Silencing of METTL3 prevents the proliferation, migration, epithelial-mesenchymal transition, and renal fibrosis of high glucose-induced HK2 cells by mediating WISP1 in m6A-dependent manner.

Diabetic nephropathy (DN) is one of the most serious complications in diabetic patients. And m6A modifications mediated by METTL3 are involved multiple biological processes. However, the specific function and mechanism of METTL3 in DN remains unclear. DN model mice were first established with streptozotocin, and WISP1 expression was confirmed by qRT-PCR. Then the influences of WISP1 or/and METTL3 on the proliferation, migration, and epithelial-mesenchymal transition (EMT) and fibrosis-related proteins of high glucose (HG)-induced HK2 cells or HK2 cells were tested through CCK-8, wound healing, and western blot. We first revealed that WISP1 was highly expressed in renal tissues of DN model mice and HG-induced HK2 cells. Functionally, WISP1 or METTL3 silencing could weaken the proliferation, migration, EMT, and fibrosis of HG-treated HK2 cells, and WISP1 or METTL3 overexpression could induce the proliferation, migration, EMT, and fibrosis of HK2 cells. Additionally, METTL3 silencing could decrease WISP1 m6A modification, and silencing of METTL3 also could notably suppress the biological functions of HG-induced HK2 cells by downregulating WISP1. Silencing of METTL3 prevents DN development process by decreasing WISP1 with m6A modification pattern. Therefore, we suggest that METTL3/WISP1 axis might be a novel therapeutic target for DN.

Bone metabolism regulation: Implications for the treatment of bone diseases.

Bone cells in the human body are continuously engaged in cellular metabolism, including the interaction between bone cells, the interaction between the erythropoietic cells of the bone marrow and stromal cells, for the remodeling and reconstruction of bone. Osteoclasts and osteoblasts play an important role in bone metabolism. Diseases occur when bone metabolism is abnormal, but little is known about the signaling pathways that affect bone metabolism. The study of these signaling pathways will help us to use the relevant techniques to intervene, so as to improve the condition. The study of these signaling pathways will help us to use the relevant techniques to intervene, so as to improve the condition. I believe they will shine in the diagnosis and treatment of future clinical bone diseases.

3D printing promotes the development of drugs.

3D printing is an emerging field that can be found in medicine, electronics, aviation and other fields. 3D printing, with its personalized and highly customized characteristics, has great potential in the pharmaceutical industry. We were interested in how 3D printing can be used in drug fields. To find out 3D printing's application in drug fields, we collected the literature by combining the keywords "3D printing"/"additive manufacturing" and "drug"/"tablet". We found that 3D printing technology has the following applications in medicine: firstly, it can print pills on demand according to the individual condition of the patient, making the dosage more suitable for each patient's own physical condition; secondly, it can print tablets with specific shape and structure to control the release rate; thirdly, it can precisely control the distribution of cells, extracellular matrix and biomaterials to build organs or organ-on-a-chip for drug testing; finally, it could print loose porous pills to reduce swallowing difficulties, or be used to make transdermal microneedle patches to reduce pain of patients.

The Nomogram Model Predicting Overall Survival and Guiding Clinical Decision in Patients With Glioblastoma Based on the SEER Database.

Background: Patients with glioblastoma have a poor prognosis. We want to develop and validate nomograms for predicting overall survival in patients with glioblastoma. Methods: Data of patients with glioblastoma diagnosed pathologically in the SEER database from 2007 to 2016 were collected by SEER*Stat software. After eliminating invalid and missing clinical information, 3,635 patients (total group) were finally identified and randomly divided into the training group (2,183 cases) and the verification group (1,452 cases). Cox proportional risk regression model was used in the training group, the verification group and the total group to analyze the prognostic factors of patients in the training group, and then the nomogram was constructed. C-indexes and calibration curves were used to evaluate the predictive value of nomogram by internal (training group data) and external validation (verification group data). Results: Cox proportional risk regression model in the training group showed that age, year of diagnosis, laterality, radiation, chemotherapy were all influential factors for prognosis of patients with glioblastoma (P < 0.05) and were all used to construct nomogram as well. The internal and external validation results of nomogram showed that the C-index of the training group was 0.729 [95% CI was (0.715, 0.743)], and the verification group was 0.734 [95% CI was (0.718, 0.750)]. The calibration curves of both groups showed good consistency. Conclusions: The proposed nomogram resulted in accurate prognostic prediction for patients with glioblastoma.

Big data-driven precision medicine: Starting the custom-made era of iatrology.

