Preoperative localization of sentinel lymph nodes using percutaneous contrast-enhanced ultrasonography in patients with breast cancer.

Background: This study aimed to investigate the feasibility of preoperative identification of sentinel lymph nodes (SLNs) by contrast-enhanced ultrasound (CEUS) for patients with breast cancer. Methods: The patients with T1-T2N0M0 breast cancer who were scheduled for primary surgical treatment were recruited. All the patients had received a periareolar intradermal injection of an ultrasonic contrast agent (SonoVue, Bracco, Milan, Italy) followed by an ultrasound to identify contrast-enhanced SLNs. A guidewire was deployed to localize the SLN. Methylene blue stain was used to help trace SLNs during the operation. The identification rate and accuracy rate were recorded. The number of SLNs labeled by two methods was counted and compared using Wilcoxon testing. Results: A total of 366 SLNs were detected in 72 patients by methylene blue intraoperatively, with a median of 5 lymph nodes [interquartile range (IQR), 4-6] per patient. A total of 95 SLNs were detected in 63 patients (87.5%) by CEUS, with a median of 1 lymph node (IQR, 1-2) per patient. The number of SLNs detected by CEUS was significantly less than that labeled by the methylene blue staining method (Z=-7.362, P=0000). Pathology confirmed 12 single metastases in all the lymph nodes examined, 10 of which were the only lymph node identified by CEUS. Conclusions: Periareolar intradermal injection of an ultrasonic contrast agent was an effective and convenient supplementary to localize SLNs. The technique was expected to improve the accuracy of axillary staging with minor surgical trauma and postoperative complications.

Identification of Forsythia suspensa (Thunb.) Vahl in different harvest periods using intelligent sensory technologies, HPLC characteristic fingerprint coupled with chemometrics.

INTRODUCTION: Forsythia suspensa (Thunb.) Vahl (FS), the fruit of Oleaceae plants, as a large part of traditional Chinese medicine, is classified as "Qingqiao (Q)" and "Laoqiao (L)" based on the harvest time. Because the maturation of FS is a gradual process, its accurate identification based on different maturity levels is an important issue. OBJECTIVES: We suggest colorimetric, electronic tongue, and high-performance liquid chromatography (HPLC) characteristic fingerprints to discriminate FS in different harvest periods. MATERIAL AND METHODS: First, FS fruits from different harvest times were collected, and then, their colour parameters, E-tongue sensory properties, HPLC characteristic fingerprints, and contents of nominal ingredients were determined. Finally, multivariate statistical analyses, including three-dimensional scatter plots, hierarchical cluster, principal component, linear discriminant, similarity, and partial least squares discriminant analyses were performed. RESULTS: The results demonstrated that the three experimental techniques could effectively discriminate FS based on different harvest times with 100% accuracy. Under the qualitative conditions, nine common peaks were identified in the HPLC fingerprints of 60 samples, among which, six peaks [variable importance in projection (VIP) > 1] could be used as index peaks for qualitative identification. In fact, the contents of quality marker components, including forsythin, phillygenin, rutin and forsythoside A, were significant different (P < 0.001) at different harvest times. Interestingly, the quality markers not only accurately reflected the maturity of FS but also showed close correlations with the colour parameters and sensory E-tongue responses. CONCLUSION: In our present investigation, bionic technologies, including a colorimeter, E-tongue analysis, and HPLC characteristic fingerprints, combined with chemometrics, were employed to develop a novel and accurate method for discriminating FS based on different harvest times.

The Adoption of Preventive Behaviors during the COVID-19 Pandemic in China and Israel.

The COVID-19 pandemic represents a massive global health crisis. The rapid transmission rate of the virus, as well as the lack of effective medications and vaccines, has posed serious challenges to controlling the spread of the disease. Dealing with this public health crisis has required major changes in people's behavior, including the adoption of social distancing measures such as avoiding meeting with family members and friends, crowded places, and public transportation. The purpose of this study is to investigate the factors associated with the adoption of these behaviors in China and Israel. We relied on the 3Cs model that has been used to predict the adoption of a specific preventive behavior (vaccinations) with the goal of testing its applicability to other preventive behaviors such as in response to the COVID-19 pandemic. The model indicates that confidence in social institutions, complacency (fear of and assessments about the risk of becoming ill) and constraints (levels of self-efficacy and confidence in being able to engage in the behaviors) are predictors of adopting preventive behaviors. Data were collected in China and Israel through an online survey of the population (n = 1406). We used latent variables and structural equation modeling to test the hypotheses derived from the 3Cs model. The findings indicate that there are some differences in the types of preventive behaviors adopted in the two countries. In Israel, higher levels of confidence predicted the adoption of avoidant behaviors and more constraints predicted engaging in fewer avoidant behaviors. In China, more constraints also contributed to the adoption of fewer avoidant behaviors, but people's level of confidence fully mediated this result. The multi-group analysis indicated that the conceptualized model fits the Chinese and Israeli data reasonably well. The findings suggest that the 3Cs model can be generalized from getting vaccinated to adopting avoidant behaviors and that the model can be used across cultures and countries.

