scholarly journals Corrigendum to Estimating Craniofacial Growth Cessation: Comparison of Asymptote- and Rate-based Methods

2021 ◽  
pp. 105566562110249
2021 ◽  
pp. 105566562110026
Author(s):  
Anna M. Hardin ◽  
Ryan P. Knigge ◽  
Hee Soo Oh ◽  
Manish Valiathan ◽  
Dana L. Duren ◽  
...  

Objective: To identify differences between asymptote- and rate-based methods for estimating age and size at growth cessation in linear craniofacial measurements. Design: This is a retrospective, longitudinal study. Five linear measurements were collected from lateral cephalograms as part of the Craniofacial Growth Consortium Study (CGCS). Four estimates of growth cessation, including 2 asymptote- (GCasym, GCerr) and 2 rate-based (GCabs, GC10%) methods, from double logistic models of craniofacial growth were compared. Participants: Cephalometric data from participants in 6 historic longitudinal growth studies were included in the CGCS. At least 1749 individuals (870 females, 879 males), unaffected by craniofacial anomalies, were included in all analyses. Individuals were represented by a median of 11 images between 2.5 and 31.3 years of age. Results: GCasym consistently occurred before GCerr and GCabs consistently occurred before GC10% within the rate-based approaches. The ordering of the asymptote-based methods compared to the rate-based methods was not consistent across measurements or between males and females. Across the 5 measurements, age at growth cessation ranged from 13.56 (females, nasion-basion, GCasym) to 24.39 (males, sella-gonion, GCerr). Conclusions: Adolescent growth cessation is an important milestone for treatment planning. Based on our findings, we recommend careful consideration of specific definitions of growth cessation in both clinical and research settings since the most appropriate estimation method may differ according to patients’ needs. The different methods presented here provide useful estimates of growth cessation that can be applied to raw data and to a variety of statistical models of craniofacial growth.


1997 ◽  
Vol 34 (4) ◽  
pp. 325-330 ◽  
Author(s):  
Kazuaki Nonaka ◽  
Yasunori Sasaki ◽  
Yoshihisa Watanabe ◽  
Ken-ichi Yanagita ◽  
Minoru Nakata

Objective: This study examined the factors related to the morphogenesis of the craniofacial complex of the CL/Fr mouse fetus affected with CLP based on the findings of a lateral cephalogram. Design: Embryo transfer experiments were performed to determine the effect of the fetus weight, dam strain, dam weight, and litter size on the intra-uterine craniofacial morphogenesis of CL/Fr mouse fetuses. On the 18th gestational day, each pregnant dam that had received CL/Fr mouse embryos was laparotomized to remove the transferred fetuses that had developed in the uteri of the cleft lip and palate (CLP)-susceptible CL/Fr strain dam and the CLP-resistant C57BL strain dam. A cephalometric observation of the craniofacial morphology of each fetus was subsequently performed. Results: Based on a multiple regression analysis, the standardized partial regression coefficients of the affected fetus weight, the dam weight, and the litter size on the maxillary size of the affected CL/Fr fetus were 0.71 (p < .01), 0.03, and −0.07. According to a least-squares analysis of variance, the dam strain effect in addition to the effect of the affected fetus weight on the maxillary size and the cranial size of the affected fetuses was significant (p < .01 for cranial size, p < .05 for maxillary size) and close to a significant level (p = .09) for the mandibular size of the affected fetuses. The adjusted maxillary size and cranial size after statistically eliminating the effects of the affected fetus weight, dam weight, and lifter size on each original craniofacial size of the affected fetuses that had developed in the CL/Er dam strain were also significantly smaller than those of the affected fetuses that had developed in the C57BL dam strain. Conclusions: The present results indicate that the craniofacial growth of the CL/Fr mouse fetus affected with CLP increased in proportion to the fetus weight. The dam strain effect, in addition to the effect of the affected fetus weight, could thus not be ignored when the etiology of the spontaneous CLP was examined, while the uterine environment, provided by the CL/Fr strain dam, retarded the intra-uterine craniofacial growth of the affected fetuses. It was therefore concluded that the dam strain effect, as well as the effect of the affected fetus weight, both play an important role on the craniofacial morphogenesis of the CL/Fr strain of the affected fetuses that developed in both strain dams.


