Three-dimensional prediction of free-flap volume in autologous breast reconstruction by CT angiography imaging

Purpose

   The diagnostic use of computer tomography angiography (CTA) to identify perforating blood vessels for abdominal free-flap breast reconstruction was extended to estimate the three-dimensional (3D) preoperative flap volume and to compare it with the real intraoperative flap weights in order to (1) evaluate the accuracy of CTA-based 3D flap volume prediction, and (2) to analyze abdominal tissue estimation for required breast volume reconstruction.

Methods

   Preoperative CTA was performed in 54 patients undergoing unilateral breast reconstruction with a free, deep, inferior epigastric artery perforator flap. 3D flap volumes ( \(\hbox {cm}^{3}\) ) based on CTA data were calculated and compared with the actual intraoperative flap weight (g). In addition, a breast volume to flap volume ratio was calculated to analyze whether the estimated 3D abdominal flap volume would match that of the breast to be removed.

Results

   40 CTA data sets (74.1 %) fulfilled the technical requirements for a reliable determination of flap volume. 3D CTA flap volume prediction showed no relevant differences to the actual flap weight (p = 0.44) and high correlations (r = 0.998, \(p < 0.001\) ), allowing a prediction accuracy within 0.29 \(\pm \) 3.0 % (range: from \(-\) 8.77 to 5.67 %) of the real flap weight. Significantly larger flap volumes were harvested compared with the actually required breast volumes ( \(p < 0.001\) ), leading to an average of 21 % of the remnant flap tissue potentially being discarded.

Conclusions

   CTA-based 3D flap volume prediction provides accurate preoperative guidelines concerning the needed amount of abdominal tissue that can be harvested to achieve acceptable symmetry.     

Alloxan-glucose interaction: Effect on incorporation of14C-leucine into pancreatic islets of rat

Summary The acute effect of alloxan on the incorporation of¹⁴C-leucine into isolated rat islets of Langerhans was studied. I.v. administration of alloxan (40 mg/kg body weight) in rats inhibited the subsequentin vitro incorporation of¹⁴C-leucine into (pro-)insulin in the isolated islets. Glucose (750 mg/kg body weight), when administered 5 min prior to alloxan, completely protected the islets against alloxan toxicity. The protective effect of glucose was partly reversed when the concentration of alloxan was raised to 80 mg/kg body weight. Similar results of inhibition of (pro-)insulin biosynthesis by alloxan and its protection by glucose were obtained when isolated rat islets were exposed to alloxan and/or glucosein vitro. Islets exposed to glucosein vitro immediately after alloxan exposure showed a slower rate of inhibition of (pro-)insulin biosynthesis, as compared to islets washed before exposure to D-glucose. In view of these findings, it is suggested that there is a common recognition site on B-cell for alloxan and glucose. CDRI Communication No. 2617.     

In vitro conversion of proinsulin to insulin by cathepsin B in isolated islets and its inhibition by cathepsin B antibodies

Summary Purified bovine cathepsin B, when incubated with isolated rat islets of Langerhans, completely converts proinsulin to insulin as demonstrated by the incorporation of¹⁴C-leucine into islet proteins, releasing lysine as the only basic amino acid. Cathepsin B antibodies raised in rabbit inhibited the above conversion. CDRI Communication No. 2703     

Insulin like activity in (−) epicatechin

Summary Water extract of the bark of plant ofPterocarpus marsupium Roxb is used as an antidiabetic drug in indigenous medicine in India. (−) Epicatechin, its active principle, has been found to be insulinogenic. The presentin vitro study reports some insulin like activities of (−) epicatechin. Like insulin, (−) epicatechin stimulates oxygen uptake in fat cells and tissue slices of various organs, increases glycogen content of rat diaphragm in dose-dependent manner with corresponding increase in U¹⁴-C glucose uptake, and inhibits theophylline induced lipolysis in isolated fat pads in dose-dependent manner. Experiments on competitive binding of¹²⁵I-insulin and (−) epicatechin to liver cell plasma membrane indicate that insulin does not share binding site with (−) epicatechin. (−) Epicatechin at a concentration of up to 1 mM does not effect the release of glucagon from the isletsin vitro. Thus, (−) epicatechin has insulinogenic as well as insulin like properties. C.D.R.I. Communication no 4499.     