Hepalatide ameliorated progression of nonalcoholic steatohepatitis in mice.

BACKGROUND: No FDA-approved medications are available for the treatment of nonalcoholic steatohepatitis (NASH). The present study aimed to assess the effects of Hepalatide, a sodium taurocholate cotransporting polypeptide (NTCP) receptor-binding agent, on metabolic and histopathologic changes of a mouse model of NASH caused by high fat/calorie diet plus high fructose/glucose in drinking water (HFCD-HF/G) for 16 weeks. METHODS: Male mice were randomly divided into 4 groups: controls (normal diet), HFCD-HF/G group, HFCD-HF/G plus low or high dose of Hepalatide (20 or 60 mg/kg, LH or HH, s.c. from 9 to 16 weeks). RESULTS: Compared to HFCD-HF/G-fed mice, serum triglyceride and cholesterol levels in mice fed HFCD-HF/G plus LH or HH were decreased. The treatment with Hepalatide decreased serum alanine aminotransferase levels significantly. Liver histology and TUNEL staining showed that Hepalatide remarkably attenuated inflammation, hepatocellular steatosis and apoptosis. Hepalatide treatment decreased fasting blood glucose, serum insulin and HOMA insulin resistance index in the HH group. Moreover, Masson's staining, semi-quantitative score of fibrosis, and hydroxyproline content demonstrated that Hepalatide mitigated fibrotic progression in this murine NASH model. Additionally, most components of liver and few serum bile acids were increased in mice treated with HH. CONCLUSION: Hepalatide effectively alleviated the pathological process, metabolic profile, hepatocellular steatosis and injury, insulin resistance, halted hepatic fibrotic progression in a mouse model of NASH, most likely through the increase of serum bile acids.

Succinate-GPR-91 receptor signalling is responsible for nonalcoholic steatohepatitis-associated fibrosis: Effects of DHA supplementation.

BACKGROUND AND AIMS: Treatment of non-alcoholic steatohepatitis (NASH) is challenging, because suppressing fibrotic progression has not been achieved consistently by drug candidates currently in clinical trials. The aim of this study was to investigate the molecular interplays underlying NASH-associated fibrosis in a mouse NASH model and human specimens. METHODS: Mice were divided into 4 groups: Controls; NASH (high fat/Calorie diet plus high fructose and glucose in drinking water, HFCD-HF/G) for 16 weeks; HFCD-HF/G plus docosahexaenoic acid (DHA) for 16 or 8 weeks. RESULTS: Along with NASH progression, fibrotic deposition was documented in HFCD-HF/G-fed mice. Liver succinate content was significantly increased along with decreased expression of succinate dehydrogenase-A (SDH-A) in these mice; whereas, GPR-91 receptor expression was much enhanced in histology compared to control mice, and co-localized histologically with hepatic stellate cells (HSCs). Succinate content was increased in fatty acid-overloaded primary hepatocytes with significant oxidant stress and lipotoxicity. Exposure to succinate led to up-regulation of GPR-91 receptor in primary and immortalized HSCs. In contrast, suppression of GPR-91 receptor expression abolished succinate stimulatory role in GPR-91 expression and extracellular matrix production in HSCs. All these changes were minimized or abrogated by DHA supplementation in vivo or in vitro. Moreover, GPR-91 receptor expression correlates with severity of fibrosis in human NASH biopsy specimens. CONCLUSION: Succinate accumulation in steatotoic hepatocytes may result in HSC activation through GPR-91 receptor signalling in NASH progression, and the cross-talk between hepatocytes and HSC through GPR-91 signalling is most likely to be the molecular basis of fibrogenesis in NASH.

Impaired mitophagy triggers NLRP3 inflammasome activation during the progression from nonalcoholic fatty liver to nonalcoholic steatohepatitis.

