Biomedical subjects

D Li

Publications and source records attributed to D Li.

At least 487 records · Page 27Linked to original sources

PubMed1998

The elucidation of the structure of thalicoside F, A. minor oleanane glycoside from Thalictrum minus L.

A new triterpenoid saponin, thalicoside F was isolated from the above-ground part of Thalictrum minus L. (Ranunculaceae family) collected in Eastern Siberia (Russia). The structure of thalicoside F was elucidated by a combination of 1D- and 2D-NMR spectroscopy and mass spectroscopy, and was determined to be C47H74O17{3-beta-O-[alpha-L-rhamnopyranosyl-(1-->2)-beta-D- glucopyranosyl-(1-->4)-alpha-L-arabinopyranosyl]-11 alpha, 12 alpha-epoxyoleanane-28,13 beta-olide}.

Carbohydrate Sequence↗

PubMed1998

A rational strategy for enhancing the affinity of vancomycin towards depsipeptide ligands.

Glycopeptide antibiotics with enhanced affinity for model depsipeptide ligands may also exhibit enhanced efficacy against bacteria exhibiting the vanA resistance phenotype. To design modified agents with enhanced affinity for these ligands, and better understand why traditional agents have low affinity for depsipeptide ligands, free energy perturbation studies were performed on vancomycin derivatives by means of molecular dynamics simulation. The results suggest that modifications of the asparagine side chain on residue 3 of the antibiotic which enhance its hydrophobicity will enhance the affinity of glycopeptide antibiotics for depsipeptide ligands, and act synergistically with other modifications that enhance the efficacy of these agents against vanA-positive bacteria.

Alanine↗

PubMed1998

Endogenous insulin-like growth factor-I is obligatory for stimulation of rat inhibin alpha-subunit expression by follicle-stimulating hormone.

Insulin-like growth factor-I (IGF-I) is essential for FSH-dependent steroidogenesis by rat granulosa cells (GC), but whether IGF-I is required for other FSH-dependent functions is unknown. To investigate the role of IGF-I in the mechanisms of FSH-stimulated inhibin alpha-subunit (Inh-alpha) production, rat GC were cultured with FSH, IGF-I, insulin-like growth factor-binding protein (IGFBP)-4, IGFBP-5, and/or anti-IGF-I antibody. Inh-alpha protein and mRNA levels were measured in conditioned medium and cells by Western immunoblotting and Northern analysis, respectively. Inh-alpha expression was increased by FSH (3.5-fold) and IGF-I (2.5-fold), and the effects were dose and time dependent. FSH stimulation of Inh-alpha was attenuated by IGFBP-4 or -5 in a dose-dependent fashion, and the effects were reversed by IGF-I. Anti-IGF-I antibody mimicked the inhibitory effects of IGFBP-4 and -5. Forskolin, cholera toxin, and 8-bromo-cAMP increased Inh-alpha production approximately 3.5-fold, and the effects were blocked by IGFBP-4 or -5. Increases in Inh-alpha by FSH, IGF-I, forskolin, cholera toxin, and 8-bromo-cAMP were totally blocked by the protein tyrosine kinase inhibitor, tyrphostin A23. In summary, these results suggest that the stimulation of Inh-alpha expression by FSH requires activation of protein tyrosine kinases by endogenously produced IGF-I. We propose that the IGF-I signaling is obligatory for FSH stimulation of Inh-alpha expression in rat GC.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1998

Activin-induced inhibin alpha-subunit production by rat granulosa cells requires endogenous insulin-like growth factor-I.

Inhibin-alpha subunit (Inh-alpha) gene expression is important for granulosa cell (GC) differentiation and prevention of ovarian tumorigenesis. Studies on Inh-alpha regulation have implicated activin and insulin-like growth factor-I (IGF-I) in the mechanisms of expression. Here we present evidence that endogenously produced IGF-I plays an obligatory role in activin-induced Inh-alpha production. Primary cultures of rat GC were incubated with increasing concentrations of various regulatory molecules, and the levels of Inh-alpha protein and its mRNA were measured in conditioned medium and cells, respectively. Recombinant activin A stimulated Inh-alpha expression, and the effects were dose- and time-dependent. The receptor tyrosine kinase inhibitor tyrphostin A23 caused a dose-dependent inhibition of activin-dependent Inh-alpha expression, whereas the inactive isomer, A63, had no effect. The stimulatory effect of activin was also blocked in a dose-dependent manner by added IGF binding protein-4 or -5, and the effects were reversed by IGF-I. Moreover, increasing concentrations of an anti-IGF-I antibody had a similar inhibitory effect on activin-stimulated Inh-alpha expression. Collectively, these results suggest, for the first time, that endogenously produced IGF-I is required for activin stimulation of Inh-alpha expression in cultured rat GC.

