Hereditary factors in the craniofacial morphology of Angle's Class II and Class III malocclusions

Background. Previous studies have shown that environmental cadmium exposure could disrupt salivary gland function and is associated with dental caries and reduced bone density. Therefore, this cross-sectional study attempted to determine whether tooth decay with tooth loss following cadmium exposure is associated with some dental or skeletal traits such as malocclusions, sagittal skeletal pattern, and tooth decay. Methods. Between August 2019 and June 2020, 60 orthodontic patients with no history of previous orthodontics, functional appliances, or surgical treatment were examined. The patients were stratified into two groups according to their urine cadmium concentrations: high (>1.06 µg/g creatinine, n = 28) or low (<1.06 µg/g creatinine, n = 32). Results. The patients were 25.07 ± 4.33 years old, and most were female (female/male: 51/9 or 85%). The skeletal relationship was mainly Class I (48.3%), followed by Class II (35.0%) and Class III (16.7%). Class I molar relationships were found in 46.7% of these patients, Class II molar relationships were found in 15%, and Class III molar relationships were found in 38.3%. The mean decayed, missing, and filled surface (DMFS) score was 8.05 ± 5.54, including 2.03 ± 3.11 for the decayed index, 0.58 ± 1.17 for the missing index, and 5.52 ± 3.92 for the filled index. The mean index of complexity outcome and need (ICON) score was 53.35 ± 9.01. The facial patterns of these patients were within the average low margin (26.65 ± 5.53 for Frankfort–mandibular plane angle (FMA)). There were no significant differences in the above-mentioned dental indices between patients with high urine cadmium concentrations and those with low urine cadmium concentrations. Patients were further stratified into low (<27, n = 34), average (27–34, n = 23), and high (>34, n = 3) FMA groups. There were no statistically significant differences in the urine cadmium concentration among the three groups. Nevertheless, a marginally significant p-value of 0.05 for urine cadmium concentration was noted between patients with low FMA and patients with high FMA. Conclusion. This analysis found no association between environmental cadmium exposure and dental indices in our orthodontic patients.

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Genetic Control of Recombination Partner Preference in Yeast Meiosis: Isolation and Characterization of Mutants Elevated for Meiotic Unequal Sister-Chromatid Recombination

Genetics ◽

10.1093/genetics/153.2.621 ◽

1999 ◽

Vol 153 (2) ◽

pp. 621-641 ◽

Cited By ~ 10

Author(s):

Dawn A Thompson ◽

Franklin W Stahl

Keyword(s):

Sister Chromatid ◽

Meiotic Recombination ◽

Class Ii ◽

Class Iii ◽

Viability Analysis ◽

Isolation And Characterization ◽

Recombination Checkpoint ◽

Recombination Pathway ◽

Checkpoint Genes ◽

Sister Chromatid Recombination

AbstractMeiotic exchange occurs preferentially between homologous chromatids, in contrast to mitotic recombination, which occurs primarily between sister chromatids. To identify functions that direct meiotic recombination events to homologues, we screened for mutants exhibiting an increase in meiotic unequal sister-chromatid recombination (SCR). The msc (meiotic sister-chromatid recombination) mutants were quantified in spo13 meiosis with respect to meiotic unequal SCR frequency, disome segregation pattern, sporulation frequency, and spore viability. Analysis of the msc mutants according to these criteria defines three classes. Mutants with a class I phenotype identified new alleles of the meiosis-specific genes RED1 and MEK1, the DNA damage checkpoint genes RAD24 and MEC3, and a previously unknown gene, MSC6. The genes RED1, MEK1, RAD24, RAD17, and MEC1 are required for meiotic prophase arrest induced by a dmc1 mutation, which defines a meiotic recombination checkpoint. Meiotic unequal SCR was also elevated in a rad17 mutant. Our observation that meiotic unequal SCR is elevated in meiotic recombination checkpoint mutants suggests that, in addition to their proposed monitoring function, these checkpoint genes function to direct meiotic recombination events to homologues. The mutants in class II, including a dmc1 mutant, confer a dominant meiotic lethal phenotype in diploid SPO13 meiosis in our strain background, and they identify alleles of UBR1, INP52, BUD3, PET122, ELA1, and MSC1-MSC3. These results suggest that DMC1 functions to bias the repair of meiosis-specific double-strand breaks to homologues. We hypothesize that the genes identified by the class II mutants function in or are regulators of the DMC1-promoted interhomologue recombination pathway. Class III mutants may be elevated for rates of both SCR and homologue exchange.

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Genetics and epigenetics of class II and class III malocclusions

Journal of Physics Conference Series ◽

10.1088/1742-6596/1943/1/012091 ◽

2021 ◽

Vol 1943 (1) ◽

pp. 012091

Author(s):

M Subono ◽

I R N Alima ◽

E I Auerkari

Keyword(s):

Class Ii ◽

Class Iii

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Lifestyle modification for weight loss: effects on cardiorespiratory capacity in Patients with Class II and Class III Obesity

Obesity Science & Practice ◽

10.1002/osp4.544 ◽

2021 ◽

Author(s):

Finn Wammer ◽

Andrea Haberberger ◽

Anita Dyb Linge ◽

Tor Åge Myklebust ◽

Sveinung Vemøy ◽

...

