Effects of water chemistry on microfabric and micromechanical properties evolution of coastal sediment: A centrifugal model study.

Water chemistry alteration induced strength weakening of natural sediment, which leads to the differential settlement of infrastructures in coastal areas, has caused numerous disasters and engineering failures. To thoroughly understand the underlying mechanisms of how water chemistry influences the microfabric and mechanical properties evolution of coastal sediments, herein, the authors adopted centrifuge test, X-ray diffraction (XRD), and atomic force microscope (AFM) to quantitatively study the structure anisotropy index (i.e., orientation index (OI)), micromorphological property (i.e., root mean square height (Sq)), and micromechanics (i.e., microscale apparent modulus) of clay sediments in different water chemistry conditions and gravity gradients. The results show that the change rule of OI is: OIsaline > OIalkaline > OIwater > OIacid, along the vertical sedimentary depth. Randomly distributed clay flocs and loose flocculated soil skeleton (mainly consisted by edge-to-face (EF) and edge-to-edge (EE) contact of the kaolinite platelets) are associated with the acidic water chemical conditions. The action of supergravity and face-to-face (FF) repulsive contact mode lead to high degree of anisotropy of kaolinite sediments in alkaline environment. Clay platelets are compacted closely under the synergetic effect of centrifugal pressure and prevailing van der Waals attraction (reduction of electric double layer repulsion) in saline environment. The change of 1/Sq is highly consistent with the change of OI at different depths in different water chemical environments. Along the sedimentary depth (i.e., transition from the normal gravity (1 g) to supergravity (8000 g)), the microscale apparent modulus of kaolinite sediment was found to be the highest in alkaline environment. As the water chemistry changes from alkaline to acidic, however, the microscale apparent modulus of kaolinite aggregate decreased, and it showed the smallest in the saline environment.

CCNB1 and CCNB2 involvement in the pathogenesis of psoriasis: a bioinformatics study.

OBJECTIVE: The cell cycle-related proteins cyclin B1 (CCNB1) and cyclin B2 (CCNB2) are potentially involved in the underlying mechanisms of psoriasis. The present study aimed to explore this possibility using bioinformatics approaches. METHODS: CCNB1 and CCNB2 protein levels were evaluated in 14 psoriasis patients and five healthy controls by enzyme-linked immunosorbent assays, and their mRNA levels were evaluated using data from four publicly available datasets (GSE53552, GSE41664, GSE14905, and GSE13355). Comparison of high- and low-expressing groups were performed to reveal CCNB1- and CCNB2-related differentially expressed genes, which were then assessed based on gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. Correlation analyses between CCNB1 and CCNB2 levels and immune infiltration, as well as typical targets of psoriasis, were also performed. RESULTS: Overall, 12 CCNB1 and CCNB2 common immune-related targets potentially involved in psoriasis were identified. These could regulate the cell cycle of through multiple pathways. In addition, CCNB1 and CCNB2 were found to potentially support the release of key molecular targets of psoriasis through the regulation of mast cell activation and macrophage polarization. CONCLUSIONS: These findings suggest that CCNB1 and CCNB2 may represent valuable molecular biomarkers of psoriasis, contributing to its onset and progression.

Crystal transformation and self-assembly theory of microbially induced calcium carbonate precipitation.

Microbially induced calcium carbonate precipitation (MICP) is ubiquitous in the earth's lithosphere and brings the inspiration of bionic cementation technology. Over recent years, MICP has been proposed as a potential solution to address many environmental and engineering issues. However, the stability of cemented precipitations generated via MICP technology, especially the characteristics and change mechanism of crystal forms, is still unclear, which substantially hindered the understanding of biomineralization and prohibited the application and upscaling of MICP technology. Here, Sporosarcina pasteurii was selected as a model microbe to induce calcium carbonate mineralization in a series of standard nutrient solutions. The authors studied the process of precipitation from amorphous calcium carbonate to calcite crystal form and revealed the assembly behavior and mechanism of precipitations by FTIR, SEM, TEM and EDS. In the two crystal forms of induced calcium carbonate, the relative position and content of C, O, N, P and Ca elements were only slightly different. The molecular attachment and structural match of organic matrix made the crystals form change. Finally, a self-assembly theory was proposed to MICP, and it provided a solid theoretical basis for the technical specification of MICP technology in engineering application. KEY POINTS: • Organic matrix is intensively involved in MICP by forming functional groups. • Molecular attachment and structural match cause calcite crystal evolution. • A self-assembly theory is proposed for MICP.