Activins↗

PubMed1998

Contrast-enhanced magnetic resonance imaging of the coronary arteries. A review.

The advent and continued improvement of T1-shortening contrast media have revolutionized magnetic resonance angiography (MRA) of the entire body in recent years. The technical basis for contrast-enhanced MRA is fast three-dimensional (3D) imaging. A brief historic review of the technical advances in MR coronary artery imaging clearly points to the importance of improved gradient capabilities that led to the development and wide application of fast 3D imaging. The use of contrast agents in coronary artery imaging has been expected for many years, given its success in other parts of the body. Nevertheless, because of the potential difficulties and unique characteristics of fast 3D imaging in the heart, the utility of contrast agents in coronary artery imaging has been systematically investigated only in the last 2 years. Initial experience from our group and others showed that contrast agents have great potential in pushing MR coronary artery imaging to a much higher level in terms of speed and signal-to-noise ratio (SNR), and intravascular agents are more desirable than extracellular agents. Nevertheless, because of the technical challenges and the diversity of methods used for coronary artery imaging, much more effort is needed to continue to improve the imaging techniques and further to define the roles of contrast agents in coronary artery imaging.

Animals↗

PubMed1998

Induction of Ca2+-calmodulin signaling by hard-surface contact primes Colletotrichum gloeosporioides conidia to germinate and form appressoria.

Hard-surface contact primes the conidia of Colletotrichum gloeosporioides to respond to plant surface waxes and a fruit-ripening hormone, ethylene, to germinate and form the appressoria required for infection of the host. Our efforts to elucidate the molecular events in the early phase of the hard-surface contact found that EGTA (5 mM) and U73122 (16 nM), an inhibitor of phospholipase C, inhibited (50%) germination and appressorium formation. Measurements of calmodulin (CaM) transcripts with a CaM cDNA we cloned from C. gloeosporioides showed that CaM was induced by hard-surface contact maximally at 2 h and then declined; ethephon enhanced this induction. The CaM antagonist, compound 48/80, completely inhibited conidial germination and appressorium formation at a concentration of 3 microM, implying that CaM is involved in this process. A putative CaM kinase (CaMK) cDNA of C. gloeosporioides was cloned with transcripts from hard-surface-treated conidia. A selective inhibitor of CaMK, KN93 (20 microM), inhibited (50%) germination and appressorium formation, blocked melanization, and caused the formation of abnormal appressoria. Scytalone, an intermediate in melanin synthesis, reversed the inhibition of melanization but did not restore appressorium formation. The phosphorylation of 18- and 43-kDa proteins induced by hard-surface contact and ethephon was inhibited by the treatment with KN93. These results strongly suggest that hard-surface contact induces Ca2+-calmodulin signaling that primes the conidia to respond to host signals by germination and differentiation into appressoria.

Amino Acid Sequence↗

PubMed1998

Perception of foreign cigarettes and their advertising in China: a study of college students from 12 universities.

OBJECTIVE: To examine how deeply foreign cigarette advertising had penetrated the Chinese market when a new ban on cigarette advertising was enacted in February 1995. DESIGN: A survey using self-completion questionnaires administered in college classrooms from November 1994 to March 1995. SETTINGS: Eight universities and four medical schools in three Chinese cities: Beijing, Wenzhou, and Hangzhou. SUBJECTS: 1896 college students who agreed to complete a written questionnaire. The mean age was 21.2 years; 39.5% of respondents were female. RESULTS: Four of the top eight cigarette brands most familiar to the respondents were foreign: Marlboro, 555, Kent, and Hilton. Advertisements for the foreign brands were much more likely to be seen than those for the domestic brands; those for Marlboro were reported most often (29.7%), followed by 555 (21.8%) and Kent (18.1%). Among smokers, Marlboro was the most preferred foreign brand, by 44.2%. The preference for Marlboro was also correlated with smokers having seen its advertisements. Most respondents, 71.8%, believed that cigarette advertising should be banned. CONCLUSIONS: The previous restrictions on cigarette advertising in China failed to prevent a large portion of the population from seeing and understanding the advertisements. Before the 1995 advertising ban took effect, strict limitations on imports of foreign cigarettes notwithstanding, certain highly advertised brands such as Marlboro achieved wide recognition and even consumer preference. Stricter restrictions are suggested as previous ones have failed to achieve their intended effects.