Reactive and reparative fibrillar collagen remodelling in the hypertrophied rat left ventricle: two experimental models of myocardial fibrosis

STUDY OBJECTIVE--The aim was to compare the temporal sequence and structural relationship between perivascular and interstitial fibrosis and microscopic scarring seen in the left ventricle in response to either a transient or sustained stimulus to fibrosis. DESIGN--In 72 male Wistar rats (250-350 g) the transient stimulus model was based on the administration of isoprenaline (500 micrograms.kg-1) while the sustained stimulus model was produced by abdominal aortic banding with right renal artery constriction. Serial sections of myocardium were examined and compared at 4 and 12 weeks in each model and to corresponding controls. EXPERIMENTAL MATERIAL--The collagen specific stain, Sirius Red F3BA, was used to determine collagen volume fraction and the fibrillar nature of the fibrous tissue response seen by light microscopy. MEASUREMENTS AND MAIN RESULTS--Following isoprenaline a stable reparative fibrosis of the endomyocardium and increase in collagen volume fraction was seen without an interstitial or perivascular fibrosis of the non-involved myocardium. In unilateral renal ischemia, on the other hand, a progressive perivascular fibrosis was evident throughout the myocardium and from which fibrillar collagen extended into the extracellular space between muscle bundles creating an interstitial fibrosis; microscopic scarring of the endomyocardium became evident at 12 weeks. CONCLUSIONS--The reactive perivascular fibrosis of intramyocardial coronary arteries seen in renovascular hypertension is a progressive process that leads to an interstitial fibrosis and eventual microscopic scarring. In contrast, the endomyocardial scarring that follows isoprenaline induced myocyte necrosis is stable and intramural vessels in remote regions are not involved.     

Genetic study of patients with dexamethasone-suppressible aldosteronism without the chimeric CYP11B1/CYP11B2 gene

Glucocorticoid-remediable aldosteronism is an inherited disorder caused by a chimeric gene duplication between the CYP11B1 (11beta-hydroxylase) and CYP11B2 (aldosterone synthase) genes. The disorder is characterized by hyperaldosteronism and high levels of 18-hydroxycortisol and 18-oxocortisol, which are under ACTH control. The diagnosis of glucocorticoid-remediable aldosteronism had been traditionally made using the dexamethasone suppression test; however, recent studies have shown that several patients with primary aldosteronism and a positive dexamethasone suppression test do not have the chimeric CYP11B1/CYP11B2 gene. The aim of this work was to evaluate whether other genetic alterations exist in CYP11B genes (gene conversion in the coding region of CYP11B1 or in the promoter of CYP11B2) that could explain a positive dexamethasone suppression test and to determine another genetic cause of glucocorticoid-remediable aldosteronism. We also evaluated the role of 18-hydroxycortisol as a specific biochemical marker of glucocorticoid-remediable aldosteronism. We studied eight patients with idiopathic hyperaldosteronism, a positive dexamethasone suppression test, and a negative genetic test for the chimeric gene. In all patients we amplified the CYP11B1 gene by PCR and sequenced exons 3-9 of CYP11B1 and a specific region (-138 to -284) of CYP11B2 promoter. We also measured the levels of 18-hydroxycortisol, and we compared the results with those found in four subjects with the chimeric gene. None of eight cases showed abnormalities in exons 3-9 of CYP11B1, disproving a gene conversion phenomenon. In all patients a fragment of 393 bp corresponding to a specific region of the promoter of CYP11B2 gene was amplified. The sequence of the fragment did not differ from that of the wild-type promoter of the CYP11B2 gene. The 18-hydroxycortisol levels in the eight idiopathic hyperaldosteronism patients and four controls with chimeric gene were 3.9 +/- 2.3 and 21.9 +/- 3.5 nmol/liter, respectively (P < 0.01). In summary, we did not find other genetic alterations or high levels of 18-hydroxycortisol that could explain a positive dexamethasone suppression test in idiopathic hyperaldosteronism. We suggest that the dexamethasone suppression test could lead to an incorrect diagnosis of glucocorticoid-remediable aldosteronism.     