Rigidified Cavitand Hosts in Water: Bent Guests, Shape Selectivity, and Encapsulation.

We report the synthesis and characterization of two water-soluble container compounds (cavitand hosts) with rigidified open ends. One cavitand uses four (CH2)4's as spacers to bridge the adjacent walls, while another cavitand uses four CH2CH2OCH2CH2's bridges and features a wider open end. The spacers preorganize the deep cavitands into vase-like, receptive shapes and prevent their unfolding to the unreceptive kite-like conformation. Cycloalkane guests (C6-C8) and small n-alkanes (C5-C7) form 1:1 complexes with the cavitands and move freely in the cavitands' spaces. Hydrophilic compounds 1,4-dioxane, tetrahydrofuran, tetrahydropyran, pyridine, and 1-methylimidazole also showed good binding affinity to the new cavitands. Longer alkanes (C11-C14) and n-alcohols (C11-C16) are taken up with a -CH3 group fixed at the bottom of the cavity and the groups near the rim in compressed conformations. The methylene bridges appear to divide the cavitand into a narrow hydrophobic compartment and a broader space with exposure to the aqueous medium. Longer alkane guests (C15-C18), N,N-dimethyldioctylammonium, and dioctylamine induce the formation of capsules (2:1 host:guest complexes). The new cavitands showed selectivity for p/m-cresol isomers and xylene isomers. The cavitand with CH2CH2OCH2CH2 bridges bound long-chain α,ω-diols (C13-C15) and diamines in folded, U-shaped conformations with polar functions exposed to the aqueous medium. It was used to separate o-xylene from its isomers by using simple extraction procedures.

Icariin protects cardiomyocytes against ischaemia/reperfusion injury by attenuating sirtuin 1-dependent mitochondrial oxidative damage.

BACKGROUND AND PURPOSE: Icariin, a major active ingredient in traditional Chinese medicines, is attracting increasing attention because of its unique pharmacological effects against ischaemic heart disease. The histone deacetylase, sirtuin-1, plays a protective role in ischaemia/reperfusion (I/R) injury, and this study was designed to investigate the protective role of icariin in models of cardiac I/R injury and to elucidate the potential involvement of sirtuin-1. EXPERIMENTAL APPROACH: I/R injury was simulated in vivo (mouse hearts), ex vivo (isolated rat hearts) and in vitro (neonatal rat cardiomyocytes and H9c2 cells). Prior to I/R injury, animals or cells were exposed to icariin, with or without inhibitors of sirtuin-1 (sirtinol and SIRT1 siRNA). KEY RESULTS: In vivo and in vitro, icariin given before I/R significantly improved post-I/R heart contraction and limited the infarct size and leakage of creatine kinase-MB and LDH from the damaged myocardium. Icariin also attenuated I/R-induced mitochondrial oxidative damage, decreasing malondialdehyde content and increasing superoxide dismutase activity and expression of Mn-superoxide dismutase. Icariin significantly improved mitochondrial membrane homeostasis by increasing mitochondrial membrane potential and cytochrome C stabilization, which further inhibited cell apoptosis. Sirtuin-1 was significantly up-regulated in hearts treated with icariin, whereas Ac-FOXO1 was simultaneously down-regulated. Importantly, sirtinol and SIRT1 siRNA either blocked icariin-induced cardioprotection or disrupted icariin-mediated mitochondrial homeostasis. CONCLUSIONS AND IMPLICATIONS: Pretreatment with icariin protected cardiomyocytes from I/R-induced oxidative stress through activation of sirtuin-1 /FOXO1 signalling.

Simvastatin reverses cardiomyocyte hypertrophy via the upregulation of phosphatase and tensin homolog expression.