Adolescent↗

PubMed1998

Ox-LDL induces apoptosis in human coronary artery endothelial cells: role of PKC, PTK, bcl-2, and Fas.

Oxidized low-density lipoprotein (ox-LDL) plays a critical role in the development of atherosclerosis. Recent studies show that ox-LDL may induce apoptosis of cultured rabbit smooth muscle cells and human macrophages. This study was designed to determine the modulation by ox-LDL of apoptosis in cultured human coronary arterial endothelial cells (HCAEC) during hypoxia-reoxygenation and to determine underlying mechanisms. When HCAEC were approximately 85% confluent, the cells were exposed to hypoxia (24 h)-reoxygenation (3 h), native LDL, or ox-LDL. Fragmented DNA end-labeling, DNA laddering, and light and electron microscopy were used to determine changes characteristic of apoptosis. Ox-LDL (20 microg/ml) increased apoptosis during hypoxia-reoxygenation compared with hypoxia-reoxygenation alone (P < 0.05). Low concentrations of ox-LDL (5 microg/ml) and native LDL (20 microg/ml) under identical conditions had no effect on the degree of apoptosis. Ox-LDL markedly decreased endogenous superoxide dismutase activity and increased lipid peroxidation in HCAEC. The presence of ox-LDL, but not native LDL, in cultured HCAEC resulted in the activation of protein kinase C (PKC) and protein tyrosine kinase (PTK). The specific PKC and PTK inhibitors significantly reduced ox-LDL-mediated apoptosis of HCAEC (P < 0.05). Hypoxia-reoxygenation significantly increased Fas expression and decreased bcl-2 expression in HCAEC lysate as determined by Western analysis. Ox-LDL further increased Fas expression and decreased bcl-2 expression. These data indicate that ox-LDL enhances hypoxia-reoxygenation-mediated apoptosis in HCAEC. Ox-LDL-mediated apoptosis of HCAEC appears to involve activation of PKC and PTK. In addition, ox-LDL modulates Fas and bcl-2 protein expression in HCAEC. This study also suggests that ox-LDL is more important than native LDL in hypoxia-reoxygenation-induced apoptosis.

Animals↗

PubMed1998

Effects of okadaic acid, calyculin A, and PDBu on state of phosphorylation of rat renal Na+-K+-ATPase.

Several indirect lines of evidence suggest that protein kinases and phosphatases modulate the activity of renal Na+-K+-ATPase. The aim of this study was to examine whether such regulation may occur via modulation of the state of phosphorylation of Na+-K+-ATPase. Slices from rat renal cortex were prelabeled with [32P]orthophosphate and incubated with the inhibitors of protein phosphatase (PP)-1 and PP-2A, okadaic acid (OA) and calyculin A (CL-A), respectively, the protein kinase C (PKC) activator, phorbol 12,13-dibutyrate (PDBu), or the PP-2B inhibitor, FK-506. Phosphorylation of Na+-K+-ATPase alpha-subunit was evaluated by measuring the amount of [32P]phosphate incorporation into the immunoprecipitated protein. Incubation with either OA, CL-A, or PDBu caused four- to fivefold increases in the amount of [32P]phosphate incorporation into immunoprecipitated Na+-K+-ATPase alpha-subunit. OA and PDBu had a synergistic effect on the state of phosphorylation of Na+-K+-ATPase alpha-subunit. FK-506 did not affect Na+-K+-ATPase phosphorylation, neither alone nor in the presence of PDBu. Each of the drugs, OA, CL-A, and PDBu, inhibited the activity of Na+-K+-ATPase in microdissected proximal tubules. PDBu potentiated OA-induced inhibition of Na+-K+-ATPase activity. Inhibition of Na+-K+-ATPase required a lower dose of CL-A than of OA. On the basis of the inhibitory constant values of CL-A and OA for PP-1 and PP-2A, it is concluded that the tubular effect is mainly due to inhibition of PP-1. The PP-1 activity in rat renal cortex was approximately 1.5 nmol Pi. mg protein-1. min-1. Using a monoclonal anti-alpha antibody that fails to recognize the subunit when Ser23 is phosphorylated by PKC, we demonstrated that the dose response of PDBu inhibition of Na+-K+-ATPase correlated with the dose response of phosphorylation of the enzyme. The results suggest that the state of phosphorylation and activity of proximal tubular Na+-K+-ATPase are determined by the balance between the activities of protein kinases and phosphatases.

