Diabetes insipidus with impaired osmotic regulation in septo-optic dysplasia and agenesis of the corpus callosum.

The clinical and endocrinological findings in 24 children with septo-optic dysplasia and/or agenesis of the corpus callosum are described with particular reference to posterior pituitary function. Nine had diabetes insipidus. The prevalence of diabetes insipidus was similar in children with complete and incomplete forms of septo-optic dysplasia. Maintenance of normal osmotic balance was very difficult in six of these children, even after the introduction of treatment with vasopressin, either as desmopressin, or lysine vasopressin spray in one of the early cases.     

Osgood-Schlatter lesion: fracture or tendinitis? Scintigraphic, CT, and MR imaging features.

To determine whether the Osgood-Schlatter lesion (OS) is produced by avulsion fracture or injury to the patellar tendon, all images obtained in 28 cases of OS in 20 patients (16 scintigrams, 34 computed tomographic [CT] scans, and 27 magnetic resonance [MR] images) were retrospectively analyzed. In 21 cases, imaging was performed before and after treatment; in 20 cases, relief from pain was complete at the time of repeat examination. In all patients (100%), abnormal size of the tendon, decreased attenuation, and increase in signal intensity were compatible with the CT and MR imaging appearance of tendinitis. Distended deep infrapatellar bursa was a frequent finding, particularly on MR studies. These abnormalities had partially disappeared at follow-up examination. An ossicle was seen in only nine of 28 cases (32%); in three of seven cases with follow-up, the ossicle remained nonunited to the tibial tuberosity on follow-up studies despite relief from symptoms. This implies that healing of fracture is not essential for relief from symptoms. These results strengthen the argument that in most cases of OS, insult to the tendon and associated soft tissues, rather than avulsion fracture, causes OS.     

Safety Concerns Affecting Delivery of Home Health Care

Abstract Factors influencing the remarkable growth of home health care include increased elderly population, decreased average length of hospital stay, and technological advancements that reduce the need for hospitalization. Societal changes have prompted increasing concern about personal risk to home care providers. The purpose of this pilot study was to: 1) ascertain factors related to perception of risk by home health care administrators and staff and to identify strategies used by home health care administrators to reduce risk to staff; and 2) determine whether quality of care is affected when home-visit situations present risk. A convenience sample of 36 home health care administrators and 62 staff was surveyed about risks and measures provided by the home health care agency to minimize risk. Factors associated with risk are geographic location, high incidence of crime, inappropriate patient or caregiver behavior, infectious diseases, and evening assignments. Strategies used to minimize risk include safety programs, preplanning of visits, personal protective equipment, escorts, and buddy systems. Perceived ability to refuse high-risk assignments, however, is questionable, as 66% of the staff stated that they leave a situation "as soon as possible." These findings will be used to strengthen inservice programs and to provide a basis for future studies.     

G-protein Activation Decreases Isoflurane Inhibition of N-type Ba2+ Currents

Background: G-protein activation mediates inhibition of N-type Ca2+ currents. Volatile anesthetics affect G-protein pathways at various levels, and activation of G-proteins has been shown to increase the volatile anesthetic potency for inhibiting the electrical-induced contraction in ileum. The authors investigated whether isoflurane inhibition of N-type Ba2+ currents was mediated by G-protein activation.

Methods: N-type Ba2+ currents were measured in the human neuronal SH-SY5Y cell line by using the whole cell voltage-clamp method.

Results: Isoflurane was found to have two effects on N-type Ba2+ currents. First, isoflurane reduced the magnitude of N-type Ba2+ currents to a similar extent (IC50 ~ 0.28 mm) in the absence and presence of GDP[beta]S (a nonhydrolyzable GDP analog). Interestingly, GTP[gamma]S (a nonhydrolyzable GTP analog and G-protein activator) in a dose-dependent manner reduced the isoflurane block; 120 [mu]m GTP[gamma]S completely eliminated the block of 0.3 mm isoflurane and reduced the apparent isoflurane potency by ~ 2.4 times (IC50 ~ 0.68 mm). Pretreatment with pertussis toxin or cholera toxin did not eliminate the GTP[gamma]S-induced protection against the isoflurane block. Furthermore, isoflurane reduced the magnitude of voltage-dependent G-protein-mediated inhibition of N-type Ba2+ currents, and this effect was eliminated by pretreatment with pertussis toxin or cholera toxin.     

pH and energy dependent transport of ketoprofen across rat jejunum in vitro.

The aim of this study was to elucidate transport mechanisms of ketoprofen (monocarboxylic acid with pK(a) 4.6) across rat jejunum in vitro using side-by-side diffusion cells. When the tissue was incubated on the mucosal and serosal sides with buffer of pH 7.51 (pH of the mucosal surface was 7.08), ketoprofen permeated faster in the mucosal-to-serosal than in the opposite direction. No asymmetry in transport was observed when 2 mM mucus disrupting agent 1,4-dithio-DL-threitol (pH of the mucosal surface increased to 7.21) was added to the mucosal side. Mucosal-to-serosal permeability of ketoprofen increased three times when the pH of the incubation medium was changed from 8.06 (pH of the mucosal surface was 7.34) to 6.07 (pH of the mucosal surface was 5.95), while no pH dependence was found under ATP-depletion caused by sodium azide. In the ketoprofen concentration range from 0.125 to 5 mM no saturation of transport was observed. Moreover, ketoprofen transport was not changed in the presence of 2 mM benzoate, 10 and 20 mM acetate, 20 mM L-lactate (substrates for monocarboxylate transporter 1, MCT1) and 1 mM alpha-cyano-4-hydroxy-cinnamic acid (an inhibitor of MCT1). These results indicate that ketoprofen is transported across rat jejunum in vitro by pH and energy dependent transport mechanisms, and most probably not by MCT1.