Periodontal surgery of vertical bony defects with or without synthetic bioabsorbable barriers. 12-month results

The aim of the present study was to clinically and radiographically compare guided tissue regeneration (GTR) therapy with bioabsorbable polyglactin 910 barriers and conventional periodontal surgery in intrabony defects. In 26 patients with advanced periodontitis, 29 teeth exhibiting interproximal intrabony defects were treated; 15 by conventional periodontal surgery (control) and 14 by GTR (test). Before and 12 months after surgery, clinical parameters were assessed and standardized radiographs were taken. On the radiographs the distances from the cemento-enamel junction (CEJ) to the alveolar crest (AC), and the CEJ to the most apical extension of the bony defect (BD) were measured using a computer-assisted analyzing device (LMSRT). Twelve months after surgery, 24 patients with 27 lesions were available for examination. For both methods statistically significant (P < 0.001) probing depth (PD) reduction (mean +/- standard deviation) of -4.49 +/- 1.94 mm (n = 13, test) and -3.22 +/- 1.48 mm (n = 14, control), as well as clinical attachment gain (CAL-V) of 3.41 +/- 1.59 mm (test) and 2.07 +/- 1.10 mm (control), was observed. Radiographic changes of the distance CEJ to AC of -0.95 +/- 1.72 mm (n = 9, test), and -0.98 +/- 1.53 mm (n = 11, control) were not significant. A significant bony fill (distance CEJ-BD) of 1.05 +/- 1.22 mm was observed for the test group (P < 0.01); the 0.68 +/- 2.04 mm bony gain for the control group was not statistically significant. The PD reduction (P < 0.05) and attachment gain (P < 0.01) in the test group was statistically significantly more favorable than in the control group. Twelve months after surgery, statistically more favorable PD reduction and attachment gain was observed using polyglactin 910 barriers than compared to conventional flap surgery. Hence, the use of bioabsorbable barriers for therapy of intrabony defects may be recommended.     

Polycyclic aromatic hydrocarbon-DNA adducts in human placenta and modulation by CYP1A1 induction and genotype

This study investigated the relationship in human placenta between polycyclic aromatic hydrocabon (PAH)-DNA adduct levels and two biomarkers of cytochrome P4501A1 (CYP1A1): gene induction evidenced by CYP1A1 mRNA, and a genetic polymorphism, the CYP1A1 MspI RFLP. CYP1A1 codes for an inducible enzyme system that catalyzes the bioactivation of PAHs. Prior research found a high correlation in human lung tissue between CYP1A1 activity and DNA damage from PAHs. The CYP1A1 Mspi RFLP has been linked in some studies to risk of lung cancer. The relationships in human placenta between DNA damage, CYP1A1 activity and genotype have not been well characterized and may be relevant to risks from transplacental PAH exposure. The study cohort consisted of 70 newborns from Krakow, Poland, a city with elevated air pollution, and 90 newborns from nearby Limanowa, an area with lower air pollution but greater indoor coal use. Contrary to results seen previously in lung tissue, CYP1A1 mRNA was not significantly correlated with PAH-DNA adduct levels in the placenta. Smoking (self-reported maternal and infant plasma cotinine) was significantly associated with CYP1A1 mRNA levels (P < 0.01), but not with PAH-DNA adduct levels. Placental PAH-DNA adduct levels were significantly higher in infants with the CYP1A1 MspI restriction site compared with infants without the restriction site (P < 0.01), implicating a genetic factor in inter-individual variation in DNA damage in human placenta. Further studies are needed to determine the relevance of this finding to risk of transplacental carcinogenesis.     

Calmodulin is essential for estrogen receptor interaction with its motif and activation of responsive promoter

Calmodulin (CaM) has been reported to have affinity for the estrogen receptor (ER). Observations reported here reveal a direct physical interaction between purified CaM and ER. This direct ER-CaM interaction may be an initial event preceding the assembly of ER plus auxiliary proteins into the active ER complex with its DNA motif, the estrogen response element. We demonstrate that CaM is an integral component of this complex by using a system reconstituted from purified ER and nuclear extract from ER-negative breast cancer cells and also with ER-depleted nuclear extract of an ER-positive breast cancer cell line. Although CaM is essential for formation of this complex, it is not sufficient, suggesting roles also of auxiliary proteins. CaM also is functionally required for activation of an ER-responsive promoter, in the 17beta-estradiol-ER pathway of hormone action and regulation of 17beta-estradiol-responsive gene expression that is associated with proliferation of mammary epithelial cells.     

Establishing the psychometric properties of the DSM-III-R personality disorders: implications for DSM-V

In this study, symptom (item) level data were used to perform a psychometric analysis of the DSM-III-R personality disorders (PDs). Determined for each PD criteria set were convergent validity, discriminant validity, and internal consistency. The results indicated that the majority of the PD criteria sets (6 of the 11 ) possessed adequate convergent validity, although discriminant validity was problematic for most of these disorders. Internal consistency was also weak for the PD criteria sets, with only 3 of the 11 exceeding a minimum cutoff score of .70. The present study employed a methodology modeled after the one reported by Morey (1988a), and the results of the two studies were highly similar. Consistent findings across the two data sets can be taken to reflect the actual psychometric properties of the DSM-III-R PDs. The success of our replication demonstrates the potential that large-scale psychometric investigations hold for aiding the development and refinement of the DSM PDs.     