Animals↗

PubMed1998

Myocardial angiotensin II receptor expression and ischemia-reperfusion injury.

The renin-angiotensin system plays an important role in myocardial ischemia-reperfusion injury. Angiotensin II (Ang II) contributes to the evolution of ischemic coronary events through its hemodynamic, hemostatic and mitogenic effects. Angiotensin-converting enzyme (ACE) inhibitors and Ang II receptor antagonists have been shown to be cardioprotective in experimental animal models, with ischemia-reperfusion injury and in patients with congestive heart failure. Ang II receptors include at least two different subtypes, AT1 and AT2. Both AT1 and AT2 are expressed in the rat heart. Myocardial AT1 receptor density increases in association with ACE expression, and AT1 receptor activation is related to collagen formation following myocardial infarction in rats. Studies from the authors' laboratory have shown significant myocardial dysfunction in association with a concurrent increase in AT1 receptor expression in the rat myocardium immediately following a brief period of ischemia and reperfusion. Application of antisense oligodeoxynucleotides (AS-ODN) directed at AT1 receptor messenger RNA and AT1 receptor antagonist, losartan, significantly attenuates myocardial dysfunction induced by ischemia-reperfusion in the isolated rat heart. These observations suggest that myocardial AT1 receptor expression is involved in myocardial dysfunction following ischemia-reperfusion. Unlike losartan, which upregulates the plasma Ang II level, administration of AS-ODN does not affect plasma Ang II level. Although the reason for this is not clear, the difference in plasma Ang II levels implies that AS-ODN may be, at least theoretically, more beneficial than losartan in limiting ischemia-reperfusion-induced cardiac dysfunction. Apoptosis, or programmed cell death, also contributes to the outcome of myocardial ischemia-reperfusion injury. Recent studies from the authors' laboratory have demonstrated that Ang II induces apoptosis in cultured human coronary artery endothelial cells via activation of AT1 receptors and this can be blocked by losartan. These observations collectively underscore the importance of myocardial AT1 receptor expression in ischemia-reperfusion injury.

Animals↗

PubMed1998

Serial sputum cell counts in the management of chronic airflow limitation.

This case study illustrates the usefulness of serial induced sputum cell counts from cytospins to investigate the nature of airway inflammation in a patient presumed to have prednisone-dependent asthma for 30 yrs. She had bronchiectasis and chronic airflow limitation. Exacerbations of breathlessness were associated with an increase in chronic airflow limitation with little or no sputum. Induced sputum showed elevated total cell and neutrophil counts at each exacerbation with no increase in the proportion of eosinophils. Pathogenic bacteria were cultured at each flare-up. The dose of prednisone was reduced progressively and each exacerbation was treated with an appropriate antibiotic without increasing the dose of prednisone, as was the case previously. The infections were associated with bronchiectasis of the right upper lobe which was removed. Examination of the specimen confirmed neutrophilic infiltration and did not show the usual airway structural changes of asthma. These results provide further evidence of the value of sputum cell counts in practice, in this case to prevent overtreatment with prednisone in a patient with recurrent deteriorations in airflow which were due to recurrent infections.

Asthma↗

PubMed1998

Developmental changes in galanin receptors in the quail oviduct and the effect of ovarian sex steroids on galanin receptor induction.

