Urinoma: an unusual case of emesis in a brain-injured child.

The evaluation of acute emesis in a multiple-trauma paediatric patient with severe traumatic brain injury can present a difficult but not unusual problem in the rehabilitation unit. The differential diagnosis will be discussed in a paediatric case in which emesis was related to a urinoma, secondary to ureteropelvic disruption, compressing the duodenum. We present a case of a 6-year-old Caucasian girl with severe brain injury who developed emesis while in rehabilitation. An X-ray of the abdomen revealed a shadow over the right psoas. Subsequently mild compression of the duodenum was diagnosed by computerized tomography, and ultrasound demonstrated a large fluid collection inferior to the right kidney. A large volume of urine was drained and a catheter placed. Pyelogram revealed apparent disruption of the right ureteropelvic junction, which was confirmed intraoperatively. The kidney was removed secondary to severe parenchymal abnormalities. The emesis subsequently resolved. Differential diagnosis of acute onset of emesis in the paediatric brain-injured patient should include a careful search for underlying previously unrecognized problems.

Antisera against three connexin43 fragments react with a 43-kD protein localised to gap junctions in myocardium and human myometrium.

Gap junctions are thought to play an essential role in the control of parturition. In this study we attempted to synthesise three short peptides which match the portion of the amino acid sequence of the connexin43, protein predicted from the nucleotide sequence of cDNA clone and to produce an anti-peptide antibody which would detect gap junction protein in human myometrium. Three peptides were synthesized: (1) RKEEKLNKKEEE, (2) EJKKFKYGJEEH and (3) KNRVKGRSDPYH. Antibodies against these peptides were raised in rabbits, screened for reactivity and specificity using dot blot assays and used for immunocytochemical staining of heart and myometrial tissues.

The amino acids that constitute sequence gamma 268-282 of fibrinogen are not involved in fibrin monomer polymerization.

Congenitally abnormal fibrinogens with impaired fibrin monomer polymerization have been described to contain single amino-acid substitutions localized in certain positions of the gamma 275-330 peptide region. To evaluate the role of the amino-acid sequence in the vicinity of Arg275 in fibrin monomer polymerization, the peptide fragment corresponding to gamma 268-282 was synthesized and used to obtain peptide-specific antibodies. These antibodies, when purified immunochemically on the immobilized peptide, bound to the intact fibrinogen and fibrin monomers with the same binding affinity. However, they did not recognize the gamma 268-282 epitopes on the denatured and reduced fibrinogen molecules. The lack of influence of antipeptide antibodies on fibrin monomer polymerization indicates that the gamma 268-282 peptide is not directly involved in the structure of the polymerization site in the D domain of fibrinogen. It is suggested that substitution of Arg275 either by His or Cys in abnormal fibrinogens results probably in conformational changes which disturb a proper orientation of the polymerization site and reduce its expression.

Allosteric interaction of components of the replitase complex is responsible for enzyme cross-inhibition.

The enzymes of DNA polymerization and DNA precursor synthesis are assembled in the replitase complex during the S phase of the cell cycle. Cross-inhibition is a phenomenon shown by enzymes of the replitase complex, in which inhibition of one enzyme of the complex leads to inhibition of a second, unrelated enzyme. This inhibition occurs only in vivo and only during S phase. The second enzyme shows no inhibition in vitro. In this study, using Chinese hamster embryo fibroblast cells, we have shown that direct allosteric interactions, i.e., structural interaction from a remote site within the replitase complex, is the cause of cross-inhibition of thymidylate synthase activity by the inhibitors of ribonucleotide reductase and DNA polymerase, because disruptions of the deoxynucleotide pools, which would be predicted for alternative explantations, do not occur. Cross-inhibition of DNA polymerase by hydroxyurea is demonstrated by the cessation of DNA synthesis when ribonucleotide reductase block is circumvented by the provision of all four deoxynucleosides. In addition to the cross-inhibition for thymidylate synthase and DNA polymerase, we have also presented evidence, on the basis of alterations of the in vivo conversion of deoxyuridine to dUMP, that cross-inhibition also occurs for the enzyme thymidine kinase. This conclusion is further supported by the lack of inhibition of the similar process in RNA synthesis, because enzymes of RNA synthesis are not included in the replitase complex. To facilitate the measurements, we have introduced a novel method of distinguishing between thymidine and deoxyuridine derivatives, making use of the fact that a tritium label placed in the 5'-position of deoxyuridine is removed on conversion to thymidine by methylation, whereas a tritium placed in the 6'-position is not.

Effects of feeding pattern and dietary regimen on growth and adipose tissue cellularity in polygenic obese mice.