The aim of the present study was to investigate the effects of simvastatin on the protein kinase B (PKB) signaling pathway and the expression of phosphatase and tensin homolog (PTEN). The effects of simvastatin were analyzed by administering the drug orally to male spontaneously hypertensive rats (SHRs) at a dose of 10 mg/kg/day, while the control animals received an equal volume of saline. The systolic pressure (mmHg) of the rat tail artery was measured prior to the initiation of the experiment, and once a week until the end of the experiment. At the end of the experiment, the animals were euthanized and the hearts were removed. The left ventricular and interventricular septum were weighed, after which the left ventricular mass/body mass ratio was calculated. In addition, cardiomyocytes isolated from Sprague Dawley rats were cultured with 15% fetal bovine serum to induce hypertrophy, following which the cells were treated with different doses of simvastatin. The in vitro effects were assessed by measuring the surface area of the cardiomyocytes, while the rate of protein synthesis was measured using a 3H-leucine incorporation assay and western blot analyses. Simvastatin was demonstrated to inhibit cardiomyocyte hypertrophy in the in vivo and in vitro experiments. Notably, simvastatin increased PTEN expression and inhibited PKB expression in the SHR model, as well as in the cardiomyocytes in culture. In addition, the use of PTEN antisense oligodeoxynucleotides was revealed to inhibit the effects of simvastatin on cardiomyocytes. Therefore, these results indicated that simvastatin was able to reverse cardiomyocyte hypertrophy in vivo and in vitro, possibly by increasing the expression of PTEN.

[Effects of glutamine induced heat shock protein 70 overexpression on atrial fibrosis and connexin 43 remodeling in isoprenaline-treated rats].

OBJECTIVE: To explore the effects of glutamine (Gln) induced heat shock protein 70(Hsp70) overexpression on atrial fibrosis and connexin 43 remodeling in isoprenaline(ISO)treated rats and related mechanisms. METHODS: Forty male SD rats were randomly divided into five groups (n = 8 each group): control group, DMSO group, ISO 5 mg×kg(-1)×d(-1) group (Fibrosis group), ISO 5 mg×kg(-1)×d(-1) + Ala-Gln 0.75 mg×kg(-1)×d(-1) group (Intervention group) and ISO 5 mg×kg(-1)×d(-1) + QUE 100 mg× kg(-1)×d(-1) + Ala-Gln 0.75 mg×kg(-1)×d(-1) + DMSO group (QUE group).Rats were killed after 7 d. The AngII expression in myocardial tissue was detected by radioimmunoassay; myocardial fibrosis was observed by HE staining.Collagen volume fractions were quantified by Masson staining and as the indicators of atrial fibrosis. The expressions of Hsp70, p-JNK1/2/3, c-Jun and Cx43 were determined with immunohistochemical method. RESULTS: AngII content was similar between the control group [(68.51 ± 10.76) pg/L] and DMSO [(71.47 ± 11.49) pg/L] group (P > 0.05), and significantly increased in fibrosis group [(211.25 ± 49.49) pg/L], intervention group [(185.32 ± 54.85) pg/L] and QUE [(189.90 ± 42.12) pg/L] group (P < 0.01 vs. control group). Atrial fibrosis was significantly higher in the fibrosis group [(29.485 ± 9.966)%] and QUE group [(25.060 ± 8.581)%] but not in the intervention group [(7.861 ± 1.867)%] compared to control group [(6.842 ± 1.674)%] and DMSO group [(7.108 ± 1.343)%]. The expression of Hsp70 was similar among the control group (0.160 ± 0.023), DMSO group (0.163 ± 0.022), fibrosis group (0.166 ± 0.028) and QUE (0.168 ± 0.027) group (P > 0.05) while significantly upregulated in the intervention group (0.215 ± 0.018) (P < 0.01 vs. control group). The expressions of p-JNK1/2/3 and c-Jun were similar between control group (0.151 ± 0.016;0.163 ± 0.022) and DMSO group (0.154 ± 0.021;0.164 ± 0.024)(P > 0.05), while significantly upregulated in fibrosis group (0.202 ± 0.025; 0.254 ± 0.044) and QUE group (0.196 ± 0.024; 0.251 ± 0.027) (P < 0.01 vs. control group) but not in intervention group (0.160 ± 0.025; 0.168 ± 0.024)were not changed obviously (P > 0.05 vs. control group). The content of Cx43 was similar between control group and DMSO group (0.231 ± 0.035 vs. 0.220 ± 0.032, P > 0.05), and was linearly distributed in intercalated disc of the cardiomyocytes, however, the content of Cx43 was significantly reduced (P < 0.01) and the Cx43 distribution was disordered in fibrosis group (0.163 ± 0.013) and QUE group (0.165 ± 0.024), while these changes were not found in intervention group. CONCLUSION: Glutamine could reduce the atrial fibrosis and Cx43 remodeling in isoprenaline-treated rats by up-regulating Hsp70 and inhibiting JNK signaling pathway activation through down-regulating p-JNK1/2/3 and c-Jun expression.