Keyword(s):

Weight Loss ◽

Lifestyle Modification ◽

Class Ii ◽

Class Iii ◽

Class Iii Obesity

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Evaluation of the Nasolabial Angle in Orthodontic Diagnosis: A Systematic Review

Applied Sciences ◽

10.3390/app11062531 ◽

2021 ◽

Vol 11 (6) ◽

pp. 2531

Author(s):

Vincenzo Quinzi ◽

Licia Coceani Paskay ◽

Nicola D’Andrea ◽

Arianna Albani ◽

Annalisa Monaco ◽

...

Keyword(s):

Systematic Review ◽

Hyaluronic Acid ◽

Class Ii ◽

Cochrane Library ◽

Class Iii ◽

Palatal Expansion ◽

Rapid Palatal Expansion ◽

Nasolabial Angle ◽

Registration Number ◽

Teeth Extraction

Background: This study is a systematic literature review aiming at identifying the variation of the average nasolabial angle (NLA) in various orthodontic situations. The NLA is one of the key factors to be studied in an orthodontic diagnosis for the aesthetics of the nose and facial profile. Methods: Out of 3118 articles resulting from four search engines (PubMed, Cochrane Library, Turning Research Into Practice (TRIP) and SciELO), the final study allowed the analysis and comparison of only 26 studies. These included studies have considered the NLA in the following cases: teeth extraction, class II malocclusion, class III malocclusion, rapid palatal expansion (RPE), orthognathic surgery, and non-surgical rhinoplasty with a hyaluronic acid filler. Results: The results indicate that teeth extraction and the use of hyaluronic acid fillers significantly affect the NLA. Conclusions: This systematic review shows that a statistically significant change in NLA values occurs in: extractive treatments of all four of the first or second premolars in class I patients; in class II patients with upper maxillary protrusion; in patients with maxillary biprotrusion, except for cases of severe crowding; and in patients undergoing non-surgical rhinoplasty with a hyaluronic acid filler. Trial registration number: PROSPERO CRD42020185166

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Atypical, Non-V600 BRAF Mutations as a Potential Mechanism of Resistance to EGFR Inhibition in Metastatic Colorectal Cancer

JCO Precision Oncology ◽

10.1200/po.19.00102 ◽

2019 ◽

pp. 1-10 ◽

Cited By ~ 1

Author(s):

Benny Johnson ◽

Jonathan M. Loree ◽

Alexandre A. Jacome ◽

Shehara Mendis ◽

Muddassir Syed ◽

...

Keyword(s):

Colorectal Cancer ◽

Metastatic Colorectal Cancer ◽

Stable Disease ◽

Kinase Activity ◽

Class Ii ◽

Activity Level ◽

Class Iii ◽

Braf Mutations ◽

Egfr Inhibition ◽

Mechanism Of Resistance

PURPOSE Atypical, non-V600 BRAF ( aBRAF) mutations represent a rare molecular subtype of metastatic colorectal cancer (mCRC). Preclinical data are used to categorize aBRAF mutations into class II (intermediate to high levels of kinase activity, RAS independent) and III (low kinase activity level, RAS dependent). The clinical impact of these mutations on anti-EGFR treatment efficacy is unknown. PATIENTS AND METHODS Data from 2,084 patients with mCRC at a single institution and from an external cohort of 5,257 circulating tumor DNA (ctDNA) samples were retrospectively analyzed. Overall survival (OS) was calculated using Kaplan-Meier and log-rank tests. Statistical tests were two-sided. RESULTS BRAF mutations were harbored by 257 patients, including 36 with aBRAF mutations: 22 class III, 10 class II, four unclassified. For patients with aBRAF mCRC, median OS was 36.1 months, without a difference between classes, and median OS was 21.0 months for patients with BRAFV600E mCRC. In contrast to right-sided predominance of tumors with BRAFV600E mutation, 53% of patients with aBRAF mCRC had left-sided primary tumors. Concurrent RAS mutations were noted in 33% of patients with aBRAF mCRC, and 67% of patients had microsatellite stable disease. Among patients with aBRAF RAS wild-type mCRC who received anti-EGFR antibodies (monotherapy, n = 1; combination therapy, n = 10), no responses to anti-EGFR therapy were reported, and six patients (four with class III aBRAF mutations, one with class II, and one unclassified) achieved stable disease as best response. Median time receiving therapy was 4 months (range, 1 to 16). In the ctDNA cohort, there was an increased prevalence of aBRAF mutations and subclonal aBRAF mutations ( P < .001 for both) among predicted anti-EGFR exposed compared with nonexposed patients. CONCLUSION Efficacy of anti-EGFR therapy is limited in class II and III aBRAF mCRC. Detection of aBRAF mutations in ctDNA after EGFR inhibition may represent a novel mechanism of resistance.

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