Activation of inflammation is an important mechanism in the development of nonalcoholic steatohepatitis (NASH). This study aims to delineate how mitophagy affects NLRP3 inflammasome activation in hepatic lipotoxicity. Mice were fed a high fat/calorie diet (HFCD) for 24 weeks. Primary rat hepatocytes were treated with palmitic acid (PA) for various periods of time. Mitophagy was measured by protein levels of LC3II and P62. NLRP3, caspase-1, interleukin (IL)-18, and IL-1ß at mRNA and protein levels were used as indicators of inflammasome activation. Along with steatotic progression in HFCD-fed mice, ratio of LC3II/ß-actin was decreased concurrently with increased levels of liver P62, NLRP3, caspase-1, IL-1ß, IL-18, and serum IL-1ß levels in late-stage NASH. PA treatment resulted in mitochondrial oxidative stress and initiated mitophagy in primary hepatocytes. The addition of cyclosporine A did not change LC3II/Τοmm20 ratios; but P62 levels were increased after an extended duration of PA exposure, indicating a defect in autophagic activity. Along with impaired mitophagy, mRNA and protein levels of NLRP3, caspase-1, IL-18 and IL-1ß were upregulated by PA treatment. Pretreatment with MCC950, N-acetyl cysteine or acetyl-L-carnitine reversed inflammasome activation and a pyroptotic cascade. Additionally, mitophagic flux was partially recovered as indicated by increases in LC3II/Tomm20 ratio, parkin, and PINK1 expression, and decreased P62 expression. The findings suggest that impaired mitophagy triggers hepatic NLRP3 inflammasome activation in a murine NASH model and primary hepatocytes. The new insights into inflammasome activation through mitophagy advance our understanding of how fatty acids elicit lipotoxicity through oxidant stress and autophagy in mitochondria.

Adipose tissue transplantation ameliorates lipodystrophy-associated metabolic disorders in seipin-deficient mice.

Seipin deficiency is responsible for type 2 congenital generalized lipodystrophy with severe loss of adipose tissue and can lead to hepatic steatosis, insulin resistance (IR), and dyslipidemia in humans. Adipose tissue secretes many adipokines that are central to the regulation of metabolism. In this study, we investigated whether transplantation of normal adipose tissue could ameliorate severe hepatic steatosis, IR, and dyslipidemia in lipoatrophic seipin knockout (SKO) mice. Normal adipose tissue from wild-type mice was transplanted into 6-wk-old SKO mice. At 4 mo after adipose tissue transplantation (AT), the transplanted fat survived with detectable blood vessels, and the reduced levels of plasma leptin, a major adipokine, were dramatically increased. Severe hepatic steatosis, IR, and dyslipidemia in SKO mice were ameliorated after AT. In addition, abnormal hepatic lipogenesis and ß-oxidation gene expression in SKO mice were improved after AT. Our results suggest that AT may be an effective treatment to improve lipodystrophy-associated metabolic disorders.

Characterization of a murine nonalcoholic steatohepatitis model induced by high fat high calorie diet plus fructose and glucose in drinking water.

There are varieties of murine models of nonalcoholic steatohepatitis (NASH) with different pathophysiologic characteristics. For preclinical assessment, a standardized model would allow comparisons of various pharmacotherapeutic candidates in efficacy, pharmacokinetics, pharmaco-metabolism, and adverse effects under a same system. The present study aims to characterize murine NASH models by comparing end-points of major abnormalities. NASH was induced by feeding high fructose/glucose in drinking water (HF/G), high-fat/calorie diet (HFCD), and in combination (HFCD-HF/G) in mice for 8 or 16 weeks. HF/G feeding caused a minimal fat accumulation and increase in free fatty acids (FFA). In contrast, HFCD-HF/G feeding resulted in a remarkable increase in body weight, subcutaneous and visceral adipose tissue, macrosteatosis with a nearly seven-fold increase in triglyceride and FFA content, accompanied with marked hepatocellular injury, inflammatory responses, fibrosis, and insulin resistance, and represented as typical NASH in histopathology, metabolic, and adipokine profiles in a progressive manner. Meanwhile, mice fed HFCD displayed significant steatosis, necroptosis, fibrosis, insulin resistance, metabolic, and adipokine profiles, and the extent is less than those fed HFCD-HF/G. Significant MCP-1, CCR-2, and NLRP-1/3 activation were found in mice fed HFCD and HFCD-HF/G for 16 weeks, whereas gene expression of CPT-1 and ACOX-1 was down-regulated in these two groups in comparison to the controls. Nuclear receptors, such as SREBP-1c, FXR, LXR-α, PPAR-α, and PPAR-γ, were strikingly elevated in the HFCD-HF/G group. In conclusion, feeding HFCD-HF/G resulted in a reliable NASH model in mice with remarkable necroptosis, steatosis, fibrosis, and insulin resistance as well as a disordered profile of lipid metabolism and adipokine, and HFCD caused significant NASH features in histopathology and metabolic profiles only at a late stage. Whereas HF/G feeding barely led to minimal fat accumulation, some changes at molecular levels and metabolic disturbance in mice.

