The complete healing of wounds is the final step in a highly regulated response to injury. Although many of the molecular mediators and cellular events of healing are known, their manipulation for the enhancement and acceleration of wound closure has not proven practical as yet. We and others have established that adenosine is a potent regulator of the inflammatory response, which is a component of wound healing. We now report that ligation of the Gαs-linked adenosine receptors on the cells of an artificial wound dramatically alters the kinetics of wound closure. Excisional wound closure in normal, healthy mice was significantly accelerated by topical application of the specific A2A receptor agonist CGS-21680 (50% closure by day 2 in A2 receptor antagonists. In rats rendered diabetic (streptozotocin-induced diabetes mellitus) wound healing was impaired as compared to nondiabetic rats; CGS-21680 significantly increased the rate of wound healing in both nondiabetic and diabetic rats. Indeed, the rate of wound healing in the CGS-21680–treated diabetic rats was greater than or equal to that observed in untreated normal rats. These results appear to constitute the first evidence that a small molecule, such as an adenosine receptor agonist, accelerates wound healing in both normal animals and in animals with impaired wound healing.

Lateral canthoplasty is a useful method to restore eyelid function and to protect the ocular surfaces. The success of the procedure depends on the proper analysis of periorbital anatomy as it relates to the specific indication for lateral canthoplasty. We report the experience with 1565 lateral canthoplasties with emphasis on the evaluation of newer techniques that better address anatomic and functional requirements. Between 1981 and 1994, 1565 lateral canthoplasties were performed in 684 patients. Of these, 1369 "reconstructive" lateral canthoplasties were performed in 586 patients and 196 "cosmetic" lateral canthoplasties were performed in 98 patients. All operations were performed by a single surgeon (Jelks), and follow-up ranged from 1 to 14 years. The evolution of the operative technique for lateral canthoplasty has been toward an operation that corresponds with the anatomy of the individual. Indications for the procedure include lateral canthal dystopia, horizontal lid laxity, ectropion, entropion, lid margin eversion, lid retraction with or without soft-tissue deficiency, and aesthetic improvement. The types of procedures performed will be reviewed in detail. The evaluation of the newer forms of lateral canthoplasty as unique reconstructive tools and as adjuncts to aesthetic surgery will be discussed.

To obtain optimum proficiency in performing LCR, a minimum of 38 M-L procedures is required. Operative and patient outcomes improve beyond the early learning curve.

A 54-year-old man presented with rectal pain and bleeding secondary to ulcerated, necrotic rectal and cecal masses that resembled colorectal carcinoma upon colonoscopy. These masses were later determined to be benign amebomas caused by invasive Entamoeba histolytica , which regressed completely with medical therapy. In Western countries, the occurrence of invasive protozoan infection with formation of amebomas is very rare and can mistakenly masquerade as a neoplasm. Not surprisingly, there have been very few cases reported of this clinical entity within the United States. Moreover, we report a patient that had an extremely rare occurrence of two synchronous lesions, one involving the rectum and the other situated in the cecum. We review the current literature on the pathogenesis of invasive E. histolytica infection and ameboma formation, as well as management of this rare disease entity at a western medical center.

The anti-inflammatory mechanism of sulfasalazine is not well understood. It has recently been shown that sulfasalazine inhibits 5-aminoimidazole-4-carboxamidoribonucleotide (AICAR) transformylase, an enzyme involved in de novo purine biosynthesis. We recently demonstrated that methotrexate promotes intracellular AICAR accumulation, thereby increasing adenosine release and diminishing inflammation, so we tested the hypothesis that sulfasalazine similarly promotes intracellular AICAR accumulation. We studied adenosine release and the state of inflammation in in vitro and in vivo models of the inflammatory process. The adhesion of stimulated neutrophils (FMLP) to endothelial cells preincubated with sulfasalazine was inhibited in a dose-dependent manner. Elimination of extracellular adenosine by addition of adenosine deaminase or inhibition of adenosine by the adenosine A2 receptor antagonist 3,7-dimethyl-1-propargylxanthine (DMPX) completely reversed the anti-inflammatory effect of sulfasalazine (at concentrations <1 microM in this in vitro model. To determine whether this phenomenon was relevant to inhibition of inflammation in vivo, we studied the effect of sulfasalazine (100 mg/kg/day by gastric gavage for 3 days) on leukocyte accumulation in the murine air pouch model of inflammation. Treatment with sulfasalazine markedly decreased the number of leukocytes that accumulated in the inflamed (carrageenan, 2 mg/ml) air pouch. Injection of either adenosine deaminase or DMPX, but not the A1 receptor antagonist 8-cyclopentyl-dipropylxanthine, significantly reversed the anti-inflammatory effects of sulfasalazine treatment. Sulfasalazine increased the exudate adenosine concentration from 127 +/- 64 nM to 869 +/- 47 nM. Moreover, sulfasalazine treatment promoted a marked increase in splenocyte AICAR concentration from 35 +/- 6 to 96 +/- 3 pmols/10(6) splenocytes, which is consistent with the in vitro observation that sulfasalazine inhibits AICAR transformylase. These results indicate that sulfasalazine, like methotrexate, enhances adenosine release at an inflamed site and that adenosine diminishes inflammation via occupancy of A2 receptors on inflammatory cells. Our studies provide evidence that sulfasalazine and methotrexate may be described as a newly recognized family of anti-inflammatory agents that share the property of using adenosine as an antagonist of inflammation.

A man aged 83 years with vague perirectal symptoms had a delayed diagnosis of Paget's disease of the anus. A lack of thorough digital rectal examination failed to diagnose a mixed adenonueroendocrine tumour of the rectum in a timely matter.

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