In the U.S., helping the noncompliant child and parent child interaction therapy represent behavioral family therapy programs that are empirically supported for treating the conduct problems of 2-to 7-year old children. This study examined how caregivers in China would view behavioral family therapy. Caregivers in Hangzhou, China reported the perceived age of deviance for behavioral family therapy targets (e.g., noncompliance) and rated the acceptability of behavioral treatment components (e.g., timeout). Chinese caregivers agreed with EuropeanAmerican culture on considering noncompliance, aggression, tantrums, and negative talk deviant during the preschool period. Overall, Chinese caregivers considered all the following nine behavioral family therapy components acceptable: contingent praise, responsive play, ignoring deviant attention seeking, authoritative instruction-giving, warnings, chair timeouts, ignoring tantrums during timeout, room backups for chair timeouts, and immediate timeouts for aggression. However, specific parental reservations were found regarding backup procedures for chair timeouts, particularly room backups. Possible treatment accommodations of behavioral family therapy for Chinese families are discussed.
Solid pseudopapillary tumors (SPTs) are a rare pancreatic neoplastic lesion. Familial aggregation has not been reported in this disease. The objectives of this study were to report the history, clinicopathological features, and gene mutations of 3 familial cases of SPT. Three female cases of SPT presented in 1 family. Eight family relatives, 5 healthy volunteers, and 8 patients with SPT acted as controls. Histological examination and immunohistochemistry were performed on the surgical tumor specimens. Polymerase chain reaction-single-strand conformation polymorphism and gene sequencing were performed on genomic DNA extracted from blood. All 3 patients underwent surgical treatment, 2 patients died (3 months and 5 months after surgery), whereas neither recurrence nor metastasis was observed in the other patient during 2-year follow-up. The tumors from the 3 cases had identical immunoreactivity to a series of molecular markers. A Leu104Val mutation of protease serine 1 (PRSS1) was observed in the familial patients and 2 healthy male family members; no β-catenin or adenomatous polyposis coli mutations were detected in the familial cases. This study indicates the possibility of genetic involvement in the pathogenesis of SPT. Family history may be a positive predictive factor for malignancy in SPT.
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