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Brown planthopper, Nilaparvata lugens Stal., (BPH) was the most devastating insect pest on rice in many partS of Asia. The Outbreak of BPH? which is resistant to many synthetic insecticides can cause total rice crop loss. This research was done to evaluate the efficiency of mangostin from the pericarp of mangosteen fruit extract (Garcina mangostana L.) as the alternative control of BPH. The pericarp of mangosteen fruit was extracted by Soxhlet apparatus using ethanol as a solvent and purified by chromatography method then qualified structure by 2D-NMR, MS and IR. The crude extracts contained mangostin ca. 2.956% w/w. This extract was trailed by the topical sprayer method with 1st, 2nd, 3rd, 4th and 5th nymph and adult BPH shows toxicity in term of LC50 ca. 1.39, 2.26, 5.44, 4.49, 4.03 and 3.84 % w/v at 24 h exposure, respectively. The in vitro enzyme activity from BPH survived after 24 h exposure and showed to inhibit the carboxylesterase (CarE), acetylchoinesterase (AchE) and glutathione-S-transferase (GST) activities which the correction factors of CarE, AchE and GST indicated ca. 1.21-2.05 fold, 1.24-2.50 fold and 1.01-3.34 fold, respectively. Moreover, the data shows that the carboxylesterase may play an important role to detoxify this extract. The results suggested that pericarp of mangosteen fruit extract which have mangostin as active ingredient compound shows mechanism as the inhibitor of detoxification enzymes. Thus, it is likely to be uses this extract as an insecticide alternative to the control of BPH.

Insulin-like growth factor (IGF)-I is an important regulator of bone metabolism. Clinical observations suggest that different anatomic sites within the adult skeleton respond differently to hormonal and therapeutic treatment, and recent studies on bone marrow stromal cells in culture show that there are skeletal site-dependent differences in the gene expression of IGF-I. The actions of IGF-I and -II on bone cells are known to be modulated by the IGF binding proteins (IGFBP)-1 through -6 and the Type I and Type II IGF receptors. Therefore, we compared the expression of IGFBP-1 through -6 in adult female rat bone marrow stromal cell cultures derived from two separate skeletal sites: vertebrae and femurs. The cultures were maintained simultaneously under conditions that support osteoblast differentiation from osteoprogenitors present in the femoral and vertebral marrow cell populations. We also addressed whether IGFBP messenger RNA levels are regulated by thyroid hormone (T(3)) and dexamethasone (dex) treatment in femoral vs. vertebral marrow stromal cells in vitro, since steroid hormones play an important role in skeletal function. Northern blot analyses revealed that there are distinct skeletal site differences in the gene expression of IGFBPs. The vertebral marrow cultures express IGFBP-2 through -6 mRNAs, with IGFBP-2, IGFBP-4, and IGFBP-6 mRNAs predominating. The femoral marrow stromal cell cultures express only IGFBP-4 and IGFBP-6. Importantly, vertebral marrow cultures have much higher IGFBP mRNA steady-state levels than femoral cultures for all the detected IGFBP transcripts. IGFBP-1 is not detected in either femoral or vertebral cultures. In addition to a skeletal site difference, we show that T(3) and dex regulate the expression of specific IGFBP mRNAs. T(3) treatment also upregulates IGF-I protein secretion by vertebral marrow stromal cell cultures. Interestingly, the type I receptor for IGF-I was expressed equivalently in cultures from the two skeletal sites. These findings have important implications for the anatomical site specificities of hormonal responses that are noted in the skeleton., (Copyright 2001 Wiley-Liss, Inc.)

