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Objective: According to current guidelines, the first line of treatment for mild-to-moderate dehydration is oral rehydration; the second line is rehydration through a nasogastric tube. Both methods are widely underused. This study was conducted to evaluate parents' attitudes towards rehydration methods used in pediatric emergency departments., Design: 100 questionnaires were distributed to parents of children who visited emergency room due to gastroenteritis and suspected dehydration., Results: 75 of the parents expected their child to get IV fluids. 49 of them would refuse to consider oral rehydration. 75 of the parents would refuse to consider insertion of nasogastric tube. Parents whose children were previously treated intravenously tended to be less likely to agree to oral treatment. Parents were more prone to decline oral rehydration if the main measurement of dehydration was the child's clinical appearance, clinical appearance with vomiting, or child's refusal to drink and were more likely to agree if the main measurement was diarrhea, diarrhea with clinical appearance, or clinical personnel opinion., Conclusions: This is the first study to examine parents' expectations. We found that in the majority of cases, parents' expectations contradict current guidelines. Efforts should be taken to educate parents in order to allow full implementation of the guidelines.

Background: The etiology of bone marrow failure, a prominent feature of paroxysmal nocturnal hemoglobulinuria, is presently unknown., Objectives: To evaluate the possible influence of cellular immune mechanisms in the bone marrow failure of PNH., Methods: We studied marrow erythroid colony formation in a patient with paroxysmal nocturnal hemoglobinuria without hypoplastic/aplastic marrow complications., Results: In vitro assays revealed a pronounced inhibition of primitive erythroid (BFU-E) progenitor cell growth by marrow T lymphocytes. Removal of T cells prior to culture resulted in a 4.5-fold enhancement of BFU-E numbers. Reevaluation of in vitro erythropoiesis during steroid administration indicated a persistent, albeit less prominent, T cell inhibitory effect., Conclusion: Our findings provide the first direct evidence for a cellular immune inhibitory phenomenon accompanying PNH.

Background: Laser assisted ventilation of the middle ear with a defocused laser beam has been performed on adults in an office setting without anesthesia., Objective: The purpose of this study was to evaluate the efficacy and safety of a highly controlled, char-free CO2 flashscanner technology for the ventilation of the middle ear in young children, at this stage under general anesthesia, and later without anesthesia., Methods: A CO2 flashscanning laser, in conjunction with a micromanipulator, was used on 21 SOM patients ages 3-7 years old, with followup at 2 months. Operating time is approximately 5 minutes., Results: Postoperative results show average patency of 2-3 weeks without adverse effects. Of the treated patients, 53% did not require a second treatment, whereas 47% still suffered from otitis media and needed a second treatment., Conclusion: The CO2 flashscanner laser technology is effective and safe for middle ear ventilation and provides excellent control of the perforation diameter. It is already being performed in an office setting with sedation on a limited basis with very promising preliminary results. Based on the current study and on 70 additional cases with longer interval followup, we anticipate the office technique to become widely used in the future.

For immune surveillance and function to be effective, T lymphocytes constantly recirculate via lymph and blood between lymphoid organs and body tissues. To enable efficient cell movement and migration, cell adhesion to components of the basement membrane and the extracellular matrix (ECM) must be a rapid and transitory process. Whether phosphorylation and dephosphorylation of cellular proteins are involved in this phenomena was explored by monitoring the adhesion of T cells to immobilized ECM proteins. A short exposure of 51Cr-labeled human CD4+ T cells to phorbol esters in vitro induced a rapid beta 1-integrin-mediated adhesion to both fibronectin and laminin, as determined by inhibition with anti-integrin antibodies. Adhesion was reversible; detachment from the immobilized ECM ligands occurred between 20 and 120 min without further intervention. This T cell adhesion was regulated by the activation of protein kinase C because (a) staurosporine and H-7 inhibitors of protein kinase C suppressed T cell adhesion, and (b) PMA-induced down-regulation of intracellular levels of protein kinase C was associated with the abrogation of the T cell adhesiveness to fibronectin and laminin. Furthermore, inhibition of protein phosphatases activity by okadaic acid delayed the detachment of the T cells from fibronectin or laminin. Thus, we suggest that T cell-ECM interactions such as adhesion and detachment are regulated, respectively, by protein kinase C and protein phosphatases.

