No abstract

The aims of this investigation were to cephalometrically study the short-term skeletal and dental modifications induced by rapid palatal expansion in a sample of 20 patients (10 male, 10 female), aged 6-10 years (mean age 8 years) in mixed dentition with a uni- or bilateral posterior crossbite, a mild skeletal Class II malocclusion, and an increased vertical dimension (FMA, SN/\GoGn), and to compare them with an untreated matched control group of 20 subjects (10 male and 10 female), mean age 8 years. Cephalometric analysis showed that the maxilla displayed a tendency to rotate downwards and backward, resulting in a statistically significant increase of the SN/\PP angle (T0 = 9*95 degrees, T1 = 11*60 degrees, P < 0*01) and the SN-ANS linear value (T0 = 49*50 mm, T1 = 51*10 mm, P < 0*05). In addition, there was a statistically significant alteration of the anterior total facial height N-Me (T0 = 113*15mm, T1 = 114*15 mm, P < 0*05) and for the dental upper molar measurement U6-PP (T0 = 19*70 mm, T1 = 20*30 mm, P < 0*05). The small alterations found in the anterior total facial height and in the sagittal angles agree with previous studies, and suggest that RPE can be also used in subjects with a tendency to vertical growth and a skeletal Class II malocclusion.

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The Beckwith-Wiedemann syndrome (BWS) is a rare genetic disorder, linked to an alteration on the short arm of chromosome 11 that comprises multiple congenital anomalies. Macroglossia is the predominant finding, with subsequent protrusion of dentoalveolar structures, which results in a protruding mandible, anterior open bite, abnormally obtuse gonial angle and increased mandibular length. A less-invasive treatment with orthopaedic appliances in a patient with early tongue reduction is presented. This work summarizes the oral signs linked to macroglossia, and highlights the influence of macroglossia on mandibular growth structures. In our opinion, glossotomy could be carried out in the paediatric patient as a preventive measure in that it curbs the tongue's influence on skeletal growth and dramatically reduces the duration and extensiveness of subsequent treatment.

Background and aims-Recent studies have shown that the age-specific seroprevalence of H pylori infection parallels hepatitis A (HAV), suggesting similar modes of transmission. The aim of this study was to investigate the seroepidemiology of H pylori and HAV in the same setting. Patients-A sample of 705 resident subjects (273 men, age range 1-87 years, median 50) who attended the outpatient medical centre of the rural town of Cirò, Southern Italy (11 000 inhabitants) for blood testing were recruited. Methods-All subjects completed a structured questionnaire. A serum sample was drawn from each subject and assayed for H pylori IgG by a validated in house enzyme linked immunosorbent assay. Antibodies to HAV were determined in 466 subjects (163 men, age range 1-87 years, median 49). A measure of agreement between H pylori and HAV seropositivity, the statistic, was used. Results-Overall, 446 (63%) subjects were seropositive for H pylori. Of the 466 subjects screened for both H pylori and HAV, 291 (62%) were seropositive for H pylori and 407 (87%) for HAV. Crosstabulation of these data showed that 275 (59%) were seropositive and 43 (9%) seronegative for both H pylori and HAV, 16 (3%) were seropositive for H pylori, and 132 (28%) were seropositive for HAV (OR = 5.6, CI 3 to 10). There was a parallel, weakly correlated (r = 0.287) rise in the seroprevalence of the two infections with increasing age. However, the agreement between H pylori and HAV seropositivity was little better than chance ( = 0.21) and in those aged less than 20 years it was worse than chance ( = -0.064). Furthermore, multiple logistic regression analysis did not show any risk factor shared by both infections. Conclusions-The correlation between H pylori and HAV reflects the age-specific seroprevalence of both infections rather than a true association. This study provides evidence against a common mode of transmission of H pylori and HAV.

The aim of this article is to show the use of the Balters' Bionator in pseudo-Class III treatment. The importance of differentiating between true Class III and pseudo-Class III is emphasized. The therapeutic results of a Balters' Bionator appliance are presented in three case reports of subjects in the mixed dentition. In this stage of development it is possible to correct an isolated problem. The use of the Bionator III in this kind of malocclusion enabled the correction of a dental malocclusion in a few months and therapeutic stability of a mesially-positioned mandible encouraging favourable skeletal growth.

Ultrasonographic fetal measurements from 293 singleton pregnancies were obtained within 7 days of delivery. Biparietal diameter, abdominal circumference, femur length, and actual birth weight data of the first 93 fetuses in the study were used as variables to determine the best mathematical model for relating estimated fetal weight to biparietal diameter, abdominal circumference, and femur length. With the aid of a computer, three regression equations were derived. R eliable estimation of fetal weight is important in the management of many problems in pregnancy. Numerous sonographic formulas exist for the estimation of the fetal weight. These have been applied in clinical settings, and experience has confirmed their general usefulness. However, difficulty has been encountered in two subgrol}ps: the SGA fetus 1 .2 and the unusually large fetus.3-~ The best estimates of fetal weight traditionally have been obtained with the equation of Shepard and coworkers, which relies on AC and BPD measurements, 4 and with the equations of Hadlock and colleagues, which relies on AC with or without FL, HC, and BPO.J6

SHOC2 is a scaffold protein mediating RAS‐promoted activation of mitogen‐activated protein kinase (MAPK) signaling in response to extracellular stimuli. A recurrent activating mutation in SHOC2 (p.Ser2Gly) causes Mazzanti syndrome, a RASopathy characterized by features resembling Noonan syndrome and distinctive ectodermal abnormalities. A second mutation (p.Met173Ile) supposed to cause loss‐of‐function was more recently identified in two individuals with milder phenotypes. Here, we report on the third RASopathy‐causing SHOC2 mutation (c.807_808delinsTT, p.Gln269_His270delinsHisTyr), which was found associated with prenatal‐onset hypertrophic cardiomyopathy. Structural analyses indicated a possible impact of the mutation on the relative orientation of the two SHOC2's leucine‐rich repeat domains. Functional studies provided evidence of its activating role, revealing enhanced binding of the mutant protein to MRAS and PPP1CB, and increased signaling through the MAPK cascade. Differing from SHOC2 S2G, SHOC2 Q269_H270delinsHY is not constitutively targeted to the plasma membrane. These data document that diverse mechanisms in SHOC2 functional dysregulation converge toward MAPK signaling upregulation.