[Effects of rootstocks on the growth and berry quality of Vitis vinifera cv. Cabernet Sauvignon grapevine in Changli zone, Hebei Province, China].

Cabernet Sauvignon grafted onto seven rootstocks 188-08, 5BB, SO4, 3309C, 110R, 5C and 101-14M, with the own-rooted vines as control, were investigated to study the effects of different rootstocks on the growth, fruit quality and yield of Cabernet Sauvignon in Changli zone, Hebei Province, China. The results showed that Cabernet Sauvignon grafted on 5BB and 5C significantly increased the trunk diameter, and 5C significantly increased one-year-old shoot diameter. 188-08, 5BB and 5C as rootstock obviously improved berry soluble solid content, in addition 188- 08 and 5BB significantly increased berry reducing sugar content. The vines on 101-14M and 3309C significantly decreased berry titratable acid content. The rootstock 5C and 101-14M significantly raised grape skin phenol and anthocyanin contents, and rootstock 101-14M significantly increased tannin content in grape skin. Cabernet Sauvignon grafted onto 3309C, 110R, 5C and 101-14M obviously got higher yield per vine than own-rooted vines. Growing parameter, grape quality index and yield per vine grafted on seven rootstocks and own-rooted vine were synthetically evaluated by fuzzy evaluation method, and the synthetical effects of vine grafted on seven rootstocks were better than own-rooted vine, with the order of scores from high to low as 5C, 101-14M, 3309C, 5BB, 188-08, 110R and SO4 under Changli unique climate and environment conditions.

[Studies on keratocystic odontogenic tumors].

Keratocystic odontogenic tumors (KCOTs, previously known as odontogenic keratocysts) are aggressive, noninflammatory jaw lesions with a putative high growth potential and a propensity for recurrence. This article puts together a summary of the serial studies related to KCOTs undertaken by the author's research group in recent years. Intraosseous jaw cysts with a solely orthokeratinized lining epithelium have been suggested to differ from the typical KCOTs. We report 20 cases of such cyst type under the term of 'orthokeratinized odontogenic cyst (OOC)'. Apart from the presence of a keratinizing epithelial lining, the OOC lacks the other histological features of KCOT, exhibits little if any tendency to recur, has no apparent association with NBCCS, may be cured by simple enucleation, and may thus constitute its own clinical entity. Mutations in PTCH1 gene are responsible for NBCCS and are related in tumors associated with this syndrome. We have so far detected 26 PTCH1 mutations (2 mutations occurred twice) in 10 out of 34 (29.4%) sporadic and 14 out of 16 (87.5%) NBCCS-associated KCOTs. The 26 mutations consisted of 10 frameshift, 2 nonsense, 3 aberrant splicing, 4 in-frame insertion/deletion/ duplication and 7 missense mutations. Two missense mutations in PTCH2 were also detected in 2 out of 15 NBCCS related KCOT patients. By contrast, no pathogenic mutation was detected in SMO. Thus, our data, together with reports from other groups, indicate that defects of PTCH1 are involved in the pathogenesis of syndromic as well as sporadic KCOTs. The pathogenic role of PTCH2 requires further investigation. A series of in vitro studies on bone resorption of KCOTs and ameloblastomas were undertaken by this group. The results indicate that odontogenic lesions could promote bone resorption in vitro and it is likely to be related to some of the cytokines secreted by the lesions.

[PTCH gene mutations in odontogenic keratocysts].

OBJECTIVE: To investigate the frequency, type and distribution of PTCH mutations in odontogenic keratocysts (OKC) and to analyze the molecular pathological relationship between sporadic OKC and OKC associated with nevoid basal cell carcinoma syndrome (NBCCS). METHODS: Genomic DNA was extracted from 8 cases of OKC lesions (4 sporadic OKCs and 4 NBCCS-related OKCs). PTCH gene mutations were detected by PCR-direct sequencing. RESULTS: Six novel PTCH mutations were identified in 6 out of 8 cases (2 sporadic and 4 NBCCS-related OKCs). Two of these were missense mutations leading to substitution of an amino acid residue respectively. The other 4 mutations were identified as insertion or deletion ranging from one single base to 7 bases, three of which caused frame-shift leading to premature truncation of PTCH protein and one resulted in an insertion of 2 amino acid residues. All these identified mutations were novel and have not been previously described. CONCLUSIONS: PTCH gene mutation is a common event in NBCCS-related OKCs and could also be detected in some sporadic OKCs. Abnormalities of PTCH gene may be involved in the pathogenesis of OKC.