The intracellular sodium concentration and intracellular volume of human red blood cells were determined from 23Na and 1H NMR spectra. It is shown that sodium dissolved in the intracellular water has a concentration higher than that previously published. The intracellular sodium concentration measured was 11.4 +/- 3.1 mM. A comparison of different NMR methods used to determine sodium concentration is given.

We report three cases of combined anemia, neutropenia and thrombocytopenia in patients with visceral leishmaniasis (kala-azar). Using immunofluorescence techniques and the common antiglobulin (Coombs') test, we showed membrane-associated antiplatelet, antineutrophil and antierythrocytic IgG antibodies in all three cases. Treatment with sodium stibogluconate raised the patients' platelet, neutrophil and erythrocyte count. At that time no antibodies were detected on peripheral blood cells. Immunological studies performed on these patients did not show marked abnormalities except for reduced T-helper cells and elevated OKM1-positive cells, which normalized after recovery. As bone marrow suppression was not found, it is suggested that pancytopenia resulted from rapid destruction of antibody-coated blood cells. Whether these antibodies are specific is not clear.

Mice immunized to bovine insulin were observed to develop anti-idiotypic antibodies which behaved in in vitro assays as antibodies to the insulin receptor. The studies described here were undertaken to investigate the effects of these antibodies in vivo on the physiology of glucose homeostasis and the state of insulin receptors. Mice developing anti-idiotypic receptor antibodies manifested abnormal fasting blood glucose concentrations: a period of hypoglycemia followed by a period of hyperglycemia. Moreover, the mice were deficient in their ability to respond to a glucose load. Changes in the number and activity of insulin receptors were associated with these physiological aberrations. In an insulin binding assay, adipocytes obtained from immunized mice had only 40% of the number of insulin receptors demonstrable on the adipocytes of control mice. The lipogenic response of the affected adipocytes was also relatively insensitive to insulin, and in addition, they manifested only 70% of the maximal response to high concentrations of insulin. Thus, development of anti-idiotypic receptor antibodies appeared to be associated with insulin resistance of adipocytes and abnormal glucose homeostasis.

The effects of racemic propranolol and its constituent isomers were studied on ganglionic stimulation produced in situ by close arterial injection of 5-HT and DMPP to the superior cervical ganglion. Ganglion stimulation was recorded in terms of the resultant contraction of the nictitating membrane. d,l-Propranolol caused a biphasic antagonism of the ganglion stimulant effect of 5-HT. At low doses, 0.5-10 mug, the antagonism was surmountable by increasing the amount of 5-HT. The l-isomer (0.2-4 mug) but not d-propranolol also caused antagonism. At higher doses, 0.1-5 mg, both d,l- and d-propranolol caused a second type of blockade of 5-HT which was not surmountable and resembled that seen with procaine. The ganglion stimulant effects of DMPP and acetylcholine were only antagonised by the higher doses of d- and d,l-propranolol. d,l-Propranolol did not reduce the direct stimulation by 5-HT on the muscle of the nictitating membrane.

1 Four beta-adrenoceptor blocking agents, (+/-)- and (+)-propranolol, practolol and oxprenolol, were found to antagonize, apparently competitively, the responses of both the rat isolated stomach and uterus to 5-hydroxytryptamine (5-HT).2 The pA(2) values for each of these agents as antagonists of the contractile action of 5-HT on the rat stomach were found to be: (+/-)-propranolol, 6.08; (+)-propranolol, 4.94; practolol, 3.43; and oxprenolol, 5.99. These values were very similar to the corresponding figures for antagonism of 5-HT-induced contractions of the uterus.3 pA(2) values for antagonism of adrenaline-induced relaxations by the four blocking agents on the rat stomach and uterus did not differ from the values for 5-HT blockade.4 To antagonize contractile responses to acetylcholine of the rat stomach it was necessary to give 100 times more (+/-)-propranolol than was needed to antagonize responses to 5-HT.

An analogue of epidermal growth factor (EGF) which is virtually devoid of biological activity retains receptor binding activity but cannot form cell surface clusters or patches. Bivalent anti-EGF antibodies restore both bioactivity and patch formation. The sensitivity of fibroblasts to native EGF can also be enhanced greatly by these antibodies, especially in hormone-resistant cell lines.