Precision medicine is a new therapeutic concept and method emerging in recent years. The rapid development of precision medicine is driven by the development of omics related technology, biological information and big data science. Precision medicine is provided to implement precise and personalized treatment for diseases and specific patients. Precision medicine is commonly used in the diagnosis, treatment and prevention of various diseases. This review introduces the application of precision medicine in eight systematic diseases of the human body, and systematically presenting the current situation of precision medicine. At the same time, the shortcomings and limitations of precision medicine are pointed out. Finally, we prospect the development of precision medicine.

Mannose: Good player and assister in pharmacotherapy.

Mannose is a monosaccharide widely distributed in body fluids and tissues, especially in the nerve, skin, testicles, retina, liver and intestines. It is used to synthesize glycoproteins and participate in immune regulation. In recent years, mannose has been applied more and more widely in the biomedical context as people have a deeper understanding of its biological effects. This review introduces the use of mannose in treating various diseases (including cancer, urinary tract infections, type 1 diabetes, and diabetic wounds), preventing pancreatic fistula, and improving magnetic resonance imaging for acute pancreatitis. We also demonstrate that mannose has the potential for clinical applications.

GWAS in cancer: progress and challenges.

The genome-wide association study (GWAS) is an effective method to detect single-nucleotide polymorphisms (SNPs) of multiple individual genes based on linkage disequilibrium (LD). GWAS examines genotypes and distinguishing gene characteristics that are exhibited in diseases. In the past few decades, more and more literature has reported the results of applying GWAS to study tumors. Although many pleiotropic loci associated with complex phenotypes have been identified by GWAS, the biological functions of many genetic variation loci remain unclear, and the genetic mechanisms of most complex phenotypes cannot be systematically explained. In this article, we will review the new findings of several tumor types, and categorize the new sites and mechanisms that have recently been discovered. We linked the mechanisms of action of various tumors and searched for links to related gene expression pathways. We found that susceptible sites can be divided into hub genes and peripheral genes; the two interact to link gene expression in a variety of diseases.

Microsatellite instability: a review of what the oncologist should know.

The patients with high microsatellite instability (MSI-H)/mismatch repair deficient (dMMR) tumors recently have been reported that can benefit from immunotherapy, and MSI can be used as a genetic instability of a tumor detection index. However, many studies have shown that there are many heterogeneous phenomena in patients with MSI tumors in terms of immunotherapy, prognosis and chemotherapy sensitivity. Here we mainly review the research results of MSI detection methods, the mechanisms of MSI occurrence and its relationship with related tumors, aiming to make a brief analysis of the current research status of MSI and provide comparable reference and guidance value for further research in this field.

A prognostic model guides surgical resection in cervical squamous cell carcinoma.

BACKGROUND: To explore the independent risk factors of cervical squamous cell carcinoma and establish a Nomogram model to predict the prognosis of patients. METHODS: We randomly divided the total data of patients with cervical squamous cell carcinoma from 2010 to 2015 obtained from the SEER database and cleaned them into training and verification cohorts. The Cox proportional hazard regression model was used to perform univariate and multivariate analyses on the three cohorts of data including the total data. After the intersection, the independent factors and their nomograms with statistical significance were obtained, and the degree of differentiation and calibration between predicted results and real values were obtained by using C-index and calibration map respectively. In addition, the ROC curve was used for correction and evaluation, and the 1-, 3- and 5-year overall and specific survival rates of patients were finally predicted. RESULTS: We found age, surgical condition of the primary site and tumor size were all independent factors of cervical cancer. The high-risk survival rates of patients at 1, 3 and 5 years were 77.7%, 48.6% and 36.4%, respectively. We determined that minimally invasive hysterectomy and uterine-preserving surgery (UPS) have a better survival rate for early (stage I) tumors or tumor diameter less than 20 mm. For the late (stage III-IV) or tumor diameter greater than 20 mm, auxiliary open hysterectomy after radiotherapy, and requires careful evaluation of the postoperative residual tumor is the best policy. CONCLUSIONS: The constructed nomograms could predict overall survival with good performance, and guide surgical resection in cervical squamous cell carcinoma.

Transcriptional regulation in model organisms: recent progress and clinical implications.

