[Correlation between polymorphism of angiotensin-converting enzyme gene and the lower extremity atherosclerosis in type 2 diabetes mellitus patients].

Objective: To explore the correlation between polymorphism of the angiotensin-converting enzyme (ACE) gene and lower extremity atherosclerosis (LEA) in type 2 diabetes mellitus (T2DM) patients. Methods: A total of 380 patients diagnosed with T2DM in Department of Endocrinology from June 2015 to March 2016 were enrolled and divided into two groups: group A had no LEA (n=120) and group B had LEA(n=260). Color doppler ultrasound was used to detect the vascular lesions of the patients. For all patients in groups A and B, the polymerase chain reaction (PCR) was applied to determined the insertion/deletion polymorphism in intron 16 of the ACE gene of the patients. Then the blood pressure, blood lipid, glycated hemoglobin, and renal function were measured. Furthermore, the measured data was compared between the two groups. Multivariate logistic regression analysis was used to analyze the independent risk factors for LEA. Results: There was no significant statistical difference in age, sex, smoking and disease course between the two groups. The frequencies of DD genotype and D allele in the ACE gene of group B were much higher than those in group A. More specifically, DD genotype frequency was 18.8% in group B and 9.2% in group A, D allele frequency was 36.8% in group B and 29.2% in group A (all P<0.05). Multivariate logistic regression analysis showed that DD genotype in ACE gene (OR=2.744, 95% CI: 1.326-5.682), systolic blood pressure (OR=1.725, 95% CI: 1.072-2.778), total cholesterol (OR=3.785, 95% CI: 1.796-7.978), and glycated hemoglobin (OR=2.612, 95% CI: 1.602-4.258) were risk factors for LEA in T2DM patients. Conclusions: ACE gene insertion/deletion polymorphism was associated with the incidence of LEA in T2DM patients. DD genotype of the ACE gene may be a genetic risk factor for T2DM patients with concurrent atherosclerosis.

Subgaleal Drain Placement Improves Surgical Outcomes After Primary Cranioplasty in Craniosynostosis Patients.

BACKGROUND: There is no published data addressing the use of postoperative subgaleal drains in patients undergoing primary cranioplasty for craniosynostosis. We conducted a retrospective chart review in this population of patients, comparing outcomes of those who received postoperative drains with those who did not. We hypothesize that the subgaleal drains can significantly diminish postoperative facial edema and reduce the length of hospital stay. METHODS: We conducted a retrospective chart review of all patients undergoing primary cranioplasty for craniosynostosis with subgaleal drain placement (May 2010-March 2012). A comparison group without drain placement was matched appropriately to establish a comparison of outcomes. We determined whether subgaleal drainage led to improvement in postoperative facial edema, reduced length of hospital stay, postoperative changes in hematocrit (Hct), and complication rates. RESULTS: Of the 50 patients in this cohort, 25 patients had received subgaleal drains. The mean length of stay was 2.4 versus 3.5 days for the respective drained and undrained cohorts (P = 0.03). There was no significant difference in the mean decline in Hct between drained and undrained patients, with the mean Hct drop of 4.8% versus 5.0%, respectively (P = 0.83). Postoperative seroma formation developed in 3 undrained patients (17%) versus none in the drained cohort (0%). Although subjective, drained patients were observed to achieve quicker resolution of facial swelling and earlier recovery of eye opening. CONCLUSIONS: There is clinical benefit in subgaleal drain placement as earlier resolution of postoperative facial edema and a significantly shortened length of hospital stay was found among the drained cohort. Future studies warrant prospective clinical trials to establish the safety and efficacy of using subgaleal drains in cranial remodeling procedures of craniosynostosis.

Does Formal Research Training Lead to Academic Success in Plastic Surgery? A Comprehensive Analysis of U.S. Academic Plastic Surgeons.

INTRODUCTION: It is currently unknown whether formal research training has an influence on academic advancement in plastic surgery. The purpose of this study was to determine whether formal research training was associated with higher research productivity, academic rank, and procurement of extramural National Institutes of Health (NIH) funding in plastic surgery, comparing academic surgeons who completed said research training with those without. METHODS: This was a cross-sectional study of full-time academic plastic surgeons in the United States. The main predictor variable was formal research training, defined as completion of a postdoctoral research fellowship or attainment of a Doctor of Philosophy (PhD). The primary outcome was scientific productivity measured by the Hirsh-index (h-index, the number of publications, h that have at least h citations each). The secondary outcomes were academic rank and NIH funding. Descriptive, bivariate, and multiple regression statistics were computed. RESULTS: A total of 607 academic surgeons were identified from 94 Accreditation Council for Graduate Medical Education-accredited plastic surgery training programs. In all, 179 (29.5%) surgeons completed formal research training. The mean h-index was 11.7 ± 9.9. And, 58 (9.6%) surgeons successfully procured NIH funding. The distribution of academic rank was the following: endowed professor (5.4%), professor (23.9%), associate professor (23.4%), assistant professor (46.0%), and instructor (1.3%). In a multiple regression analysis, completion of formal research training was significantly predictive of a higher h-index and successful procurement of NIH funding. CONCLUSION: Current evidence demonstrates that formal research training is associated with higher scientific productivity and increased likelihood of future NIH funding.

Gene miles-apart is required for formation of otic vesicle and hair cells in zebrafish.

Hearing loss is a serious burden to physical and mental health worldwide. Aberrant development and damage of hearing organs are recognized as the causes of hearing loss, the molecular mechanisms underlining these pathological processes remain elusive. Investigation of new molecular mechanisms involved in proliferation, differentiation, migration and maintenance of neuromast primordium and hair cells will contribute to better understanding of hearing loss pathology. This knowledge will enable the development of protective agents and mechanism study of drug ototoxicity. In this study, we demonstrate that the zebrafish gene miles-apart, a homolog of sphingosine-1-phosphate receptor 2 (s1pr2) in mammals, has an important role in the development of otic vesicle, neuromasts and survival of hair cells. Whole-mount in situ hybridization of embryos showed that miles-apart expression occurred mainly in the encephalic region and the somites at 24 h.p.f. (hour post fertilization), in the midbrain/hindbrain boundary, the brainstem and the pre-neuromast of lateral line at 48 h.p.f. in a strict spatiotemporal regulation. Both up- and downregulation of miles-apart led to abnormal otoliths and semicircular canals, excess or few hair cells and neuromasts, and their disarranged depositions in the lateral lines. Miles-apart (Mil) dysregulation also caused abnormal expression of hearing-associated genes, including hmx2, fgf3, fgf8a, foxi1, otop1, pax2.1 and tmieb during zebrafish organogenesis. Moreover, in larvae miles-apart gene knockdown significantly upregulated proapoptotic gene zBax2 and downregulated prosurvival gene zMcl1b; in contrast, the level of zBax2 was decreased and of zMcl1b enhanced by miles-apart overexpression. Collectively, Mil activity is linked to organization and number decision of hair cells within a neuromast, also to deposition of neuromasts and formation of otic vesicle during zebrafish organogenesis. At the larva stage, Mil as an upstream regulator of bcl-2 gene family has a role in protection of hair cells against apoptosis by promoting expression of prosurvival gene zMcl1b and suppressing proapoptotic gene zBax2.