Measuring the Pressure in the Superficial Inferior Epigastric Vein to Monitor for Venous Congestion in Deep Inferior Epigastric Artery Perforator Breast Reconstructions: A Pilot Study

During deep inferior epigastric artery perforator (DIEP) flap dissection, we noted that in many cases the superficial vein on the ipsilateral side of the flap was engorged and tense, and in others, it was empty. This led us to believe that the pressure is increased as the result of preferential outflow through the superficial vein in some cases, which could result in venous congestion of the flap if this vessel was not anastomosed. To test this hypothesis, we measured the venous pressure in the superficial venous system before and after flap dissection. The pressure in the superficial inferior epigastic vein of a DIEP flap was measured in 26 consecutive flaps to investigate the correlation between the pressure and venous congestion of the flap. The first measurement was performed at the beginning of the dissection, and the second measurement was taken after the flap had been completely raised on a single perforator. The mean increase in pressure after flap dissection was 10.6 mm Hg (mu = 10.6; range -1 to 31; O +/- 7.0 mm Hg). Clinical signs of venous congestion were observed in one case. In this case, the increase in venous pressure was with 31 mm Hg, also the highest. Although the results of this report are preliminary, they indicate that the pressure in the superficial vein of DIEP flaps might be of predictive value for venous congestion

Rare and Common Variants Conferring Risk of Tooth Agenesis

We present association results from a large genome-wide association study of tooth agenesis (TA) as well as selective TA, including 1,944 subjects with congenitally missing teeth, excluding third molars, and 338,554 controls, all of European ancestry. We also tested the association of previously identified risk variants, for timing of tooth eruption and orofacial clefts, with TA. We report associations between TA and 9 novel risk variants. Five of these variants associate with selective TA, including a variant conferring risk of orofacial clefts. These results contribute to a deeper understanding of the genetic architecture of tooth development and disease. The few variants previously associated with TA were uncovered through candidate gene studies guided by mouse knockouts. Knowing the etiology and clinical features of TA is important for planning oral rehabilitation that often involves an interdisciplinary approach

Inhibition of neoplastic development in the liver by hepatocyte growth factor in a transgenic mouse model.

Overexpression of the c-myc oncogene is associated with a variety of both human and experimental tumors, and cooperation of other oncogenes and growth factors with the myc family are critical in the evolution of the malignant phenotype. The interaction of hepatocyte growth factor (HGF) with c-myc during hepatocarcinogenesis in a transgenic mouse model has been analyzed. While sustained overexpression of c-myc in the liver leads to cancer, coexpression of HGF and c-myc in the liver delayed the appearance of preneoplastic lesions and prevented malignant conversion. Furthermore, tumor promotion by phenobarbital was completely inhibited in the c-myc/HGF double transgenic mice, whereas phenobarbital was an effective tumor promoter in the c-myc single transgenic mice. The results indicate that HGF may function as a tumor suppressor during early stages of liver carcinogenesis, and suggest the possibility of therapeutic application for this cytokine

Rare and Common Variants Conferring Risk of Tooth Agenesis

To access publisher's full text version of this article click on the hyperlink belowWe present association results from a large genome-wide association study of tooth agenesis (TA) as well as selective TA, including 1,944 subjects with congenitally missing teeth, excluding third molars, and 338,554 controls, all of European ancestry. We also tested the association of previously identified risk variants, for timing of tooth eruption and orofacial clefts, with TA. We report associations between TA and 9 novel risk variants. Five of these variants associate with selective TA, including a variant conferring risk of orofacial clefts. These results contribute to a deeper understanding of the genetic architecture of tooth development and disease. The few variants previously associated with TA were uncovered through candidate gene studies guided by mouse knockouts. Knowing the etiology and clinical features of TA is important for planning oral rehabilitation that often involves an interdisciplinary approach.Swedish Society of Medicine Swedish Brain Foundation National Institutes of Health (NIH) (National Institute of Dental and Craniofacial Research) Danish National Research Foundation Danish Regional Committees Pharmacy Foundation Egmont Foundation March of Dimes Birth Defects Foundation Health Foundation Novo Nordisk Foundation Oak Foundation fellowship Novo Nordisk Foundation NI