Given an abstract, generate a keyword (a noun phrase) that best describes the focus or contribution of the paper. Such keywords can be directly from the given abstract or outside it.

Abstract: 17 beta-Estradiol (E2) affects the sensitivity of pituitary cells to several neurohormones as LHRH, TRH, or dopamine, presumably by modulating receptor coupling mechanisms. We attempted to pinpoint the membrane processes underlying this modulation and studied the effect of E2 on pituitary membrane phospholipid methylation. Anterior pituitary membranes prepared from ovariectomized (ovx) or ovx plus E2-treated rats were assayed for phospholipid methylation. Methylated phospholipids were separated by TLC. Incorporation of [3H]methyl groups into phospholipids increased with membrane concentration and incubation time with S-adenosyl-L-methyl [3H]methionine; it was not Mg2+ dependent and was inhibited in a dose-dependent manner by S-adenosyl-L-homocysteine, methyltransferase inhibitor. pH was found to be critical. Formation of phosphatidyl-monoethanolamine, phosphatidyl-dimethylethanolamine, and phosphatidylcholine was markedly stimulated by treatment with E2. The effect increased progressively when animals were killed 15 h to 5 days after E2 implantation. The response involved a shift in the maximum velocity (Vmax) although there was no change in the available substrate for the methylating enzyme. This change in Vmax probably reflects changes in the amount of the methylating enzyme itself. Administration of 17 alpha-estradiol, an inactive stereoisomer of E2 was ineffective, pointing to a stereospecific interaction. After differential centrifugation of pituitary membranes, the highest specific methyltransferase activity was found in light mitochondrial (L) and microsomal (P) fractions and the lowest in nuclei (N) and the heavy mitochondrial (M) fractions. After sucrose density gradient centrifugation, methylated phospholipids were preferentially recovered from fractions corresponding to the endoplasmic reticulum and/or secretory granules. E2 treatment for 5 days did not modify the subcellular distribution of methyltransferase activity but stimulated it in all fractions; in contrast, it did not modify the activity of the other enzymes measured as fraction markers. Under the same experimental conditions, phospholipid methylation in membranes prepared from cortex, and anterior and mediobasal hypothalamic structures was not affected by the steroid, with the exception of a slight increment of [3H]methyl incorporation into mediobasal hypothalamic membrane phospholipids after 5 days of E2 treatment. These results indicate that E2-induced changes in pituitary responsiveness might be concomitant with selective effects of the steroid on specific membrane enzymatic activities involved in coupling mechanisms.
Animal

Abstract: We reviewed the computed tomographic findings after 1055 intracranial operations to determine the incidence of postoperative extradural hematomas. There were 11 medium and 5 large hematomas after 1055 operations (1.0%). Ten of the 16 hematomas were operated upon (10/1055, 0.9%). Four of the 10 hematomas were seen after 278 brain tumor removals (1.4%), another four after 190 aneurysmal operations (2.1%), one after 14 intracerebral hematoma removals (7.1%), and the last one after 251 ventricular shunting or drainage procedures (0.4%). In 4 of the 10 operated hematomas, sites were regional, in five sites were adjacent, and in one the site was distant. All of the five adjacent hematomas extended downward from a lower rim of the operative locus. Causes were analyzed in the three types of the hematomas. In case of the regional hematomas, the causes were incomplete hemostasis of the dura mater or the bone in all four patients, nonperformance of central stay sutures in three, systemic hypertension in one, and hypofibrinogenemia in one. In the adjacent hematomas, we could find dural separation at an edge of craniotomy in all five patients, abrupt collapse of the brain in all, ventricular dilatation in two, and systemic hypertension during immediate postoperative period in two. In one distant hematoma, ventricular dilatation and ventricular shunting procedure were themselves thought to be the causal factors.
Adolescence

Abstract: A controlled prospective study to evaluate the efficacy of expired ipecac syrup was conducted at two regional poison control centers in New England. During a 6-month period, 200 study patients treated with expired ipecac syrup and 200 control patients treated with unexpired ipecac syrup were evaluated. There were no statistical differences between the control and study groups in patient characteristics (age and sex) and product characteristics (general class, emetic potential, pretreatment, previously opened bottles, and manufacturer). In both control and study groups, emesis occurred in 100% of cases with 90% of patients vomiting with the first dose. The mean time to emesis was 24.7 minutes and 24.8 minutes in the study and control groups, respectively. Expired preparations ranged from 1 month to greater than 4 years postexpiration, with the duration of expiration not altering the mean time to emesis. Mean time to emesis between the two groups was also not affected by manufacturer, pretreatment with milk, or whether the ipecac syrup bottle was previously opened. We conclude that expired ipecac syrup (up to 4 years postexpiration date) is an effective emetic.

Child, Preschool