The effect of varying feed intake and feeding pattern during the early postweaning period on growth, body composition and adipose tissue cellularity was studied in polygenic obese and control normal mice. Male mice were assigned to the following dietary treatments at 4.5 wk of age: stock diet fed ad libitum(AL), four palatable foods cafeteria-fed(CF), stock diet fed every 2 h by automatic feeders adjusted for maximum intake(MI), fed same procedure as MI but restricted to produce 70% of the gain of mice fed ad libitum(RE), and stock diet fed one meal/d the same amount fed RE mice(PM). Mice were killed after 5 wk on treatment. Cafeteria-fed control mice were heavier (P less than .05) than RE control mice, but they were not different (P greater than .05) from AL, MI and PM control mice, while CF obese mice were heavier and RE obese mice were smaller than AL, MI and PM obese mice (P less than .05). Cafeteria-fed mice were fatter than mice from all other treatments in both the obese and control lines. Maximum intake, PM and RE mice were fatter than AL mice but this effect was only significant in the obese line. Alterations in feeding pattern can affect body composition even though body weight may not show a correlated response. Cafeteria-fed obese mice had larger fat pads and more small (less than 40 micron) and large (greater than 110 micron) adipocytes than other obese mice. Results indicate that the difference in the development of obesity on cafeteria diet was due primarily to genetic effects while the increase in percentage fat after restriction on MI, PM and RE treatments was due mainly to the acute change of feeding pattern.

Mechanisms of hydroxylation by cytochrome P-450: metabolism of monohalobenzenes by phenobarbital-induced microsomes.

The monohydroxylation of halobenzenes by phenobarbital-induced rat liver microsomes was studied. The p-halophenol was found to be the major metabolite from all four halobenzenes; o-halophenol formation decreased as the halogen atom size increased. Vmax for total hydroxylation (ortho and para products) correlated well with the sigma + Hammett constant with a negative rho value. This implies a positively charged intermediate in the rate-determining step. Vmax for either ortho or para hydroxylation alone did not correlate with a Hammett constant, implying that the product-determining step occurs after the rate-determining step. Rate-determining formation of a radical cation intermediate is postulated to explain this data.

Effects of hormones on mammary adenosine 3',5'-monophosphate levels and metabolism in normal and adrenalectomized lactating rats.

Prostaglandin E1 (PGE1) T4, and epinephrine (Epi) were incubated with mammary tissue slices from normal and adrenalectomized (Adx) rats and Adx rats receiving cortisol (Adx + C). PGE1, T4, and the combination of Epi, T4, and PGE1 increased mammary slice cAMP levels in all groups. No differences were observed among treatment groups in basal cAMP levels or responses to hormones. Glucose-1-14C oxidation and incorporation into lipids were stimulated by PGE1, T4, and the combination of EPi, T4, and PGE1 in normal rats. Responses were depressed by adrenalectomy and reversed by cortisol. PGE1, T4, and the combination of EPi, T4, and PGE1 depressed glucose-6-14C oxidation. Fatty acid synthesis from glucose-6-14C was stimulated by Epi, PGE1, and T4 in tissues from normal and Adx + C rats, but not in those from Adx rats. Glycerol synthesis was unchanged. Pyruvate-1-14C and pyruvate-2-14C oxidation were uneffected by adrenalectomy or hormones. Fatty acid synthesis was depressed by adrenalectomy and reversed by cortisol. T4 and the combination of Epi, T4, and PGE1 depressed triacylglycerol and fatty acid synthesis in all groups. Glycerol synthesis was unchanged. Hormonal effects were much more pronounced when glucose was the substrate. This suggests that cAMP effects on glucose metabolism are manifest at a site between hexose-P and pyruvate, and further, that a primary effect of adrenalectomy may be to reduce the responsiveness of this site to cAMP. Linear regression analyses comparing cAMP levels with glucose and pyruvate metabolic parameters further support this conclusion.

Unsuspected nonmedullary carcinoma of the thyroid in patients with hyperparathyroidism.

All patients with hyperparathyroidism seen in a large referral military hospital within a twenty month period underwent neck exploration by one of us (HN). Three patients were found to have an unsuspected solid thyroid nodule measuring 0.5 to 1.5 cm. All were widely excised by thyroid lobectomy and isthmectomy and found to be follicular or papillary carcinoma of the thyroid. These three patients join thirty-one previously reported clinical cases documenting an association between parathyroid adenoma and nonmedullary carcinoma of the thyroid. Because of the high potential for malignancy in this clinical setting, we urge careful examination and palpation of the thyroid gland during neck exploration for hypercalcemia in order to detect and cure "early" malignancies of the thyroid.

Effects of adrenalectomy and glucocorticoid therapy on enzyme activities in mammary and adipose tissues from lactating rats.

Several mammary and adipose enzymes were measured in normal, adrenal-ectomized, adrenalectomized cortisol-treated, and intake-restricted lactating rats. Acetyl-CoA carboxylase, lipoprotein lipase, and triglyceride synthetase complex activities in mammary tissue were unchanged by intake restriction, decreased by adrenalectomy, and increased by glucocorticoid-replacement therapy. Malic dehydrogenase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and lipoprotein lipase activities in adipose were unchanged after adrenalectomy.