In this review, we will summarize model organisms used by scientists in the laboratory, including Escherichia coli, yeast, Arabidopsis thaliana, nematodes, Drosophila, zebrafish, mice and other animals. We focus on the progress in research exploring different types of E. coli in the human body, and the specific molecular mechanisms by which they play a role in humans. First, we discuss the specific transcriptional regulation mechanism of E. coli in cell development, maturation, ageing and longevity, as well as tumorigenesis and development. Then, we discuss how the synthesis of some important substances in cells is regulated and how this affects biological behaviour. Understanding and applying these mechanisms, presumably, can greatly improve the quality of people's lives as well as increase their lifespan. For example, some E. coli can activate certain cells by secreting insulin-like growth factor-1, thus activating the inflammatory response of the body, while other E. coli can inactivate the immune response of the body by secreting toxic factors.

Dose-related histopathology and bone remodeling characteristics of the knee articular cartilage and subchondral bone induced by glucocorticoids in rats.

The aim of the current study was to investigate histopathological changes and bone remodeling in the knee articular cartilage and subchondral bone in rats following treatment with glucocorticoids. A total of 30 3-month-old female Sprague-Dawley rats were randomly divided into either a vehicle control group or one of three experimental groups wherein dexamethasone (Dex) was administered at a dose of 1.0, 2.5 or 5.0 mg/kg (Dex1.0, Dex2.5 and Dex5.0, respectively), for 8 weeks. Articular cartilage and the epiphyseal subchondral bone of the proximal tibias were evaluated by histopathology or for bone remodeling using histomorphometry. No histological changes were identified in the knee articular cartilage but the bone formation rate of the subchondral bone was lower in the Dex1.0 group compared with that of the control group. Compared with the control and the Dex1.0 group, the width of the articular cartilage and the subchondral plate were larger, with abnormal morphology and increased apoptosis of chondrocytes, decreased cell/matrix volume ratio in the cartilage and fewer blood vessels in the subchondral plate in the Dex2.5 and Dex5.0 groups. A higher Dex dose resulted in more severe inhibition of bone formation, a greater number of apoptotic osteocytes and constrained bone resorption. All microstructure parameters indicated no significant changes in the Dex2.5 group but exhibited deterioration in the Dex5.0 group compared with the normal and Dex1.0 group. There were no significant differences in morphological changes, or in static and dynamic bone indices between the Dex2.5 and Dex5.0 groups. In conclusion, long-term glucocorticoid use induced dose-related histopathological changes in the knee articular cartilage, along with unbalanced bone remodeling and osteopenia in the subchondral bone. The degree of damage to the articular cartilage was milder and transformed from compensation to degeneration at higher doses.

WISP1 silencing confers protection against epithelial-mesenchymal transition of renal tubular epithelial cells in rats via inactivation of the wnt/ß-catenin signaling pathway in uremia.

Uremia can affect hepatic metabolism of drugs by regulating the clearance of drugs, but it has not been clarified whether gene silencing could modulate the epithelial-mesenchymal transition (EMT) process in uremia. Hence, we investigated the effect of WISP1 gene silencing on the renal tubular EMT in uremia through the wnt/ß-catenin signaling pathway. Initially, microarray-based gene expression profiling of uremia was used to identify differentially expressed genes. Following the establishment of uremia rat model, serum creatinine, and urea nitrogen of rats were detected. Renal tubular epithelial cells (TECs) were transfected with shRNA-WISP1 lentivirus interference vectors and LiCI (the wnt/ß-catenin signaling pathway activator) to explore the regulatory mechanism of WISP1 in uremia in relation to the wnt/ß-catenin signaling pathway. Then, expression of WISP1, wnt2b, E-cadherin, α-SMA, c-myc, Cyclin D1, MMP-2, and MMP-9 was determined. Furthermore, TEC migration and invasion were evaluated. Results suggested that WISP1 and the wnt/ß-catenin signaling pathway were associated with uremia. Uremic rats exhibited increased serum creatinine and urea nitrogen levels, upregulated WISPl, and activated wnt/ß-catenin signaling pathway. Subsequently, WISP1 silencing decreased wnt2b, c-myc, Cyclin D1, α-SMA, MMP-2, and MMP-9 expression but increased E-cadherin expression, whereas LiCI treatment exhibited the opposite trends. In addition, WISP1 silencing suppressed TEC migration and invasion, whereas LiCI treatment promoted TEC migration and invasion. The findings indicate that WISP1 gene silencing suppresses the activation of the wnt/ß-catenin signaling pathway, thus reducing EMT of renal TECs in uremic rats.

The development of bone microstructure, metabolism and biomechanics in lumbar vertebra under short-term glucocorticoid exposure.