We have recently isolated an oviposition-inducing peptide from mature quail oviducts identified as avian galanin. This peptide evoked vigorous contractions of the uterine oviduct through binding to receptors located in the uterus. The questions arising from these findings are: what changes occur in galanin receptors in the uterus during maturation, and what is the hormonal factor(s) that induces uterine galanin receptors? Therefore, the present study examined changes in uterine galanin receptors with age and the effect of administration of ovarian sex steroids on galanin receptors in the quail. Immature females reared under long day (LD) photoperiods from 4 weeks of age demonstrated a progressive increase in specific galanin binding per both unit uterine weight and per whole uterus concurrent with uterine development during 4-13 weeks. Scatchard plot analyses of the binding to the uterine preparation showed that the equilibrium dissociation constant (Kd) was about 0.30-0.34 nM regardless of age, and the change in galanin binding during uterine development was due to a change in the number of binding sites. Plasma 17beta-estradiol and progesterone concentrations were almost constant between 4-6 weeks and tended to increase thereafter. Administration of 17beta-estradiol to immature females for 1 week increased not only uterine weight but also specific galanin binding per unit uterine weight, whereas progesterone increased only the binding per unit uterine weight. Both sex steroids also induced an increase in total binding per uterus. Combined administration of 17beta-estradiol and progesterone induced marked increases in the galanin binding, and the effect was not additive but, rather, was synergistic. Scatchard plot analysis showed that the number of binding sites, but not the Kd, was increased by steroid treatment. Administration of 17beta-estradiol or progesterone increased each circulating steroid level to that relatively similar to the maximal levels observed in females exposed to LD. Thus, ovarian sex steroids may contribute at least in part as hormonal factors to galanin receptor induction, which takes place in the uterine oviduct during development.

Age Factors↗

PubMed1998

The distribution and translocation of the G protein ADP-ribosylation factor 1 in live cells is determined by its GTPase activity.

ADP-ribosylation factors (ARF) are small G proteins that play key roles in vesicular transport processes. We have studied the distribution of ARF1 in live cells using chimeras of ARF1 mutants (wild type (wt) ARF1; Q71L-ARF1 (reduced GTPase); T31N (low affinity for GTP); and (Delta)Nwt (deletion of amino acids 2-18)) with green fluorescent protein (GFP). Confocal microscopy studies showed that the wt and Q71L proteins were localized in the Golgi and cytoplasm. The (Delta)Nwt and the T31N mutants were exclusively cytoplasmic. The behavior of the wt and Q71L proteins was studied in detail. About 15% of wt-ARF1-GFP was bound to the Golgi. Bound wt-ARF1-GFP dissociated rapidly after addition of Brefeldin A (BFA). This process did not appear to be a consequence of BFA-induced disappearance of the Golgi. Photobleaching recovery showed that essentially all the ARF-GFP was mobile, although it diffused very slowly. In contrast, about 40-50% of the Q71L mutant was found in the Golgi, and its rate of dissociation in the presence of BFA was slow and biphasic. Q71L-ARF1-GFP diffused more slowly than the wt. We conclude that ARF1 proteins exist in a dynamic equilibrium between Golgi-bound and cytosolic pools, and that the translocation of ARF in live cells requires the hydrolysis of GTP by the Golgi-bound protein.

ADP-Ribosylation Factor 1↗

PubMed1998

Detection of coronary stenoses on source and projection images using three-dimensional MR angiography with retrospective respiratory gating: preliminary experience.

OBJECTIVE: Our objective was to study the ability of three-dimensional MR angiography with retrospective respiratory gating to reveal stenoses in proximal coronary arteries on source and projection images. CONCLUSION: Proximal coronary artery stenoses can be identified using three-dimensional MR angiography with retrospective respiratory gating, both with projection images and on source images alone. Reasons for missed lesions included collateral vessels and retrograde flow distal to complete occlusion and volume averaging of vessels with adjacent structures. Causes of false-positive interpretations included small foci of decreased signal intensity distal to complete occlusion, partial volume effects on individual partitions, and regions of distal vessels leaving the imaging plane.

Aged↗

PubMed1998

[A study on the effectiveness of hepatitis B vaccine among the vaccinated population].

In order to identify the effect of hepatitis B vaccine in a vaccinated population, 5890 persons from 1890 families in 13 counties/cities in Henan province were chosen for investigation under multistage cluster systematic sampling. All subjects were bled for HBsAg, anti-HBs and anti-HBc by RIA. The positive rate of HBsAg was significantly lower in vaccinates than in that non-vaccinates. There was no protective effect in those who only vaccinated for one dose. It was preferable to receive vaccination before the age of two years. If 70% of hepatitis B vaccine coverage was reached among those younger than 5 years old, the positive rate of HBsAg could reduce to 1% or even lower. Results showed that it was important to ensure an earlier and full course vaccination with high coverage.

Adolescent↗

PubMed1998

Detection of p53 gene mutations in human leukemia by PCR-SSCP analysis and direct nucleotide sequencing.