[Study of mechanical irritation effects in workers exposed to rock wool].

OBJECTIVE: To explore the effects of mechanical irritation to the skin, eyes, and upper respiratory tract in workers exposed to rock wool. METHODS: The gravimetric concentration of total dust and number concentration of fibre in the air of the rock wool workplace were determined . 109 rock wool manufacturing and processing workers were taken as the exposed group, 104 workers from an air separation plant, a papermaking plant and cover making plant were served as control group. All subjects accepted the questionnaire interview and clinical examination of the skin, eyes, nose and the pharynx. RESULTS: 10.1% of the exposed group had the irritant contact dermatitis, which showed linear trend with the current gravimetric concentration of total dust (P < 0.05) but no association with the exposure age (P > 0.05), and the detection rate of conjunctivitis of the exposed group (12.8%) was significantly higher than the control group (2.8%) (P < 0.05). The percentages of shin and eye itching symptoms of the exposed group (54.1% and 42.9%) were significantly higher than the control group (11.5% and 26.5%) (P < 0.05), but the differences among/between the exposed subgroups with different exposure level and different exposure age were not statistically significant (P > 0.05). The differences of the detection rate of chronic rhinitis and chronic pharyngitis and the percentages of the symptoms of nose and pharynx between the exposed group and control group were not statistically significant (P > 0.05), except the rhinorrhea symptom. CONCLUSIONS: Occupational exposure to rock wool had some degree of the mechanical irritation effects on the skin and eyes. The current exposure level of total dust should be emphatically controlled.

[Effects of valsartan and U0126 on atrial fibrosis and connexin40 remodeling in rats].

OBJECTIVE: To explore the effects of valsartan and MEK1/2 inhibitor U0126 on atrial fibrosis and connexin40 (Cx40) remodeling in rats treated with isoproterenol (ISO). METHODS: 32 male SD rats were randomly divided into control group (A), ISO (5 mg · kg(-1) · d(-1) for 7 days) + DMSO group (B), ISO + U0126 (0.5 mg · kg(-1) · d(-1) for 28 days) group (C, U0126 was dissolved in DMSO), ISO + valsartan (30 mg · kg(-1) · d(-1) for 28 days) + DMSO group (D). Rats were sacrificed after 28 days. The AngIIcontent in myocardial tissue was measured by radioimmunoassay, P-MEK1/2, P-ERK1/2 and Cx40 was detected by immunohistochemistry, atrial fibrosis was determined on HE and Masson stained heart sections. RESULTS: The content of AngII was significantly higher in group B, C and D compared with group A [(368.243 ± 6.283) ng/L, (357.175 ± 5.944) ng/L, (359.908 ± 2.496) ng/L vs (250.380 ± 4.261) ng/L, P < 0.01]; the degree of atrial fibrosis was significantly lower in group C and D compared with group B [CVF(10.260 ± 0.525)%, (10.238 ± 0.524)% vs (78.710 ± 1.587)%, P < 0.01] while there was no atrial fibrosis in group A [CVF(9.025 ± 0.456)%]; the expression of P-MEK1/2 and P-ERK1/2 was significantly upregulated in group B compared with group A (P-MEK1/2: 0.311 ± 0.007 vs 0.203 ± 0.009, P < 0.01; P-ERK1/2: 0.259 ± 0.003 vs 0.173 ± 0.006, P < 0.01) and significantly lower in group C and D compared with group B (P-MEK1/2: 0.212 ± 0.004, 0.213 ± 0.005 vs 0.311 ± 0.007, P < 0.01, P-ERK1/2: 0.178 ± 0.004, 0.175 ± 0.007 vs 0.259 ± 0.003, P < 0.01). The content of Cx40 was obviously reduced and the distribution of Cx40 was disordered in group B compared with A (0.199 ± 0.007 vs 0.241 ± 0.004, P < 0.01) which could be partly reversed in group C and D (0.239 ± 0.037, 0.235 ± 0.006 vs 0.199 ± 0.007, P < 0.01). All parameters in group C and D were similar (P > 0.05). CONCLUSION: The chronically elevated AngII content in myocardium may be related to atrial fibrosis and Cx40 remodeling in this model, valsartan and U0126 were equivalent on attenuating atrial fibrosis and Cx40 remodeling by inhibiting ERK pathways at different levels.

[Relationship between radiosensitivity of nasopharyngeal carcinoma and MDR1 gene polymorphism].