Abstracts Objective: This study investigated the characteristics of bone microstructure, metabolism, and biomechanics in rat's lumbar vertebra undergoing short-term glucocorticoid administration. Methods: Forty 4-month-old female Sprague-Dawley rats were treated with either vehicle (Cont) or prednisone acetate (Pre) at 3.5 mg/kg/day, respectively for periods of 7 days and 21 days. The lumbar vertebras were processed for MicroCT scan, histomorphometry analysis, mechanical compression test, in addition to Dual-Energy X-ray absorptiometry scan, respectively. Results: The connective density (Conn. D) along with trabecular connection nodes decreased while trabecular termini increased in Pre at day 21 when compared to Cont at day 21 as well as Pre at day 0. The mineralizing surface (MS/BS), mineral apposition rate (MAR), bone formation rate (BFR), osteoblast surfaces (Ob.S/BS) were lower in Pre at day 21 than that in Cont at day 21, Pre at day 0 and Pre at day 7. Only the bending stiffness of compression test decreased in Pre group at day 21 compared to age-matched control. Conclusion: The results suggested that excess prednisone significantly inhibited bone formation and slightly depressed bone resorption in the lumbar vertebra of intact rats for the duration of 21 days. Accordingly, the trabecular spatial microstructure made an adjustment yet failed to maintain the anti-compression mechanical property.

Salvianolic acid B prevents bone loss in prednisone-treated rats through stimulation of osteogenesis and bone marrow angiogenesis.

Glucocorticoid (GC) induced osteoporosis (GIO) is caused by the long-term use of GC for treatment of autoimmune and inflammatory diseases. The GC related disruption of bone marrow microcirculation and increased adipogenesis contribute to GIO development. However, neither currently available anti-osteoporosis agent is completely addressed to microcirculation and bone marrow adipogenesis. Salvianolic acid B (Sal B) is a polyphenolic compound from a Chinese herbal medicine, Salvia miltiorrhiza Bunge. The aim of this study was to determine the effects of Sal B on osteoblast bone formation, angiogenesis and adipogenesis-associated GIO by performing marrow adipogenesis and microcirculation dilation and bone histomorphometry analyses. (1) In vivo study: Bone loss in GC treated rats was confirmed by significantly decreased BMD, bone strength, cancellous bone mass and architecture, osteoblast distribution, bone formation, marrow microvessel density and diameter along with down-regulation of marrow BMPs expression and increased adipogenesis. Daily treatment with Sal B (40 mg/kg/d) for 12 weeks in GC male rats prevented GC-induced cancellous bone loss and increased adipogenesis while increasing cancellous bone formation rate with improved local microcirculation by capillary dilation. Treatment with Sal B at a higher dose (80 mg/kg/d) not only prevented GC-induced osteopenia, but also increased cancellous bone mass and thickness, associated with increase of marrow BMPs expression, inhibited adipogenesis and further increased microvessel diameters. (2) In vitro study: In concentration from 10(-6) mol/L to 10(-7) mol/L, Sal B stimulated bone marrow stromal cell (MSC) differentiation to osteoblast and increased osteoblast activities, decreased GC associated adipogenic differentiation by down-regulation of PPARγ mRNA expression, increased Runx2 mRNA expression without osteoblast inducement, and, furthermore, Sal B decreased Dickkopf-1 and increased ß-catenin mRNA expression with or without adipocyte inducement in MSC. We conclude that Sal B prevented bone loss in GC-treated rats through stimulation of osteogenesis, bone marrow angiogenesis and inhibition of adipogenesis.

[Effects of alcohol on bone metabolism and biomechanical property of mice].

This study was aimed to detect the effects of alcohol on bone metabolism and biomechanical property of growing mice. Thirty KM mice were randomly divided into 3 groups, namely basal control group (mice were killed at the beginning), normal control group (with distilled water given by gastrogavage), and 50% (V/V) alcohol group (with alcohol given by gastrogavage at the dose of 4 g x kg(-1) x d(-1) for 60 days). All mice were killed and their proximal tibia and tibial diaphysis were processed by undecalcified sections and measured by bone histomorphometry. The biomechanical properties of lumbar vertebra and femur were tested. Compared with normal control, the index of trabecular bone area (% Tb. Ar) of proximal tibial metaphysis (PTM) and the static parameter of cortical bone( Ct. Ar) both decreased obviously (P < 0.05) in alcohol group. Bone formation rate (BFR/TV) of trabecular bone and cortical bone dropped also (P < 0.05). The maximal resistibility of lumbar vertebra and structural mechanical strength of proximal femoral neck both declined significantly (P < 0.01) in alcohol group. Low dose of alcohol inhibited the bone formation rate of growing mice , thus leading to a disorder of bone metabolism and a decrease in biomechanical quality.