2021 ◽  
Author(s):  
Federica Landi ◽  
James Barraclough ◽  
Andrej Evteev ◽  
Anatoliy Anikin ◽  
Leonid Satanin ◽  
...  

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1489-1506
Author(s):  
Kathleen D Jermstad ◽  
Daniel L Bassoni ◽  
Keith S Jech ◽  
Gary A Ritchie ◽  
Nicholas C Wheeler ◽  
...  

Abstract Quantitative trait loci (QTL) were mapped in the woody perennial Douglas fir (Pseudotsuga menziesii var. menziesii [Mirb.] Franco) for complex traits controlling the timing of growth initiation and growth cessation. QTL were estimated under controlled environmental conditions to identify QTL interactions with photoperiod, moisture stress, winter chilling, and spring temperatures. A three-generation mapping population of 460 cloned progeny was used for genetic mapping and phenotypic evaluations. An all-marker interval mapping method was used for scanning the genome for the presence of QTL and single-factor ANOVA was used for estimating QTL-by-environment interactions. A modest number of QTL were detected per trait, with individual QTL explaining up to 9.5% of the phenotypic variation. Two QTL-by-treatment interactions were found for growth initiation, whereas several QTL-by-treatment interactions were detected among growth cessation traits. This is the first report of QTL interactions with specific environmental signals in forest trees and will assist in the identification of candidate genes controlling these important adaptive traits in perennial plants.


1995 ◽  
Vol 6 (3) ◽  
pp. 184-189 ◽  
Author(s):  
Steven R. Cohen ◽  
Michael L. Corrigan ◽  
Fred L. Bookstein ◽  
Carroll-Ann Trotman ◽  
Alphonse Burdi ◽  
...  

1989 ◽  
Vol 9 (10) ◽  
pp. 4196-4203
Author(s):  
A J Fornace ◽  
D W Nebert ◽  
M C Hollander ◽  
J D Luethy ◽  
M Papathanasiou ◽  
...  

More than 20 different cDNA clones encoding DNA-damage-inducible transcripts in rodent cells have recently been isolated by hybridization subtraction (A. J. Fornace, Jr., I. Alamo, Jr., and M. C. Hollander, Proc. Natl. Acad. Sci. USA 85:8800-8804, 1988). In most cells, one effect of DNA damage is the transient inhibition of DNA synthesis and cell growth. We now show that five of our clones encode transcripts that are increased by other growth cessation signals: growth arrest by serum reduction, medium depletion, contact inhibition, or a 24-h exposure to hydroxyurea. The genes coding for these transcripts have been designated gadd (growth arrest and DNA damage inducible). Two of the gadd cDNA clones were found to hybridize at high stringency to transcripts from human cells that were induced after growth cessation signals or treatment with DNA-damaging agents, which indicates that these responses have been conserved during mammalian evolution. In contrast to results with growth-arrested cells that still had the capacity to grow after removal of the growth arrest conditions, no induction occurred in HL60 cells when growth arrest was produced by terminal differentiation, indicating that only certain kinds of growth cessation signals induce these genes. All of our experiments suggest that the gadd genes are coordinately regulated: the kinetics of induction for all five transcripts were similar; in addition, overexpression of gadd genes was found in homozygous deletion c14CoS/c14CoS mice that are missing a small portion of chromosome 7, suggesting that a trans-acting factor encoded by a gene in this deleted portion is a negative effector of the gadd genes. The gadd genes may represent part of a novel regulatory pathway involved in the negative control of mammalian cell growth.


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