Autologous bone graft harvesting: a review of grafts and surgical techniques.

Spinal fusion with or without instrumentation often requires the use of bone graft. Bone graft may be autogenous or exogenous. There are various forms of bone graft which may be acquired from numerous sites. Knowledge of fusion biology is imperative for understanding the benefits and limitations of these grafts. Equally as important is the knowledge of outcome measures, management of donor-site morbidity, and potential reconstruction. This review details the methods of obtaining bone graft and details the properties of each, as well as discusses observed outcomes, donor-site morbidities, and reconstruction techniques.

hERG1 channels drive tumour malignancy and may serve as prognostic factor in pancreatic ductal adenocarcinoma.

BACKGROUND: hERG1 channels are aberrantly expressed in human cancers. The expression, functional role and clinical significance of hERG1 channels in pancreatic ductal adenocarcinoma (PDAC) is lacking. METHODS: hERG1 expression was tested in PDAC primary samples assembled as tissue microarray by immunohistochemistry using an anti-hERG1 monoclonal antibody (α-hERG1-MoAb). The functional role of hERG1 was studied in PDAC cell lines and primary cultures. ERG1 expression during PDAC progression was studied in Pdx-1-Cre,LSL-Kras(G12D/+),LSL-Trp53(R175H/+) transgenic (KPC) mice. ERG1 expression in vivo was determined by optical imaging using Alexa-680-labelled α-hERG1-MoAb. RESULTS: (i) hERG1 was expressed at high levels in 59% of primary PDAC; (ii) hERG1 blockade decreased PDAC cell growth and migration; (iii) hERG1 was physically and functionally linked to the Epidermal Growth Factor-Receptor pathway; (iv) in transgenic mice, ERG1 was expressed in PanIN lesions, reaching high expression levels in PDAC; (v) PDAC patients whose primary tumour showed high hERG1 expression had a worse prognosis; (vi) the α-hERG1-MoAb could detect PDAC in vivo. CONCLUSIONS: hERG1 regulates PDAC malignancy and its expression, once validated in a larger cohort also comprising of late-stage, non-surgically resected cases, may be exploited for diagnostic and prognostic purposes in PDAC either ex vivo or in vivo.

Evolution of the technologist specialist in gastrointestinal radiology.

Over the past few years, a program was initiated at the author's institution to train radiologic technologists to perform the fluoroscopic aspect of gastrointestinal examinations. The program was undertaken in an attempt to improve patient flow through the division, as well as in response to the decreasing number of residents being accepted into the radiology program. The results with respect to diagnostic quality of examination, improved patient flow, and patient and resident acceptance have been satisfactory.

Gastroduodenal response to low-dose glucagon.

A prospective, double-blind clinical study of the double-contrast upper gastrointestinal examination involving 240 patients was performed using glucagon in doses from 0.025 to 0.125 mg, in 0.025 mg increments. Although motility was diminished, neither gastric distension or coating was improved with the use of glucagon. However, duodenal distension and coating were markedly enhanced. The response of the pylorus was individualistic. The pylorus remained patent in most patients, and glucagon would not prevent barium spillage in the duodenum. However, in those patients with a "competent" pylorus, increasing glucagon doses produced a delay in gastric emptying. Several other variables, including weight, age, and gender, were studied and were not believed to be of clinical significance. Spontaneous gastroesophageal reflux was also increased with the use of glucagon. Glucagon mainly enhanced duodenal visualization but had no beneficial effect on the stomach or pylorus. Absolute dose is the most important factor, and all observable changes can be seen once a certain threshold dose (0.05 mg) is reached.

Control of cardiac sarcolemmal adenylate cyclase and sodium, potassium-activated adenosinetriphosphatase activities.

A plasma membrane preparation purified from guinea pig ventricles without the use of high concentrations of detergents or structure-disrupting salts was used to compare the mechanisms of controlling sodium, potassium-activated adenosinetriphosphatase (Na, K-ATPase) and adenylate cyclase activities. The basal ATPase activity of 4-6 mu moles P1/hour mg-1 protein, measured in 120 mM NaC1 or KC1, was approximately doubled in 100 mM NaC1 plus 20 mM KC1. This increment, the Na, K-ATPase, was abolished by 10-5M ouabain, the K1 for ouabain being approximately 3 X 10-7M. 1-Epinephrine had no effect on Na, K-ATPase, but NaF was inhibitory. Adenylate cyclase, which had a basal activity of approximately 50% by NaC1 or KC1 alone at concentrations up to 0.2M. There was no additional stimulation of adenylate cyclase activity when na+ K+ included together. Both 1-epinephrine and NaF cause significant stimulation of adenylate cyclase, but neither basal nor activated cyclic AMP PRODUCTION WAS INFLUENCED BY OUABAIN. Half-maximal stimulation was seen at approximately 5 X 10-6M 1-epinephrine. Both the catecholamine and NaF increased the V-max ofcardiac plasma membrane adenylate cyclase without significantly influencing Km. Increasing Ca2+ in the range between 10-7 and 10-3M inhibited basal, 1-epinephrine-stimulated, and NaF-stimulated activities. Basal rates of cyclic AMP production were more sensitive to Ca2+ than was 1-epinephrine stimulation was increased from approximately 60% in 0.5 mM EGTA to approximately 150% in 10-7M Ca2+ and 400% in 10-5M Ca2+. The inhibitory effect of Ca2+ on adenylate cyclase activity may represent a negative feed back mechanism by which elevation of intracellular Ca2+ concentration lowers cellular levels of cyclic AMP and thus reduces Ca2+ influx into the myocardium.