Thyroid hormones influence both bone formation and bone resorption. Clinical data and animal studies provide evidence of skeletal site heterogeneity (hip vs. spine) of bone responses to thyroid hormones. In vitro studies also demonstrate direct effects of thyroid hormones on cells of the osteoblast lineage. Transcriptional regulation by thyroid hormone is mediated by ligand-dependent transcription factors called thyroid hormone receptors (TRs). Two genes, c-ErbAalpha and c-ErbAbeta, generate at least four TR isoforms in the rat: TRalpha(1), c-erbAalpha(2), TRbeta(1), and TRbeta(2). Although functional TRs have been identified in cells of the osteoblast lineage, it is still not known if TR isoform expression in bone differs depending upon which skeletal site is examined. We have used ribonuclease protection assay and Northern blot analysis to simultaneously examine the expression of TR isoform mRNAs in adult rat femoral and vertebral bone. TRalpha(1), c-erbAalpha(2), and TRbeta(1) are expressed in both femur and vertebra whole bone. Bone marrow cells from both skeletal sites were also cultured under conditions whereby the osteoprogenitors differentiated into osteoblasts and formed a mineralized extracellular matrix. TRalpha(1), c-erbAalpha(2), and TRbeta(1) mRNAs are each expressed in both femoral and vertebral osteoblast cultures. The presence of TRalpha(1), c-erbAalpha(2), and beta(1) proteins was confirmed by Western analysis of nuclear protein extracts from femoral and vertebral cell cultures. These results indicate that the three predominant TR isoforms are highly expressed in bone and osteoblasts from femurs and vertebrae. Whether there are distinct mechanisms of thyroid hormone action mediated by TRalpha(1), c-erbAalpha(2), and TRbeta(1) at these separate skeletal sites remain to be shown., (Copyright 1999 Wiley-Liss, Inc.)

Somatic gene therapies require targeted transfer of the therapeutic gene(s) into stem cells that proliferate and then differentiate and express the gene in a tissue-restricted manner. We have developed an approach for gene therapy using marrow cells that takes advantage of the osteoblast specificity of the osteocalcin promoter to confine expression of chimeric genes to bone. Adherent marrow cells, carrying a reporter gene [chloramphenicol acetyltransferase (CAT)] under the control of a 1.7-kilobase rat osteocalcin gene promoter, were expanded ex vivo. After transplantation by intravenous infusion, engrafted donor cells in recipient mice were detected by the presence of the transgene in a broad spectrum of tissues. However, expression of the transgene was restricted to osteoblasts and osteocytes, as established by biochemical analysis of CAT activity and immunohistochemical analysis of CAT expression at the single cell level. Our data indicate that donor cells achieved long-term engraftment in various tissues of the recipients and that the CAT gene under control of the osteocalcin promoter is expressed specifically in bone. Thus, transplantation of multipotential marrow cells containing the osteocalcin promoter-controlled transgene provides an efficacious approach to deliver therapeutic gene expression to osteoblasts for treatment of bone disorders or tumor metastasis to the skeleton.

Osteoblast-like cell cultures have been established from the marrow of adult rat vertebrae. We have simultaneously examined the response to dexamethasone (dex) treatment in cultures of young adult female vertebral and femoral marrow cells. Alkaline phosphatase (AP) activity was analyzed as well as the expression of mRNAs for osteocalcin (OC) and insulin-like growth factor I (IGF-I). The vertebral and femoral marrow cells were maintained for 7 days in primary culture with or without 10(-8) M dex and then 6 days in secondary culture without dex or with 10(-8) M or 10(-7) M dex. All cells were examined on day 6 of secondary culture. Vertebral and femoral cultures each expressed the highest AP enzyme levels when grown with dex in primary culture (10(-8) M) and secondary culture (10(-7) M). Under all experimental conditions, vertebral cultures had lower AP enzyme activity than femoral cultures. When dex was omitted from secondary culture, OC gene expression was not detected in either vertebral or femoral passaged cells even if dex was present in primary culture. For dex conditions where OC was expressed, vertebral cultures had higher OC mRNA steady-state levels than femoral cultures. IGF-I gene expression was detected by Northern analysis in both vertebral and femoral secondary cultures. However, vertebral marrow cultures had much higher IGF-I mRNA levels compared to femoral cultures whether or not dex was present in primary culture. These findings demonstrate that dex supports the differentiation of both vertebral and femoral adult marrow osteogenic cells into osteoblasts. Our results support the hypothesis that osteoblastic marrow cultures differ depending upon which location in the skeleton they are from and that there are skeletal site-dependent differences in the insulin-like growth factor system components.