OBJECTIVE: To investigate the relationship between human multidrug resistancel gene (MDR1) polymorphisms and the radiosensitivity of nasopharyngeal carcinoma (NPC). METHODS: Blood samples were collected from 59 NPC patients, who were devided into radiosensitive or radioresistant groups according to their responses to radiation therapy. The genotypes for MDR1 polymorphisms (G2677T in exon 21 and C3435T in exon 26) and their haplotypes were determined by PCR and restriction fragment length polymorphism analysis. The results were further confirmed by sequencing. RESULTS: The 3435CC genotype was associated with a significantly better response to radiotherapy than combined 3435 CT and TT genotype (P=0.026). The 2677GG genotype was also associated with a better response in comparison with combined 2677 GT and TT genotype, but this relation was not statistically significant. Patients with 2677G-3435C haplotype had a significant better response to radiotherapy than those with the other haplotypes (P=0.017). CONCLUSION: The MDR1 G2677T and C3435T polymorphisms may help predict the response to radiotherapy in NPC patients.

[Assessment of radiation-induced liver injury with computed tomography].

OBJECTIVE: To review the appearance of radiation-induced liver injury on computer tomography for quantitative assessment of dosimetric changes in different radiological reactions and the influence of time-effect. METHODS: The focal liver reactions of 35 patients treated with three-dimensional conformal radiation therapy (3-D CRT) for liver malignancies were evaluated, with the applied doses of 36-65 Gy in 4-28 fractions completed in 8-41 days. All patients received nonenhanced CT scan and arterial-dominant phase contrast-enhanced CT scan 1-6 months after therapy. The liver tissue density in irradiated and nonirradiated liver was compared, and the reaction type and the threshold dose determined radiologically. RESULTS: On at least one follow-up examination, 51.4% of patients were found to have a focal radiation reaction in the liver. The radiation reaction was hypodense in 43.75% of the follow-up nonenhanced CT examinations and in 19.23% of arterial-dominant phase contrast-enhanced CT scans. It was hyperdense in 42.31% of arterial-dominant phase contrast-enhanced CT scans. The median threshold dose inducing a radiation reaction was 30.8 Gy (range 18-42.8 Gy). The detected threshold dose was positively correlated with the time of detection of the reaction (P=0.041), with a correlation coefficient of -0.473. On arterial-dominant phase contrast-enhanced CT scans, the threshold dose was significantly higher for hyperdense than for hypodense changes (P=0.017). In additional follow-up, the reaction volume decreased and the reaction types changed on arterial-dominant phase contrast-enhanced CT scans. CONCLUSIONS: The threshold dose can be different in different radiological reaction types on multiphase CT scans. The detected threshold dose is inversely correlated with the time of detection of the early reaction. Multiphase contrast-enhanced CT is helpful to distinguish radiation reactions from recurrent tumors.

[Three-dimensional conformal hypofractionated radiotherapy for brain metastases of non-small-cell lung carcinoma: implications for whole brain irradiation].

OBJECTIVE: To evaluate the therapeutic effect of of whole brain irradiation (WBI) in the treatment of brain metastases of non-small-cell lung carcinoma and analyze the factors affecting the patients' survival. METHODS: Ninety-three cases of brain metastases of non-small-cell lung carcinoma receiving radiotherapy between January 1998 and February 2004 were retrospectively reviewed. Of these patients, 68 were treated with three-dimensional conformal hypofractionated radiotherapy (3D-CRT) following WBI, while the other 25 underwent 3D-CRT alone. Kaplan-Meier method was used to analyze the survival rate and local control rate, and Cox proportional hazards model employed for determining prognostic factors influencing the patients' survival. RESULTS: The overall median actuarial survival of the patients was 14 months in the 3D-CRT+WBI group with 1- and 2-year actuarial survival rates of 50% and 27%, respectively, showing no significant difference from 3D-CRT group, which had a median survival of 11 months and 1- and 2-year survival rates of 45% and 15% (P=0.502, log-rank test). Actuarial 1-year local control rate in 3D-CRT+WBI group was 90% as compared to 70% in 3D-CRT group (P=0.028, log-rank test). In multivariate analyses, active extracranial disease (P=0.002) and Karnofsky Performance Scale score (P=0.034) were identified as the independent prognostic factors for the patients' survival. CONCLUSION: WBI prior to 3D-CRT does not benefit the patients with brain metastases of non-small cell lung carcinoma for their survival, but may help improve the local control rate.