Renal injury in Seipin-deficient lipodystrophic mice and its reversal by adipose tissue transplantation or leptin administration alone: adipose tissue-kidney crosstalk.

Seipin deficiency is responsible for type 2 congenital generalized lipodystrophy with severe loss of adipose tissue (AT) and could lead to renal failure in humans. However, the effect of Seipin on renal function is poorly understood. Here we report that Seipin knockout (SKO) mice exhibited impaired renal function, enlarged glomerular and mesangial surface areas, renal depositions of lipid, and advanced glycation end products. Elevated glycosuria and increased electrolyte excretion were also detected. Relative renal gene expression in fatty acid oxidation and reabsorption pathways were impaired in SKO mice. Elevated glycosuria might be associated with reduced renal glucose transporter 2 levels. To improve renal function, AT transplantation or leptin administration alone was performed. Both treatments effectively ameliorated renal injury by improving all of the parameters that were measured in the kidney. The treatments also rescued insulin resistance and low plasma leptin levels in SKO mice. Our findings demonstrate for the first time that Seipin deficiency induces renal injury, which is closely related to glucolipotoxicity and impaired renal reabsorption in SKO mice, and is primarily caused by the loss of AT and especially the lack of leptin. AT transplantation and leptin administration are two effective treatments for renal injury in Seipin-deficient mice.-Liu, X.-J., Wu, X.-Y., Wang, H., Wang, S.-X., Kong, W., Zhang, L., Liu, G., Huang, W. Renal injury in Seipin-deficient lipodystrophic mice and its reversal by adipose tissue transplantation or leptin administration alone: adipose tissue-kidney crosstalk.

Activation of pluripotent genes in hepatic progenitor cells in the transition of nonalcoholic steatohepatitis to pre-malignant lesions.

Nonalcoholic steatohepatitis is considered as a precancerous condition. However, hepatic carcinogenesis from NASH is poorly understood. This study aims to investigate the activation of pluripotent genes (c-Myc, Oct-4, KLF-4, and Nanog) and morphogenic gene (Gli-1) in hepatic progenitor cells from patient specimens and in an animal model to determine the possibility of normal stem/progenitor cells becoming the origin of NASH-HCC. In this study, expression of pluripotent and morphogenic genes in human NASH-HCC tissues was significantly upregulated compared to adjacent non-tumor liver tissues. After feeding high-fat/calorie diet plus high fructose/glucose in drinking water (HFC diet plus HF/G) for up to 12 months, mice developed obesity, insulin resistance, and steatohepatitis with significant necroptotic inflammation and fibrotic progression, as well as occurrence of hyperplastic nodules with dysplasia; and this model represents pathohistologically as a transition from NASH to NASH-HCC in a pre-carcinomatous stage. High expression of pluripotent and morphogenic genes was immunohistochemically visualized in the dysplasia areas of mouse liver, where there were many OV-6-positive cells, indicating proliferation of HOCs in NASH with fibrotic progression. Moreover, oncogenic transcription factors (c-Myc, KLF-4, and Nanog) were co-localized in these hepatic progenitor cells. In conclusion, pluripotent and morphogenic genes may contribute to the reprogramming of hepatic progenitor cells in driving these cells to be the origin of NASH-HCC in a steatotic and inflamed microenvironment.

Palmitic acid elicits hepatic stellate cell activation through inflammasomes and hedgehog signaling.

