Quantity and distribution of plaque in orthodontic patients treated with molar bands

Objective

The placement of orthodontic bands usually increases plaque accumulation due to numerous mechanical retention sites. The purpose of this investigation was to evaluate the amount and distribution pattern of biofilm in the oral (palatal and lingual) and interproximal regions surrounding orthodontic bands.

Materials and Methods

We evaluated the formation of biofilm on 32 orthodontic bands which had been placed intraorally for 6?C37?months. Two parameters were measured: the percentage of surface covered by biofilm (quantity) and the biofilm distribution pattern of accumulation. We measured these two parameters in four regions of interest: the mesial and distal interproximal regions, as well as the mesial and distal regions of the oral attachment.

Results

The quantity of biofilm formation was similar in all four regions of interest, ranging from 13.3% to 16.8%. In contrast to biofilm quantity, distribution patterns differed in the four regions. In the mesial and distal interproximal regions it appeared as extensive insular areas in 87.5% and 71.9%, respectively, whereas it appeared more often supragingival and linear in nature in regions adjacent to the oral attachment, i.e. in 65.6% and 68.8%, respectively.

Conclusion

Our results indicate that firstly, oral hygiene in the palatal and lingual regions of orthodontic bands seems as difficult as it is in the interproximal areas, thus requiring thorough hygiene in both areas. Secondly, orthodontic patients with a history of periodontal disease require special attention regarding the use of orthodontic bands.     

Cancer-promoting effect of Taiwan betel quid in hamster buccal pouch carcinogenesis

OBJECTIVE: To investigate the cancer-promoting effect of Taiwan betel quid in hamster buccal pouch carcinogenesis.
MATERIALS AND METHODS: Two hundred and fifty-two non-inbred mate adult Syrian golden hamsters were randomly divided into six groups, each containing forty-two animalS. A treatment regimen over a 14-week experimental period was employed with six animals per group being killed at seven different periods (every 2 weeks). The right buccal pouch of each animal was painted three times a week with various combinations of 7, 12-dimethylbenz[a]anthracene (DMBA), Taiwan betel quid extract, dimethyl sulfoxide (DMSO) and mineral oil.
RESULT: Both the number and size of tumors in animals concurrently treated with DMBA and betel quid were significantly higher than those in animals treated with DMBA alone in each killing period of 8, 10, 12 and 14 weekS. No visible tumors but hyperkeratosis and acanthosis were observed in pouches treated with betel quid alone for all killing periods.
CONCLUSION: Our results indicate Taiwan betel quid may be a co-carcinogen in human oral carcinogenesis, if extrapolation can be made from the current animal study.     

汉语阅读障碍儿童在本顿视觉保持测验中的反应特征

目的:比较阅读障碍儿童与正常儿童在本顿视觉保持测验中的反应特征,探索阅读障碍儿童视觉空间记忆能力的特点。方法:①2005-07/2006-05在儿童发育行为门诊遴选阅读障碍儿童20名(平均年龄10.2岁),按1∶1配对原则,选择年龄、性别、年级和家庭状况等条件与阅读障碍组相似的20名正常阅读能力儿童为对照组(平均年龄10.1岁)。②应用国内修订版本顿视觉保持测验C式B法,D式C法和E式D法对两组儿童进行个别测试。C式图卡呈现5s后让被试默画(视觉记忆能力),D式图卡让被试临摹(视觉结构能力),E式图卡呈现10s后间隔15s再让被试默画(视觉延迟记忆能力)。③对两组儿童的视觉记忆保持能力、视觉结构能力和延迟记忆能力进行测试,分别记录两组儿童测验的正确分(每一图卡根据全或无的原则记1或0分,总分0～10)及错误次数(错误类型分为遗漏或增加、变形、持续、旋转、位置错误和大小错误6个范畴),进行配对t检验。结果:40名受试者均进入结果分析。①正确得分:在视觉记忆和视觉结构能力测验中阅读障碍组低于对照组(5.00±2.45,6.60±1.82,P=0.019;7.50±2.44,8.95±1.32,P=0.015),在视觉延迟记忆测试中,两组得分比较差异不显著(P=0.077)。②总错误分:在视觉记忆和视觉结构能力测验中阅读障碍组高于对照组(7.65±4.20,4.90±3.24,P=0.016;3.20±3.93,1.15±1.46,P=0.035),在视觉延迟记忆测试中,两组得分比较差异不显著(P=0.389)。③错误类型:阅读障碍组儿童在视觉记忆能力测试中变形和持续性错误次数均显著多于对照组(3.95±2.40,1.75±1.52;0.35±0.67,0;P均<0.05),在视觉结构能力测试中变形错误次数显著多于对照组(1.35±1.69,0.35±0.75,P<0.05)。结论:阅读障碍儿童的视觉空间短时记忆能力、视觉结构和视觉运动整合能力存在缺陷。     

Benzimidazole -Resistance in Haemonchus contortus: New PCR-RFLP Method for the Detection of Point Mutation at Codon 167 of Isotype 1 β-Tubulin Gene

Background

Due to the lack of a suitable and economic test for the analysis of the polymorphism at codon 167, we developed a new PCR-RFLP technique, based on a modified forward primer (UT-HC167 MF-primer), to identify simultaneously the SNPs at codons 167 and 200 of isotype 1 β-tubulin gene of Haemonchus contortus.