[Effects of simvastatin on the left ventricular hypertrophy in spontaneously hypertensive rats and its relationship with the expression of protein kinase B].

OBJECTIVE: To investigate the effects of simvastatin on left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs) and its possible mechanism. METHODS: Sixteen male SHRs were randomly divided into 2 equal groups: treatment group and SHR control to be given simvastatin or glucose-normal saline by oral gavage for 10 weeks. Eight Wistar-Kyoto (WKY) rats were given normal saline as normal controls. Blood pressure was measured before the experiment and then once every week after the beginning of experiment. By the end of the experiment the rats were killed and their hearts were taken out to measure the left ventricle weight/body weight. RT-PCR was used to detect the mRNA expression of atrial natriuretic peptide (ANP) and of protein kinase B (PKB) in myocardium. Western blotting was used to examine the protein expression of PKB. RESULTS: (1) The systolic blood pressure of the SHR normal control and treatment groups were 221 mm Hg +/- 10 mm Hg and 217 mm Hg +/- 8 mm Hg respectively (P > 0.05) and the systolic pressure of the normal control group was 126 +/- 6 mm Hg, significantly lower than those of the 2 SHR groups (both P < 0.01). (2) The LVW/BW values of the SHR control group were 3.04 mg/g +/- 0.12 mg/g, 3.73 mg/g +/- 0.08 mg/g, and 4.10 mg/g +/- 0.13 mg/g in the normal control group, SHR treatment group and SHR control group respectively with significant difference between any 2 groups (all P < 0.01). (3) The mRNA expression levels of ANP were 0.44 +/- 0.33, 0.27 +/- 0.03, and 0.17 +/- 0.33 in the SHR control group, SHR treatment group, and normal control group respectively (P < 0.01 or P < 0.05). (4) The mRNA expression levels of PKB were 0.45 +/- 0.05, 0.32 +/- 0.03, and 0.19 +/- 0.02 in the SHR control group, SHR treatment group, and normal control group respectively (P < 0.01 or P < 0.05). CONCLUSION: Simvastatin reverses LVH and myocyte phenocyte transformation in the SHRs with the possible mechanism of decreasing the expression level of PKB.

Three-dimensional conformal radiotherapy versus intracavitary brachytherapy for salvage treatment of locally persistent nasopharyngeal carcinoma.

PURPOSE: To compare the outcomes of three-dimensional conformal radiotherapy (3D-CRT) and intracavitary brachytherapy (ICBT) as salvage treatment for locally persistent nasopharyngeal carcinoma. METHODS AND MATERIALS: Between March 1994 and November 2001, a total of 117 patients with locally persistent nasopharyngeal carcinoma received salvage treatment for 2-8 weeks (median, 4 weeks) after a full course of conventional external beam RT. Of the 117 patients, 54 were salvaged with 3D-CRT (3D group) and 63 with ICBT (BT group). No statistically significant differences were found in the patient characteristics between the two groups (p >0.05). In the 3D group, the planning target volume for 3D-CRT was defined as the persistent disease plus a 5-mm margin; three to seven static conformal coplanar or noncoplanar portals were delivered for each fraction. The median salvage dose was 24 Gy (range, 18-38 Gy), with fraction size of 2.0 Gy/d. In the BT group, a median salvage dose of 20 Gy (range, 15-30 Gy) was delivered with a (192)Ir source, at 5 Gy/fraction, twice weekly. The brachytherapy dose was prescribed at a distance of 1 cm from the center of the surface as defined by the sources, irrespective of the extent of persistent disease. The actuarial rates of survival were estimated using the Kaplan-Meier method. Potential differences in the actuarial outcomes between groups were evaluated using the Mantel log-rank test. Multivariate analyses were performed with the Cox regression proportional hazards model. RESULTS: The 5-year actuarial rates of overall survival, disease-specific survival, and local failure-free survival for the 3D group and BT group were 64.50% vs. 55.78% (p = 0.33), 70.03% vs. 59.56% (p = 0.11), and 88.93% vs. 76.28% (p = 0.07), respectively. Subgroup analysis showed that the 5-year actuarial local failure-free survival rate of patients with initially diagnosed T3-T4 disease for the 3D group and BT group was 84.01% vs. 60.50% (p = 0.03). The incidence of Grade 3-4 late complications was comparable between the two groups. Multivariate analyses performed in the whole group showed that T stage at initial diagnosis and the salvage technique (3D-CRT or ICBT) were the statistically significant, independent prognostic factors for local failure-free survival (p = 0.00 and p = 0.02, respectively). CONCLUSION: 3D-CRT seemed to provide better local control than ICBT as a salvage treatment for locally persistent nasopharyngeal carcinoma, especially in patients with initially diagnosed T3-T4 disease. CT/MRI evaluation of the extent of persistent disease is recommended for technique selection of salvage RT. Patients should be cautioned about the potentially increased complications. The optional time for salvage treatment remains controversial.