Thyroid hormones (T3 and T4) regulate bone development, growth, and turnover. Studies have suggested that different skeletal sites respond differently to thyroid hormones. Therefore, we examined the in vitro T3 responsiveness of cells committed to the osteoblast lineage as a function of skeletal location. Bone marrow cells derived from female rat femurs and vertebrae were cultured using conditions that induce osteogenic differentiation. Cells from both sites formed mineralized bone nodules in primary and secondary culture. In femoral cultures, collagen type I (coll I) and osteocalcin (OC) messenger RNA (mRNA) levels increased from the earliest time point examined (day 3) to a maximum on day 12 and thereafter declined to undetectable levels. T3 increased both OC and coll I mRNA, resulting in a continuous expression throughout the culture period. Insulin-like growth factor I (IGF-I) gene expression was detected at very low levels by Northern analysis of femoral total RNA, and T3 only marginally enhanced IGF-I mRNA levels. In vertebral cultures, OC and coll I mRNA levels also increased with time in culture, but remained expressed throughout the culture period. OC and coll I mRNA levels were not markedly altered in response to T3. In contrast to femoral cells, IGF-I gene expression was easily visualized in Northern blots from untreated vertebral cultures and was markedly increased by the addition of T3. The continuous presence of T3 (10(-7) M) in the medium for 18 days caused a marked decrease in the number of alkaline phosphatase-positive colonies formed in femoral secondary cultures, but only a slight decrease in the number in vertebral cultures. In addition, short term (6 days) exposure to T3 (10(-7) M) at the beginning of the culture period decreased alkaline phosphatase activity in femoral cultures, but not in vertebral cultures. These findings indicate that there are skeletal site-dependent differences in the in vitro responses of cells of the osteoblastic lineage to thyroid hormone.

The antenatal diagnosis of a thoracic neurenteric cyst with vertebral abnormality during routine ultrasound is described here. The diagnosis was made at 34 weeks gestation but with hindsight, the abnormality was visible on the 18-week scan. To the knowledge of the authors, this is the first recorded instance of the antenatal demonstration of a neurenteric cyst with a vertebral anomaly. With modern high-resolution machines it is possible to detect the abnormality at as early as 18 weeks gestation. As a result of early diagnosis, the mother could be counselled and both the mother and the obstetrician could be better prepared to manage the pregnancy and take early remedial action before the onset of complications, to obtain the best possible outcome for all concerned.

The saddle nose resembles a saddle, i.e., with a concave, often flattened dorsum and an apparent cephalic rotation of the nasal tip. The concavity may be present in the osseous or cartilaginous dorsum, or both. The saddle nose deformity can be divided into congenital, postinfection, postsurgical, and traumatic types. Congenital saddle nose deformity is rare, often accompanying midfacial deficiency malformation syndromes. The advent of antimicrobial therapy has helped restrict the incidence of syphilitic or leprotic saddle nose to the nonindustrialized nations. Postsurgical saddle nose deformity occurs most often as a result of the overzealous septorhinoplasty. The most common type of saddle nose deformity may be traumatic. The authors use Kazanjian and Converse's characterization of the true saddle nose as one in which the bony and/or cartilaginous portions are depressed and the projection of the nose is generally preserved. This article describes the saddle nose deformity and its etiology and proposes a management technique with minimal complications.

The gene (hprt) coding for mouse HPRT (hypoxanthine phosphoribosyltransferase) is transcribed from a promoter lacking CAAT and TATAA boxes. It is expressed ubiquitously, albeit at different levels, in all tissues and cultured cells. During investigations to characterise hprt transcription control elements required in embryonic stem (ES) cells and to develop compact hprt minigenes for gene-targeting strategies, we discovered a requirement for intron-1 sequences for expression in ES cells. The essential intron-1 element, which is 420 bp long, is located 230 bp downstream from the transcription start point and is shown to increase transcription from the hprt promoter in a position- and orientation-dependent manner. We propose that this element is an integral downstream part of the hprt promoter.