Methods

There already are several safe and easy methods for identification of point mutations at codons 198 and 200. Due to the lack of a reliable and easy method for the detection of the single nucleotide polymorphism (SNP) at codon 167, we developed an innovative PCR-RFLP technique based on a modified forward primer (UT-HC167 MF-primer), in which the nucleotide T at the position 443 was substituted through a nucleotide A creating a restriction site for restriction endonuclease SnaB I in the nucleotide sequences including codon 167. A total of 138 adult male H. contortus were collected from three different geo-climatic areas of Iran. The isolated genomic DNA of each single worm was amplified by PCR using primers flanking codon 167. The PCR product (527 bp) was then amplified by semi-nested PCR using the UT-HC167 MF-primer and the reverse primer achieving a PCR product of 451 bp in length. This PCR product was subsequently digested with the restriction endonucleases SnaB I and TaaI for analysis of the mutations at codons 167 and 200, respectively.

Results

All worms had two alleles encoding for phenylalanine (BZ^ss homozygote) for both codons.

Conclusion

Using the UT-HC167 MF-primer and a suitable reverse primer designed upstream from codon 200, it is possible to amplify a PCR product which can be used for analysis of the SNPs at all three mentioned codons using RFLP.     

Cell markers in hairy cell leukemia studied in cells from 51 patients

To determine the maturation arrest of the neoplastic cells of hairy- cell leukemia (HCL) and the spectrum of the surface markers on these cells, a series of 51 patients with this disease was studied. The cells of all but two of the patients showed monoclonal surface Ig with respect to light chains. In about one-third of the cases, only gamma heavy chain determinants were present on the cells; the majority carried multiple heavy chain determinants as documented by the application of different fluorochromes. Two patients each showed two different clones of cells, both of the same light chain type. In one of these two patients, two paraproteins were present in the serum. Intracytoplasmic Ig was found in only 4 of 39 cases, in all instances being IgM. All cases studied concerned cells with FclgG receptors; however, the density of this receptor varied. FcIgM receptors also showed a spectrum of density, with some cases showing very few FcIgM- positive cells. Receptors C3 were not observed on the hairy cells. Serum immunoglobulin levels were normal or increased. Paraproteins were found in the sera of 4 of 38 patients. These data suggest that HCL is a neoplasm of B lymphocytes. The neoplastic cells are probably arrested at a more mature stage than the cells of chronic lymphocytic leukemia. The multiple isotypes on the cells indicate a block at the "switch" phase from the small micro-carrying lymphocyte to the larger Ig- producing lymphocyte or plasma cell.     

Asialo-von Willebrand factor inhibits platelet adherence to human arterial subendothelium: discrepancy between ristocetin cofactor activity and primary hemostatic function

Platelet adherence at high wall shear rates requires plasma von Willebrand factor (vWF). Clinically, the ristocetin cofactor (RCof) activity is the only widely available assay for vWF function. When purified vWF is treated with neuraminidase to yield asialo-vWF (AS- vWF), its RCof activity is increased by 20% to 40%. AS-vWF binds to normal human platelets independently of ristocetin and induces platelet aggregation in the presence of fibrinogen. To determine whether AS-vWF also shows an enhanced capacity to support platelet adherence to subendothelium, we used the Baumgartner technique. Intact vWF, AS-vWF, or AS-vWF treated with beta-galactosidase (asialo, agalacto-vWF; AS,AG- vWF) was added to normal citrated whole blood before perfusion over human umbilical artery segments (wall shear rate, 2,600 sec-1). Four micrograms per milliliter AS-vWF caused a 69% reduction in total platelet adherence compared with citrated whole blood (P less than .001), and 4 micrograms/mL AS,AG-vWF led to a 48% reduction (P less than .005). With 4 micrograms/mL intact vWF, the platelet adherence values were not significantly different from the controls. No significant differences in subendothelial platelet thrombi or postperfusion platelet counts were evident among any of the groups. In reconstituted afibrinogenemic perfusates, 4 micrograms/mL AS-vWF caused a 42% reduction in platelet adherence (P less than .05). Thus, AS-vWF is a potent inhibitor of platelet adherence, despite its enhanced RCof specific activity. Abnormalities in vWF carbohydrate may play a role in impaired primary hemostasis in some patients with von Willebrand's disease.     

Interaction of platelet plasma membranes with thrombin-activated platelets

This study described the binding of platelet plasma membranes to either control or thrombin-activated platelets. Glycoproteins in plasma membranes isolated from human platelets were labeled by oxidation with periodate followed by reduction with [3H]NaBH4. Labeled membranes were incubated with either control or thrombin-activated platelets. The amount of membranes bound was measured by separating platelets with bound membranes from solution by rapid centrifugation through 27% sucrose and determining the amount of radioactivity associated with platelets. Five- to sevenfold more membranes bound to thrombin- activated platelets than to control platelets. This enhanced binding of labeled membranes was completely inhibited by an excess of unlabeled platelet membranes. Human erythrocyte membranes had little affinity for either washed or thrombin-activated platelets and therefore did not compete for platelet-membrane binding. Binding of platelet membranes to thrombin-treated platelets was inhibited by prior incubation of the platelets with PGI2 suggesting that the enhanced binding of membranes was to activated platelets. This study demonstrates that the purified platelet membranes have functional sites that can mediate membrane binding to platelets and that quantitation of membrane binding appears to reflect the increased aggregation capability of activated platelets.