Studies have documented biodiversity losses due to intensification of coffee management (reduc-tionPalabras Clave: agroecosistema, biodiversidad, café con sombra, café sin sombra, característico del sitio, meta análisis, producción de café

Pterygium pathogenesis is mainly related to UV light exposure. However, the exact mechanisms by which it is formed have not been elucidated. Clinical advances in surgical treatment use conjunctival autografts and amniotic membranes in combination with adjuvant therapies, including mitomycin C, β-radiation, and 5-fluoroacil, to reduce recurrence. Several studies aim to unveil the molecular mechanisms underlying pterygium growth and proliferation. They demonstrate the role of different factors, such as viruses, oxidative stress, DNA methylation, apoptotic and oncogenic proteins, loss of heterozygosity, microsatellite instability, inflammatory mediators, extracellular matrix modulators, lymphangiogenesis, cell epithelial-mesenchymal transition, and alterations in cholesterol metabolism in pterygium development. Understanding the molecular basis of pterygium provides new potential therapeutic targets for its prevention and elimination. This review focuses on providing a broad overview of what is currently known regarding molecular mechanisms of pterygium pathogenesis.

Fasting gastrointestinal motility in the human is characterized by the regular cycling activity of the migrating motor complex (MMC). Our purpose was to define the variability of the MMC within and between a group of six healthy subjects studied for 6-9 hr over six separate days with a perfused catheter system. A total of 88 phase III events was observed during 255 hr of recording in this group. The mean MMC cycling time varied significantly between subjects (range 113-230 min, P less than 0.001), and variation within subjects also was wide (SD range 58-70 min). Seventy-one percent of phase III events commenced in the gastric antrum, 18% in the proximal duodenum, 10% in the distal duodenum, and 1% in the proximal jejunum. For each subject, the velocity of propagation of phase III decreased significantly (P less than 0.001), and phase III duration increased significantly (P less than 0.001), with increasing distance from the os. In the antrum, phase I was predominant, and significant (P less than 0.006) variation between subjects was noted for percentage of MMC cycle occupied by phase I (overall mean +/- SD 55 +/- 23%). Phase II was predominant in both duodenum and jejunum (mean range 70-80%), and no significant variation was noted between subjects for percentage of MMC occupied by phase II. We conclude that human MMC activity varies widely between individuals and within the same individual when studied on separate days.

No abstract

A prospective, randomized, placebo-controlled, double-blind, multicenter clinical trial of intravenous somatostatin (Stilamin; Serono Laboratories, Inc., Randolph, MA) was performed in 102 patients with actively bleeding esophageal varices from August, 1985, to November, 1986. Patients had major hemorrhage indicated by hematemesis or melena and evidence of significant blood loss. For entry, patients had to have endoscopic demonstration of active bleeding from esophageal varices or stigmata of recent hemorrhage and bright red blood in the gastric aspirate with no other source of bleeding found. Randomized patients received identical-appearing somatostatin or placebo for a 30-hr study period. Those given somatostatin received a 250-micrograms bolus and a 250-micrograms per hr infusion with repeat bolus and doubling of the infusion if the bleeding was not controlled. In retrospect, 18 patients could not be evaluated. Of the 84 evaluable patients, 48 received somatostatin and 36 placebo. They were comparable in age, gender, severity of liver disease and history of variceal bleeding. Transfusion requirements were similar in both groups. Bleeding stopped for 12 consecutive hr during 30 hr of the study period in 31 (65%) of the somatostatin group vs. 30 (83%) of the placebo group (p = 0.06). The median time to cessation of bleeding was 2 hr in the placebo group and 3 hr in the somatostatin group. Deaths following the study period were nine (25%) in the placebo group and 15 (31%) in the somatostatin group. Within the limitations of the present study, we conclude that somatostatin was ineffective in the management of active bleeding of esophageal varices.

No abstract

The effect of increased bolus viscosity on esophageal peristaltic function was studied in six healthy volunteer subjects. Intraluminal pressure events were measured with an infused catheter system and lower esophageal sphincter pressure was monitored continuously with a Dent sleeve. Boluses with viscosities of 2.5, 8.7, 48, and 860 centipoise (cP) were compared with a water bolus. Increasing bolus viscosity to 48 and 860 cP elicited a slowing of wave velocity, an increase in wave duration, and a prolongation of lower esophageal sphincter relaxation. The initial change noted at lower viscosities was an increased duration of contraction wave. Maximal changes were noted at the 48 cP bolus. In conclusion, increased bolus viscosity significantly alters human esophageal peristalsis. These changes may be mediated by esophageal stretch reflexes or by the intrinsic properties of the esophageal musculature or both.

Exocrine pancreatic insufficiency has been observed in some diabetics with peripheral neuropathy and diarrhea. Several mechanisms may be responsible for this insufficiency: (1) pancreatic atrophy, (2) disruption of the cholinergic enteropancreatic reflexes, or (3) elevated serum levels of peptides such as glucagon and pancreatic polypeptide which are known to inhibit pancreatic exocrine secretion. To clarify the mechanism(s) involved in this exocrine pancreatic impairment, we studied 10 diabetics with diarrhea and peripheral neuropathy. Their results were compared to those of eight normal volunteers. Each subject underwent a standardized pancreatic function study which assessed nonstimulated secretion, the response to intrajejunal infusion of a mixture of amino acids, and the output following intravenous administration of secretin and cholecystokinin (CCK). In separate studies, the effect of a background infusion of bethanechol and secretin on the pancreatic response to CCK was assessed in six patients and six normal controls. Compared to normals, all diabetics exhibited a significant reduction in both enzyme and bicarbonate secretion to all stimuli. This reduction was not corrected by administering bethanechol. Plasma glucagon and pancreatic polypeptide levels in diabetics were not significantly higher than those in controls. We conclude that diabetics with diarrhea and peripheral neuropathy exhibit impairment of their exocrine pancreatic secretion and possible mechanisms for this are discussed.