AIMS: Activation of hepatic stellate cells (HSCs) plays a pivotal role at the center of the fibrogenic progression in nonalcoholic steatohepatitis (NASH). However, it is poorly understood that how various molecules interact within HSCs during the progression of NASH to fibrosis. The aim of the present study is to delineate how inflammasome molecules, hedgehog signaling and autophagy provoke HSC activation using palmitic acid (PA) as a major insult. MAIN METHODS: Inflammasome activation, hedgehog signaling activity and autophagy in PA-exposed HSCs were determined to investigate their role in activation of human and rodent HSC lines or primary HSCs. KEY FINDINGS: PA treatment elicited HSC activation reflected by increased mRNA levels of transforming growth factor-ß1, connective tissue growth factor, tissue inhibitor of metalloproteinase-1 and procollagen type I (α1). In addition, expression levels of NOD-like receptor protein 3 (NLRP3) and hedgehog signaling transcription factor Gli-1 were increased in PA-exposed HSCs. It's evident that PA treatment resulted in increased production of light chain 3-II and autophagosomes, as well as enhanced autophagy flux reflected by transduction of an adeno-associated viral vector. Whereas, reduced autophagy, which is often seen in the late stage of NASH, provoked inflammasome activation. Moreover, suppressing the Hh signaling pathway by LDE225 blocked production of light chain 3-II and autophagy flux. SIGNIFICANCE: Saturated fatty acids, such as PA, stimulate HSC activation through inflammasomes and hedgehog signaling. Meanwhile, compromised autophagy may facilitate HSC activation, implicating valuable candidates for pharmacologic intervention against the progression of fibrogenesis in NASH.

[The Development of Gene Knockout Technologies in Large and Medium Animal Models].

Technique of homologous recombination based gene targeting developed in the late 1980s and won the Nobel Prize in Physiology or Medicine in 2007. However, this technique could only performed in mice which embryonic stem (ES) cells could keep in the potential of multifunction in vitro. Therefore gene knockout technology was difficult to be applied in other species of animals for a long time. Since 2008, with the development of the new technologies, such as the new ES cell gene targeting, zinc finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs) and clusters of regularly interspaced short palindromic repeats/Cas9 (CRISPR/Cas9), building gene knockout in large and medium animals models which are similar to human in disease research becomes possible. This review describes some new gene knockout technologies in large and medium animal models for recent years.

Elastography for breast cancer diagnosis: a useful tool for small and BI-RADS 4 lesions.

The present study aimed at evaluating and comparing the diagnostic performance of B-mode ultrasound (US), elastography score (ES), and strain ratio (SR) for the differentiation of breast lesions. This retrospective study enrolled 431 lesions from 417 in-hospital patients. All patients were examined with both conventional ultrasound and elastography. Two experienced radiologists reviewed ultrasound and elasticity images. The histopathologic result obtained from ultrasound-guided core biopsy or operation excisions were used as the reference standard. Pathologic examination revealed 276 malignant lesions (64%) and 155 benign lesions (36%). A cut-off point of 4.15 (area under the curve, 0.891) allowed significant differentiation of malignant and benign lesions. ROC (receiver-operating characteristic) curves showed a higher value for combination of B-mode ultrasound and elastography for the diagnosis of breast lesions. Conventional ultrasound combined elastography showed high sensitivity, specificity, and accuracy for group II lesions (10mm

A comparison of hepatic segmental anatomy as revealed by cross-sections and MPR CT imaging.

To compare the areas of human liver horizontal sections with computed tomography (CT) images and to evaluate whether the subsegments determined by CT are consistent with the actual anatomy. Six human cadaver livers were made into horizontal slices with multislice spiral CT three-dimensional (3D) reconstruction was used during infusion process. Each liver segment was displayed using different color, and 3D images of the portal and hepatic vein were reconstructed. Each segmental area was measured on CT-reconstructed images, which were compared with the actual area on the sections of the same liver. The measurements were performed at four key levels namely: (1) the three hepatic veins, (2) the left, and (3) the right branch of portal vein (PV), and (4) caudal to the bifurcation of the PV. By dividing the sum of these areas by the total area of the liver, the authors got the percentage of the incorrectly determined subsegmental areas. In addition to these percentage values, the maximum distances of the radiologically determined intersegmental boundaries from the true anatomic boundaries were measured. On the four key levels, an average of 28.64 ± 10.26% of the hepatic area of CT images was attributed to an incorrect segment. The mean-maximum error between artificial segments on images and actual anatomical segments was 3.81 ± 1.37 cm. The correlation between radiological segmenting method and actual anatomy was poor. The hepatic segments being divided strictly according to the branching point of the PV could be more informative during liver segmental resection.

[Predictive study of HBsAg in different stages of neonatal venous blood on failure of blocking HBV mother to infant transmission].

