How to assess fetal metabolic acidosis from cord samples.

The degree of metabolic acidosis at birth has been calculated in cord artery and vein samples from 21 term fetuses with cord artery pH less than 7.20. The aim of the study was to compare base deficit values calculated from either Siggaard-Andersen alignment nomogram (BD blood) or the Acid-Base chart (BD extra cellular fluid, BDecf). BDblood was found to be consistently higher in the cord artery as compared with BDecf, 13.2 +/- 3.5 and 9.9 +/- 2.9 mmol/l (Mean +/- SD), respectively. A significant correlation was found between cord artery PCO2 and BDblood whereas BDecf appeared unaffected by PCO2. In cases with cord entanglement BDecf a-v differences were increased to 3.4 +/- 2.3 mmol/l as compared with the small a-v difference noted in acidotic cases without cord entanglement, 1.1 +/- 1.25 mmol/l. It is speculated that with acutely emerging, intermittent asphyxia due to cord compression, a cord artery and vein difference in metabolic acidosis may exist and where the vein captures the basal level and the artery the acute changes. It is concluded that BDecf in both cord artery and vein add valuable information on the mechanisms behind metabolic acidosis.     

Identification of accessory bile ducts at cholecystectomy

The presence of accessory channels between the liver and extrahepatic bile ducts has long been recognised by anatomists and the division of such ducts may be a cause of bile leakage following cholecystectomy. However, visualisation of accessory bile ducts at operation is difficult as they are often small and sometimes less than 1 mm in diameter. Cholangiography has been used to help in the identification of accessory ducts in 50 patients included in a prospective trial. X-rays were taken after dissection of the gall bladder from its bed and extravasation of contrast was seen on five occasions (10%) suggesting leakage from divided accessory ducts. The identification of damage to accessory bile ducts in 10% of patients suggests that this may occur more frequently than previously supposed.     

Preparation of protected peptidyl thioester intermediates for native chemical ligation by Nα‐9‐fluorenylmethoxycarbonyl (Fmoc) chemistry: considerations of side‐chain and backbone anchoring strategies,and compatible protection for N‐terminal cysteine*,†

Abstract: Native chemical ligation has proven to be a powerful method for the synthesis of small proteins and the semisynthesis of larger ones. The essential synthetic intermediates, which are C‐terminal peptide thioesters, cannot survive the repetitive piperidine deprotection steps of N^α‐9‐fluorenylmethoxycarbonyl (Fmoc) chemistry. Therefore, peptide scientists who prefer to not use N^α‐t‐butyloxycarbonyl (Boc) chemistry need to adopt more esoteric strategies and tactics in order to integrate ligation approaches with Fmoc chemistry. In the present work, side‐chain and backbone anchoring strategies have been used to prepare the required suitably (partially) protected and/or activated peptide intermediates spanning the length of bovine pancreatic trypsin inhibitor (BPTI). Three separate strategies for managing the critical N‐terminal cysteine residue have been developed: (i) incorporation of N^α‐9‐fluorenylmethoxycarbonyl‐S‐(N‐methyl‐N‐phenylcarbamoyl)sulfenylcysteine [Fmoc‐Cys(Snm)‐OH], allowing creation of an otherwise fully protected resin‐bound intermediate with N‐terminal free Cys; (ii) incorporation of N^α‐9‐fluorenylmethoxycarbonyl‐S‐triphenylmethylcysteine [Fmoc‐Cys(Trt)‐OH], generating a stable Fmoc‐Cys(H)‐peptide upon acidolytic cleavage; and (iii) incorporation of N^α‐t‐butyloxycarbonyl‐S‐fluorenylmethylcysteine [Boc‐Cys(Fm)‐OH], generating a stable H‐Cys(Fm)‐peptide upon cleavage. In separate stages of these strategies, thioesters are established at the C‐termini by selective deprotection and coupling steps carried out while peptides remain bound to the supports. Pilot native chemical ligations were pursued directly on‐resin, as well as in solution after cleavage/purification.     

Neoplastic and inflammatory processes of the peritoneum, omentum, and mesentery: diagnosis with CT.

Disease processes in the peritoneum, omentum, and mesentery occasionally are not recognized at radiologic examination. The authors have used computed tomography (CT) to categorize the radiologic appearances of the more common abnormalities into three basic patterns: (a) solid but relatively well-defined masses, (b) cystic-appearing masses, and (c) ill-defined or infiltrative processes. The most common solid masses to affect these anatomic regions are secondary neoplasms, which are associated with enhancement of the peritoneum on contrast material-enhanced CT scans and, typically, ascites. The various cystic-appearing masses (including cystic lymphangioma, cystic mesothelioma, teratoma, and loculated ascites) and infiltrating masses (such as peritoneal mesothelioma, retractile mesenteritis, desmoid, and carcinoid) must be differentiated on the basis of clinical findings and additional imaging findings (eg, CT depiction of fat and calcium in teratomas and the radiating appearance of carcinoids). Although the CT appearances of some of the abnormalities overlap, classifying them by pattern is helpful in narrowing the range of the differential diagnosis.