Regulation of intestinal nutrient transport is impaired in aged mice

To determine the effect of age on the regulation of intestinal nutrient absorption, we fed young (7.6-mo-old) and aged (24.8-mo-old) C57BL mice diets designed to stimulate in vitro sugar or amino acid uptake in the isolated small intestine. In each age group, diet had no effect on feeding rates and body weights. D-Glucose and D-fructose uptakes by the small intestine each increased by about two times in young and 1.5 times in aged mice fed high carbohydrate diets as compared with those fed no carbohydrate. Adaptive increases in uptake by the aged group were not only reduced but also restricted to more proximal regions of the small intestine. In both age groups, diet-stimulated increases in D-glucose transport were accompanied by parallel increases in number of Na(+)-D-glucose cotransporters as estimated by specific phlorizin binding. Diet had no effect on transporter Kd for phlorizin, turnover rate of each transporter, mucosal mass or mucosal permeability. A high protein diet stimulated the uptake of L-aspartate and L-proline in young mice and of only L-aspartate in aged mice. Uptake of essential amino acids and of nonessential amino acids sharing transporters with essential ones were not regulated. Although aged mice possess adaptive mechanisms to diet that are similar to those in young mice, the effectiveness of these mechanisms may be impaired with age and may result in malabsorption symptoms so prevalent in the elderly.     

Fluorescein angiographic characteristics of macular holes before and after vitrectomy with transforming growth factor beta-2

We evaluated the fluorescein angiographic features of full-thickness macular holes before and after vitrectomy, fluid-gas exchange, and instillation of transforming growth factor beta-2 in 43 eyes in a masked fashion to evaluate the angiographic characteristics of macular holes preoperatively and the changes that occur with successful and unsuccessful closure of the macular hole. Hyperfluorescence was present in the base of the macular hole preoperatively in 34 of 43 eyes (79.1%), was questionable in eight of 43 eyes (18.6%), and was definitely absent in only one of 43 eyes (2.3%). The hyperfluorescence in the base of the macular hole disappeared in 19 of 20 eyes (95%) with successful closure of the macular hole (P < .00001) and appeared to be caused by blocked fluorescence at the site of the macular hole. The photographic features of eyes with unsuccessful closure of the macular hole changed little, except that the size of the cuff of neurosensory detachment around the hole increased and was associated with decreased postoperative visual acuity. These angiographic changes support the presence of a glial tissue plug bridging a small defect in the fovea of eyes with successful closure of a macular hole.     

Complications of biliary stents in obstructive pancreatic malignancies. A case report and review

Biliary stents have become a common palliative measure in the treatment of unresectable obstructive pancreatic cancer. Survival after endoscopic stenting rivals that of surgical bypass. Complications involving stents are not uncommon and can be categorized as related to placement, obstruction, migration, or fracture. A case report and review of stent-related morbidity is presented. Overall complication rates range from 15 to 34%, often requiring stent replacement and occasionally requiring surgical intervention.     

Effects of GnRH antagonist on lymphocyte subpopulations in primary and secondary lymphoid tissues of female mice

PROBLEM: GnRH analogs are playing an increasing role in the treatment of many clinical disorders. Recent studies have indicated that GnRH agonists suppress immune function in mice in vivo. The present study investigated the effects of GnRH antagonist of functional lymphocyte subsets of mice in vivo. METHOD: Three- and 10-wk old female mice received 10 micrograms of Nal-Glu daily for 15 and 30 days; changes in the immunophenotypic expression of lymphocytes from thymus, bone marrow, spleen and blood were analyzed by flow cytometry. RESULTS: The administration of GnRH antagonist to pre- and postpubertal female mice induced slight increases in lymphocyte subpopulations in primary and secondary lymphoid tissues. These effects are opposite those obtained with GnRH agonist in our earlier studies in mice. CONCLUSIONS: Assuming similar effects in humans and rodents, the gonadal steroid suppression achieved by GnRH antagonist treatment has no apparent suppressive effects on the immune system.     

Blur and contrast as pictorial depth cues

OBJECTIVE: Infusion of GH secretagogues appears to be a novel endocrine approach to reverse the catabolic state of critical illness, through amplification of the endogenously blunted GH secretion associated with a substantial IGF-I rise. Here we report the dynamic characteristics of spontaneous nightly TSH and PRL secretion during prolonged critical illness, together with the concomitant effects exerted by the administration of GH-secretagogues, GH-releasing hormone (GHRH) and GH-releasing peptide-2 (GHRP-2) in particular, on night-time TSH and PRL secretion. PATIENTS AND DESIGN: Twenty-six critically ill adults (mean +/- SEM age: 63 +/- 2 years) were studied during two consecutive nights (2100-0600 h). According to a weighed randomization, they received 1 of 4 combinations of infusions, within a randomized, cross-over design for each combination: placebo (one night) and GHRH (the next night) (n = 4); placebo and GHRP-2 (n = 10); GHRH and GHRP-2 (n = 6); GHRP-2 and GHRH + GHRP-2 (n = 6). Peptide infusions (duration 21 hours) were started after a bolus of 1 microgram/kg at 0900 h and infused (1 microgram/kg/h) until 0600 h. MEASUREMENTS: Serum concentrations of TSH and PRL were determined by IRMA every 20 minutes and T4, T3 and rT3 by RIA at 2100 h and 0600 h in each study night. Hormone secretion was quantified using deconvolution analysis. RESULTS: During prolonged critical illness, mean night-time serum concentrations of TSH (1.25 +/- 0.42 mlU/l) and PRL (9.4 +/- 0.9 micrograms/l) were low-normal. However, the proportion of TSH and PRL that was released in a pulsatile fashion was low (32 +/- 6% and 16 +/- 2.6%) and no nocturnal TSH or PRL surges were observed. The serum levels of T3 (0.64 +/- 0.06 nmol/l) were low and were positively related to the number of TSH bursts (R2 = 0.32; P = 0.03) and to the log of pulsatile TSH production (R2 = 0.34; P = 0.03). GHRP-2 infusion further reduced the proportion of TSH released in a pulsatile fashion to half that during placebo infusion (P = 0.02), without altering mean TSH levels. GHRH infusion increased mean TSH levels and pulsatile TSH production, 2-fold compared to placebo (P = 0.03) and 3-fold compared to GHRP-2 (P = 0.008). The addition of GHRP-2 to GHRH infusion abolished the stimulatory effect of GHRH on pulsatile TSH secretion. GHRP-2 infusion induced a small increase in mean PRL levels (21%; P = 0.02) and basal PRL secretion rate (49%; P = 0.02) compared to placebo, as did GHRH and GHRH + GHRP-2. CONCLUSIONS: The characterization of the specific pattern of anterior pituitary function during prolonged critical illness is herewith extended to the dynamics of TSH and PRL secretion: mean serum levels are low-normal, no noctumal surge is observed and the pulsatile fractions of TSH and PRL release are reduced, as was shown previously for GH. Low circulating thyroid hormone levels appear positively correlated with the reduced pulsatile TSH secretion, suggesting that they have, at least in part, a neuroendocrine origin. Finally, the opposite effects of different GH-secretagogues on TSH secretion further delineate particular linkages between the somatotrophic and thyrotrophic axes during critical illness.