Effects of stanozolol on bone mineral density and bone biomechanical properties of osteoporotic rats.

OBJECTIVE: To evaluate the effects of stanozolol on the bone mineral density (BMD) and bone biomechanical properties of rats with glucocorticoid (GC)-induced osteoporosis (OP). METHODS: Twenty-eight male Sprague-Dawley rats of 3-month old were randomly divided into Group A (the basal control group), Group B (the age-matched control group), Group C (GC-induced OP group) and Group D (stanozolol-administrated group), 7 in each group. The rats in Group A were killed when experiment commenced, and those in Group B were given normal saline ig., while those in Groups C and D received the prednisone acetate (4.5 mg/kg, twice a week) alone and in combination with stanozolol (0.5 mg/kg, 6 times a week), respectively. Ninety days later, the bilateral femur and the 5th lumbar vertebra of the rats were isolated for BMD test using dual-energy X-ray absorptiometry scanner, and the torsion test, three-point bending test and compression test using electronic testing device. RESULTS: Compared with Group B, the mean BMD of the femur and the 5th lumbar vertebra in Group C decreased by 14.64% (P<0.01), the BMD of the bilateral distal femoral segment and the 5th lumbar vertebra decreased by 21.42% (P<0.01), 19.62% (P<0.05) and 23.48% (P<0.01) respectively. The load that the femur withstood in three-point bending test decreased by 17.1% (P<0.05), and the other biomechanical parameters also declined. When compared with Group C, the BMD in Group D increased, the torsional angle of the femur increased by 72.5% (P<0.05) and the other biomechanical parameters also tended to increase. CONCLUSIONS: BMD and biomechanical properties of the rat femur and the 5th lumbar vertebra decrease in response to a long-term GC administration, which can be prevented by stanozolol.

[Effects of stilbestrol on bone growth and metabolism in ovariectomized rats].

OBJECTIVE: To study the effects of stilbestrol on bone growth and metabolism in ovariectomized rats. METHODS: Twenty-seven 3-month-old female SD rats were randomly divided into 3 equal groups, namely the control group, ovariectomized group (OEG), and OEG+estrogen (OEG+E) group. After ovariectomy, the rats in the third group were given stilbestrol 0.022 5 mg/d x kg x b x w by intragastric gavage for 90 d. A digital image analysis system was used for the measurement of histomorphometric parameters in the proximal tibial metaphysis of the rats. The three-dimensional structure of the femur was observed with scanning electron microscope, with the blood cholesterol level determined and the main viscera weighted. RESULTS: In comparison with the control rats, the trabecular bone area (TbAr) of ovariectomized rats was significantly reduced (-65%), trabecular bone space (TbSp) enlarged (+189%), and the bone formation rate (BFR) accelerated (+91%). The cancellous bone of the femurs manifested obvious signs of thinning, roughening and resorption lacunae to cause trabecular bone discontinuance, and osteoporosis occurred. The rats treated with stilbestrol, in contrast, had increased TbAr (by 128%), reduced TbSp (by 63%), lowered BFR (by 49%), and reduced osteoclasts (by 32%). The cancellous bone of the femurs was well arranged in close connection with each other, and the high cholesterol level and endocrinic changes in response to ovariectomy was corrected by stilbestrol, which also caused the increase of the uterine weight. CONCLUSION: Stilbestrol may help prevent primary osteoporosis but may increase the risk of female genital cancer.

[Piperazinyl estrone prevents bone loss in ovariectomized rats].