The contribution of classical (beta1/2-) and atypical beta-adrenoceptors to the stimulation of human white adipocyte lipolysis and right atrial appendage contraction by novel beta3-adrenoceptor agonists of differing selectivities

The role of beta3- and other putative atypical beta-adrenoceptors in human white adipocytes and right atrial appendage has been investigated using CGP 12177 and novel phenylethanolamine and aryloxypropanolamine beta3-adrenoceptor (beta3AR) agonists with varying intrinsic activities and selectivities for human cloned betaAR subtypes. The ability to demonstrate beta1/2AR antagonist-insensitive (beta3 or other atypical betaAR-mediated) responses to CGP 12177 was critically dependent on the albumin batch used to prepare and incubate the adipocytes. Four aryloxypropanolamine selective beta3AR agonists (SB-226552, SB-229432, SB-236923, SB-246982) consistently elicited beta1/2AR antagonist-insensitive lipolysis. However, a phenylethanolamine (SB-220646) that was a selective full beta3AR agonist elicited full lipolytic and inotropic responses that were sensitive to beta1/2AR antagonism, despite it having very low efficacies at cloned beta1- and beta2ARs. A component of the response to another phenylethanolamine selective beta3AR agonist (SB-215691) was insensitive to beta1/2AR antagonism in some experiments. Because no [corrected] novel aryloxypropanolamine had a beta1/2AR antagonist-insensitive inotropic effect, these results establish more firmly that beta3ARs mediate lipolysis in human white adipocytes, and suggest that putative 'beta4ARs' mediate inotropic responses to CGP 12177. The results also illustrate the difficulty of predicting from studies on cloned betaARs which betaARs will mediate responses to agonists in tissues that have a high number of beta1- and beta2ARs or a low number of beta3ARs.     

DK UK10-A系列音箱

UK10-A系列适用于各种固定安装的高档演艺吧、慢摇吧及现场表演。该系列采用高功率扬声器单元和轻巧的箱体搭配,通过计算机优化设计,达到平滑的特性、展宽的频响特点和良好的控制覆盖性能。     

Spinal cord energy metabolism following compression trauma to the feline spinal cord

The purpose of this study was to determine the spinal cord metabolic state for 24 hours after compression trauma to the feline spinal cord. Cats were anesthetized with pentobarbital and injured by placing a 190-gm weight on the spinal cord for 5 minutes. Biochemical analysis of the injured segment revealed a significant depletion in the levels of adenosine triphosphate (ATP), phosphocreatine (P-creatine), and total adenylates for the entire 24-hour recovery period. Glucose levels initially declined, but by 1 hour had normalized, and at 8 and 24 hours were significantly supranormal. The lactate/pyruvate ratio and tissue lactate concentrations increased four and five and half times, respectively, for the first 4 hours after injury. Between 8 and 24 hours, lactate levels remained elevated, whereas the lactate/pyruvate ratio declined to contol levels as the result of a significant rise in the tissue pyruvate concentration. This sequence of metabolic changes suggested that metabolism was probably not homogeneous throughout the injured segment, and that tissue metabolic rate was depressed for the initial 4 hours after trauma then increased in metabolically active tissue for the remainder of the 24-hour recovery period. This model of spinal cord trauma results in a severe, prolonged ischemia and metabolic injury to the affected tissue. Whether these metabolic changes results from or cause the tissue damage and irreversible paraplegia associated with this type of spinal cord injury remains to be determined.     

Iodine induced thyroid disease

Although iodine prevents goiter, enlarged thyroid glands continue to be detected in subjects, especially children, in spite of adequate iodine ingestion. Iodine may cause goiter in susceptible individuals by inhibiting the organic binding of iodine as is seen in adult asthmatics, neonates born of iodine ingesting mothers and in subjects residing along the littoral of Japan. Myxedema, especially in treated Graves' disease and Hashimoto's disease, may also be precipitated by iodine. On the other hand, iodine given to euthyroid subjects in areas of endemic goiter and to subjects with nontoxic nodular goiter may induce thyrotoxicosis by disclosing diffuse autonomously functioning thyroid tissue. An indirect adverse effect of iodine upon the thyroid gland may be manifested by lymphocyte glandular infiltrates and chronic thyroiditis which were sparse or absent in thyroid glands removed from subjects living in iodine deficient areas before iodine prophylaxis and therapy. Not only has the incidence of thyroiditis increased, but the histologic and clinical distinctions between treated Graves' disease and chronic thyroiditis have become indistinct. Experimentally, chronic thyroiditis has been produced in animals following large doses of iodine. Accumulated evidence supports the concept that iodine contributes to the genesis of chronic thyroiditis.     

Human spinal arachnoid villi and granulations

A commercially available recording of Northwestern University Auditory Test No. 6 (N.U. No. 6) produced by Auditec of St. Louis was evaluated in a series of four studies. Interlist equivalence of this version was initially investigated, and then normative intelligibility functions were developed using listerners with normal hearing. Intelligibility functions for the original version of N.U. No. 6. prepared by Northwestern University, were then derived, concurrently with functions of the Auditec version, using (1) a group of listeners with normal hearing; and (2) a group with sensorineural hearing loss. The results demonstrated good interlist equivalence for the Auditec version of N.U. No. 6. The comparative intelligibility functions for the Auditec and Northwestern versions of N.U. No 6 furthermore indicated a difference between the two recordings, but it was concluded that for clinical purposes the two versions may be considered equivalent.