unknown primary melanoma and lymph node metastases and those with clinical stage II melanoma and known primary sites. The prognosis of the former patients is no worse than that of patients with lymph node metastases from a known primary site and should be treated in a comparable manner.     

Clinical experience with alpha-particle emitting 211At: treatment of recurrent brain tumor patients with 211At-labeled chimeric antitenascin monoclonal antibody 81C6.

alpha-Particle-emitting radionuclides, such as (211)At, with a 7.2-h half-life, may be optimally suited for the molecularly targeted radiotherapy of strategically sensitive tumor sites, such as those in the central nervous system. Because of the much shorter range and more potent cytotoxicity of alpha-particles than of beta-particles, (211)At-labeled agents may be ideal for the eradication of tumor cells remaining after surgical debulking of malignant brain tumors. The main goal of this study was to investigate the feasibility and safety of this approach in patients with recurrent malignant brain tumors. METHODS: Chimeric antitenascin monoclonal antibody 81C6 (ch81C6) (10 mg) was labeled with 71-347 MBq of (211)At by use of N-succinimidyl 3-[(211)At]astatobenzoate. Eighteen patients were treated with (211)At-labeled ch81C6 ((211)At-ch81C6) administered into a surgically created resection cavity (SCRC) and then with salvage chemotherapy. Serial gamma-camera imaging and blood sampling over 24 h were performed. RESULTS: A total of 96.7% +/- 3.6% (mean +/- SD) of (211)At decays occurred in the SCRC, and the mean blood-pool percentage injected dose was < or = 0.3. No patient experienced dose-limiting toxicity, and the maximum tolerated dose was not identified. Six patients experienced grade 2 neurotoxicity within 6 wk of (211)At-ch81C6 administration; this neurotoxicity resolved fully in all but 1 patient. No toxicities of grade 3 or higher were attributable to the treatment. No patient required repeat surgery for radionecrosis. The median survival times for all patients, those with glioblastoma multiforme, and those with anaplastic astrocytoma or oligodendroglioma were 54, 52, and 116 wk, respectively. CONCLUSION: This study provides proof of concept for regional targeted radiotherapy with (211)At-labeled molecules in oncology. Specifically, the regional administration of (211)At-ch81C6 is feasible, safe, and associated with a promising antitumor benefit in patients with malignant central nervous system tumors.