AIM: To determine the effect of piperazinyl estrone, a new estrogen derivative, on bone turnover, bone mass and uteri in ovariectomized rats. METHODS: Female Sprague-Dawley rats were ovariectomized (OVX) or sham operated (sham) at the age of 3 months and treated with estrone (E) at 0.75 mg.kg-1.d-1, or with piperazinyl estrone (P-E) at 1 or 10 mg.kg-1.d-1, orally, for 3 months. At the time of death, the uterine weight was measured. Bone histomorphometric analysis of proximal tibial metaphyses (PTM) was performed in undecalcified sections. RESULTS: Bone histomorphometric data showed that the percent trabecular area (% Tb.Ar) of OVX rats with bone high turnover was significantly decreased. The uteri were atrophied. The percent trabecular area (% Tb.Ar) of estrone treated group was increased in decreasing bone turnover manner. But the size and weight of uteri in this group were increased vs OVX group. The bone loss induced by OVX was preserved by P-E treatment, but the mechanism of maintaining bone is different from that of E-treated rats. P-E treatment in low dose did not decrease any bone formation indices, such as percent labeling perimeter, bone formation rate per bone volume (BFR/BV), except bone mineral apposition rate (MAR) compared with E-treated group, and maintained them at OVX level. The uteri were found to be in atrophy compared with the match dose (0.75 mg) of E-treated OVX rats. But rats treated with high dose of P-E showed the same change like E-treated group. CONCLUSION: The finding of this study shows that lower dosage of piperazinyl estrone has effect on preventing the bone losses in OVX rats, while the bone formation and the uterus are not affected, thus supporting the hypothesis that piperazinyl estrone has the potential to prevent postmenopausal bone loss in women with less side effects.

Effects of low doses of hydrochloride tetracycline on bone metabolism and uterus in ovariectomized rats.

AIM: To study the effects of low doses of hydrochloride tetracycline (Tc) on bone metabolism and uterus in the ovariectomized (Ova) rats. METHODS: Forty 3-month-old rats were randomly divided into 5 groups: sham group, Ova group, Tc1 group (1.2 mg/kg/d), Tc2 group (4.8 mg/kg/d), and estrone group (1.48 mg/kg/d), oral fed for 3 months. The proximal tibia metaphyses were processed undecalcified for quantitative bone histomorphometry and the soft tissues were processed in paraffin for pathological observation. RESULTS: Placebo-treated (lactose) Ova rats were characterized by trabecular area (TA) decreasing and their architecture worsening compared with sham controls, and bone resorption was over formation with high bone turnover. The uteri were atrophy. (2) In estrone-treated group, TA and trabecular numbers were significantly increased and the trabecular separation decreased vs Ova group. Estrone slowed down Ova-inducing bone high turnover. But the size, weight, and the endometrium of the uteri in this group were increased vs Ova group. (3) TA was increased in both Tc1 and Tc2 groups compared with Ova rats. Tc maintained bone formation indices almost at Ova level, and only decreased mineral apposition rate (MAR) in Tc1 group, and declined bone resorption perimeter. The uteri and the cell of liver and kidney almost maintained at Ova level; Tc2 decreased labeling perimeter and increased MAR in comparison with Tc1 group. The uteri were atrophy, whose size maintained at Ova level; yellow labeling was not found in bone with these doses of Tc, while yellow labeling could be seen with the doses of 30 mg/kg/d of Tc for bone marker. CONCLUSION: The two doses of Tc have similar effects on preventing bone loss in Ova rats while the bone formation and uterus are not affected. However, Tc2 does not have more effects on increasing bone mass, Tc2 causes less mild damages to the liver and kidneys.

Effects of prednisone on bone mineral density and biomechanical characteristics of the femora and lumbar vertebras in rats.

OBJECTIVE: To explore effects of prednisone on the bone mineral density (BMD) and biomechanics of the femora and lumbar vertebras in rats. METHODS: Twenty one 3-month-old male Sprague-Dawley rats weighing 226+/-12 g were randomly divided into basal control, age-matched and hormone groups. The rats in basal control group were killed at the beginning of the experiment without any treatment, and those in age-matched group were given oral normal saline (5 ml x kg(-1) x d(-1)) while the rats in hormone group received oral prednisone acetate (4.5 ml x kg(-1) x d(-1) twice a week) to establish osteoporotic models. The treatment for the latter 2 groups of rats lasted for 90 days, after which the BMD and mechanical measurements of the femurs and L5 vertebra were carried out by way of torsion, three-point bending and compression tests. The measurements were also conducted in the basal control group at the time indicated above. RESULTS: In hormone group, the total BMD of the femora and L5 vertebra was decreased by 14.64%(P<0.01), and the BMD in the right and left distal femoral segments and the vertebra decreased by 21.42% (P<0.01), 19.62% (P<0.05) and 23.48%(P<0.01), respectively, in comparison with the control group. In the meantime, the loads of three-point bending test in hormone group was decreased by 17.1%(P<0.05), whereas the rest parameters tended to decrease as compared with the control group. CONCLUSIONS: Chronic use of corticosteroid is more liable to cause bone mass loss in rat cancellous bone than in the cortical bone, and mechanical properties of the cortical and cancellous bone, especially those of the latter, will also decline, to give rise to easy bone fracture at the trabecular bone in osteoporotic conditions.