Congenital band of the vitelline artery remnant as a cause of chronic lower abdominal pain in an adult: Case report

INTRODUCTIONIntraabdominal bands of the vitelline vessel remnant are the rarest form of congenital mesodiverticluar bands which may or may not be associated with Meckel's diverticulum. In the majority of cases they cause an acute abdominal disease such as intestinal obstruction, especially in children.PRESENTATION OF CASEWe report a case of a 64 year old gentleman who experienced recurrent episodes of abdominal distension and bloating over two years. Computed tomography of his abdomen, colonoscopy, and barium follow through were all normal. Diagnostic laparoscopy revealed a single band adhesion stretching between the distal ileal mesentery and the anterior abdominal wall near the umbilicus.DISCUSSIONCongenital vascular bands are established causes of acute intestinal obstruction especially in children but are relatively uncommon. Their role in chronic abdominal pain is rare and diagnosis is difficult preoperatively. Pain in the patient was most likely due to recurrent partial twisting and untwisting of the bowel around the band.CONCLUSIONThis case not only highlights an unusual cause of chronic abdominal pain, but also the effectiveness of laparoscopy as a diagnostic tool in such patients.     

Interaction phenomena in graphene seen through quantum capacitance

Capacitance measurements provide a powerful means of probing the density of states. The technique has proved particularly successful in studying 2D electron systems, revealing a number of interesting many-body effects. Here, we use large-area high-quality graphene capacitors to study behavior of the density of states in this material in zero and high magnetic fields. Clear renormalization of the linear spectrum due to electron–electron interactions is observed in zero field. Quantizing fields lead to splitting of the spin- and valley-degenerate Landau levels into quartets separated by interaction-enhanced energy gaps. These many-body states exhibit negative compressibility but the compressibility returns to positive in ultrahigh B. The reentrant behavior is attributed to a competition between field-enhanced interactions and nascent fractional states.     

Similarities and Discrepancies in the Signaling Pathway for Nerve Growth Factor in an Insulin Producing Cell Line and a Neural Crest-Derived Cell Line

Like neuronal cells, insulin producing cells (beta cells) possess nerve growth factor (NGF) binding sites and express mRNA coding for the low- and high-affinity NGF receptors, p75^NGFR and Trk-A respectively. Although the role of NGF on neuronal cells is well documented, its function on beta cells is still unknown. As a first step towards the elucidation of the role of NGF on beta cells, we have characterized both types of NGF receptors on INS-1 cells, a beta cell line derived from a rat insulinorna and studied some early post-receptor events by comparing the signaling pathway of NGF in those cells and in PC12 cells, a well characterized NGF-responsive cell line. By polymerase chain reaction, immunocytochemistry, cross-linking and Western blot analysis, we clearly demonstrated that Trk-A and p75^NGFR, the two NGF receptors expressed in INS-1 cells and PC12 cells are similar. Moreover, upon NGF treatment, Trk-A is phosphorylated on tyrosine residues in both cell types in the same dose- and time-dependent manner. These data clearly demonstrate that the first step of NGF signal transduction is similar in PC12 and INS-1 cells. Although early responsive genes like NGFI-A and c-fos are induced in both cell types upon NGF treatment, the induction of c-jun expression is restricted to PC12 cells. Furthermore, the expression of late responsive genes, such as vgf and transin, which are induced by NGF in PC12 cells, are not induced in INS-1 cells. In conclusion, although the initial steps of NGF signal transduction are similar in PC12 and INS-1 cells, some of the later differ. These dissimilarities could suggest that NGF plays different roles in neuronal and pancreatic beta cells.