OBJECTIVE: To look for mutations of the p53 gene in leukemic patients and study the relationship between abnormalities in p53 gene and leukemogenesis. METHODS: The peripheral blood and Bone Marrow Samples were collected from 36 patients with various leukemia types including 14 cases of lymphocytic leukemia [8 cases of acute lymphocytic leukemia (ALL), 4 cases of chronic lymphocytic leukemia (CLL), 2 cases of hairy cell leukemia (HCL)] and 22 cases of myelocytic leukemia [11 cases of acute nonlymphocytic leukemia (ANLL), 11 cases of chronic myelocytic leukemia (CML)]. DNA structures of exon 5-8 of the p53 gene were scanned by PCR-SSCP (single strand conformation polymorphism analysis of polymerase chain reaction products). The appropriate DNA fragments were amplified, Purified and sequenced directly. RESULTS: By PCR-SSCP analysis, shifts in electrophoretic mobility of the p53 gene were detected in 3 of 14 patients with lymphocytic leukemia (2 ALL and 1 CLL), but none in 22 patients with myelocytic leukemia including one in blastic crisis. Direct nucleotide sequencing in one patient with ALL showed transition of CTG to CAG at codon 257 of exon 7, resulting in a change of its encoded amino acids from aspartic acid to valine. To our knowledge, the mutation at this codon has not been previously reported hitherto. CONCLUSIONS: The p53 gene mutations are specifically associated with lymphocytic leukemia. Alternations of the p53 gene may play a certain role in leukemogenesis in some cases of lymphocytic leukemia.

Exons↗

PubMed1998

Pharmacokinetics of flutamide and its metabolite 2-hydroxyflutamide in normal and hepatic injury rats.

AIM: To develop a new HPLC assay to study the pharmacokinetics of flutamide (Flu) and its active metabolite 2-hydroxyflutamide (HF) in rats. METHODS: Normal or hepatic injury rats were given i.g. Flu 50 mg.kg-1. Reverse phase HPLC was developed with a mu-Bondapak C 18 column. Internal standard was methyltestosterone. The mobile phase was a mixture of methanol:acetonitrile:water:diethyl ether = 40:20:35:1 (vol). Absorbance was measured at lambda 234 nm. RESULTS: The pharmacokinetic parameters of Flu were as follows: in normal rats, K = 0.62 +/- 0.16 h-1, Cl = 6.0 +/- 1.0 L.kg-1.h-1, AUC = 8.6 +/- 1.3 mg.L-1.h, Cmax = 2.4 +/- 0.7 mg.L-1; in hepatic injury rats, K = 0.16 +/- 0.03 h-1, Cl = 0.63 +/- 0.29 L.kg-1.h-1, AUC = 100 +/- 44 mg.L-1.h, Cmax = 6.7 +/- 2.8 mg.L-1. The pharmacokinetic parameters of HF were as follows: in normal rats, K(m) = 0.07 +/- 0.01 h-1, AUC = 219 +/- 22 mg.L-1.h, Cmax = 8.6 +/- 0.6 mg.L-1; in hepatic injury rats, K(m) = 0.05 +/- 0.01 h-1, AUC = 170 +/- 42 mg.L-1.h, Cmax = 3.8 +/- 0.8 mg.L-1. There were significant differences between the parameters of normal and hepatic injury rats (P < 0.01) except AUC of HF (P > 0.05). CONCLUSION: This HPLC assay was sensitive and precise, and the elimination of Flu and HF was inhibited significantly due to hepatic injury.

Androgen Antagonists↗

PubMed1998

[Clinical observation on benign osteolytic bone defects treated with natural non-organic bone].

It is extremely necessary to find an ideal filling material for the treatment of benign bone defect, particularly those benign osteolytic defect in children with a comparatively large cavity. From July, 1995 to December, 1996, 10 cases of benign osteolytic bone defects were treated, in which 5 cases of benign osteolytic defects, 3 cases of bone cysts, 1 case of fibrous dysplasia of bone and 1 case of non-ossifying fibroma. After through curettage of the cavity, the natural non-organic bone in cube-shaped was used to fill the prepared cavity. The results showed that the activities of the patients resumed normal in 3 to 6 months after operation. The roentgenographic examination after operation showed that the lucent spaces between NNB cubes disappeared with obvious new bone formation and the bony cavity was obliterated with newly-formed bone. There was no recurrence of the lesion during a follow-up of 7 to 24 months. It was concluded that to treat the osteolytic defect of bone with NNB was a method of choice. The new bone formation appeared early in large amount and increased rapidly.

Adolescent↗