OBJECTIVE: In this study, we discuss the predictive value of different content of HBsAg in different stages of neotal venous blood on failure of blocking mother to infant transmission of HBV. METHODS: 150 infants born of chronically HBV infected mothers who were positive of both HBsAg and HBeAg and who also had a HBV DNA virus load above 10(5) copies/ml were enrolled. These infants were given hepatitis B virus immune globin (HBIG) 200 IU immediately after birth and were given hepatitis B vaccine 10 or 20 microg at brith, 1 month and 6 months after birth. HBV serological index of these infants were test at birth, 1 month and 7 months after birth respectively. Different content of HBsAg in different stages of neonatal venus blood were analyzed to predict the failure of blocking mother to infant transmission of HBV. RESULTS: 11 infants failed in blocking of HBV mother to infant transmission. The positive rate of HBsAg at birth, 1 month and 7 months after birth were 41.26%, 10.49% and 7.69% respectively, and were 97.90%, 65.73% and 13.29% of HBeAg. The positive predictive value of HBsAg > or = 0.05 and HBsAg > or = 1 IU/ml at birth were 18.64% and 70% respectively, and were 73.33% and 100% one month after birth. CONCLUSIONS: Infants with HBsAg > or = 1 IU/ml at birth should be suspicious of failure on blocking HBV mother-to-infant transmission and it should be more credible if the infant has HBsAg > or = 1 IU/ml one month after birth. How to improve the blocking rate of neonates who were positive of HBsAg at birth and one month after birth should be the focus of our future research.

Boundaries between subsegments IVa and IVb in the human liver.

Until now there has been no definitive anatomical study of the boundary between hepatic subsegments IVa and IVb. In this study, we used a multicolor segmental corrosion cast technique and a multicolor segmental technique on plastinated slices, in combination with helical CT three-dimensional (3D) reconstruction on 15 donated fresh isolated human liver specimens. The corrosion cast technique was carried out on eight of these specimens, and the remaining seven livers were used to make horizontal plastinated slices. Examination of these specimens and observation of 20 additional liver corrosion cast specimens showed that all boundaries between hepatic segments were complex, undulating scissures rather than simple, flat planes. We also found that there was an obvious boundary between subsegments IVa and IVb, such that subsegment IVa laid posterosuperior to subsegment IVb. A tributary of a hepatic vein passed through the boundary between subsegments IVa and IVb, and could serve as an anatomical landmark of this boundary.

[Spectrophotometric determination of azithromycin by charge transfer reaction].

The charge transfer interactions of Azithromycin and 7,7,8,8-tetracyanoquinodimethane (TCNQ) or chloranilic acid (CL) were investigated by spectrophotometry. The apparent molar absorptivity of TCNQ complex is 2.7 x 10(4) L x mol(-1) x cm(-1) at 743 nm, and 5.0 x 10(4) L x mol(-1) x cm(-1) at 842 nm; and that of CL complex is 2.4 x 10(3) L x mol(-1) x cm(-1). Beers law is obeyed in the concentration range of 0-30 mg x L(-1) for TCNQ method, and 5-225 mg x L(-1) for CL method. The relative standard deviations of the two methods are 1.0% and 1.4% (n = 6), respectively. The composition of complex of Azithromycin with 7,7,8,8-tetracyanoquinodimethane or chloranilic acid is 1 : 2. This proposed method has been applied to the determination of Azithromycin in tablets with satisfactory results.

[Multi-slice spiral CT using spinal structure assessment in elderly patients with osteoporosis].

OBJECTIVE: To explore the clinical value of 64-slice spiral CT for spinal structure assessment in elderly patients with osteoporosis. METHODS: The computed radiography (CR) films and 64-slice spiral CT isotropic scanning images of 40 patients who had been diagnosed as osteoporosis by dual-energy X-ray absorptiometry (DXA) were retrospectively analyzed. The patients were divided into two groups according to their T-scores by DXA: group A (T-score was -1.0 - (-2.5)); and B group (T-score was below -2.5). RESULTS: The diagnostic results of axial CT images combined with multi-planar reconstruction (MPR) was negatively correlated with the measurement results of DXA in the diagnosis of spinal osteoporosis, and such correlation was higher in group B than in group A. Compared with CR films, axial CT images combining with MPR showed superior effectiveness in the diagnosis of osteoporosis. CONCLUSIONS: 64-slice spiral CT is better than CR in diagnosis of osteoporosis. CT-MPR and 3D reconstruction not only can be used to diagnose osteoporosis early, but also to observe the changes of skeleton's shape and overall structure.