[Value of integrated positron-emission tomography and computed tomography in gross tumor volume delineation for radiotherapy for bone metastasis].

OBJECTIVE: To evaluate the role of integrated positron-emission tomography and computed tomography (PET/CT) in gross tumor volume (GTV) delineation for three-dimensional conformal radiotherapy for bone metastasis. METHODS: Three patients with multiple bone metastases were enrolled in this study, whose primary tumors were pathologically identified as lung cancer, liver cancer and renal cell carcinoma. In each case, 6 sites of bone metastases were selected, labeled as BM1 to BM6 which located in the lumbar, thoracic vertebra, rib, ilium, scapula and thighbone respectively. The GTVs of the 6 bone metastases were delineated on the CT scans for treatment planning by 8 radiation oncologists, and the results were compared with the delineation obtained on the basis of integrated CT and PET/CT for analyzing the interobserver variability. RESULTS: For BM1-5 with obvious bone cortex lesions by the carcinoma, the GTV delineated on the basis of CT was greater than that derived from PET/CT (P<0.05), whereas for BM6 with intact bone cortex, the contrary result was observed (P<0.05). For any of these bone metastasis, the interobserver variability in GTV delineation with PET/CT was less than that with CT. CONCLUSION: PET/CT is useful for improving the accuracy of GTV delineation for the protection of the normal tissues during radiotherapy.

[Effects of chelerythrine on cell proliferation and p27 expression of cardiac fibroblasts modulated by arginine vasopressin].

OBJECTIVE: To study the effects of chelerythrine, a protein kinase C (PKC) inhibitor, on the cell proliferation and p27 expression of cardiac fibroblasts (CFs) modulated by arginine vasopressin (AVP) and to investigate the intracellular signal transduction mechanisms of AVP in CFs. METHODS: The cultured CFs of neonatal Sprague-Dawley rats were divided into 3 groups: AVP group (10(-7) mol/L AVP was added into the culture), chelerythrine group (10(-6) mol/L chelerythrine and 10(-7) mol/L AVP were added into the culture), and control group. MTT assay was used to evaluate the cell proliferation. The cultured cells were collected and propidium iodide was used to label the DNA so as to identify the cell cycle. Specific mouse-versus-rat p27 protein monoclonal antibody and fluorescein isothiocyanate-labeled secondary antibody were added into the cell suspension to label the p27 protein in the cells. Flow cytometry was used to determine the distribution of cell cycles and p27 expression. RESULTS: (1). The A value of CFs measured by MTT assay in AVP + chelerythrine group was 0.32 +/- 0.01, significantly lower than that of the AVP group (0.39 +/- 0.01, P < 0.01). (2). The percentage of CFs in S stage was 4.4% +/- 1.7% in the AVP + chelerythrine group, lower than those of the AVP group (15.5% +/- 1.4%, P < 0.01) and control group (7.5% +/- 1.0%). The PI of CFs was 20.9% +/- 1.2% in the AVP + chelerythrine group, significantly lower than that of the AVP group (31.4% +/- 1.5%, P < 0.01). The PI of the AVP group was significantly lower than that of the control group (26.0% +/- 1.0%, P < 0.01). The percentage of CFs in G(0)/G(1) stage was 79.1% +/- 1.2% in the AVP + 1 chelerythrine group, significantly higher than that in the AVP group (68.6% +/- 1.5%, P < 0.01). The percentage of CFs in G(0)/G(1) stage in the AVP group was significantly lower than that in the control group (74.0% +/- 1.0%, P < 0.01) too. (3). The expression rate of p27 protein was 91.7% +/- 2.2% in the AVP + chelerythrine group, significantly higher than that in the AVP group (63.3% +/- 1.9%, P < 0.01). CONCLUSION: PKC inhibitor remarkably reverses the CFs proliferation and p27 downregulation induced by AVP. It may be involved in the intracellular signal transduction pathway of AVP in CFs.