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Objective To compare the difference between volume computed tomography dose index (CTDIvol) and size-specific dose estimates (SSDE) in evaluating the radiation dose of abdominal CT scan.Methods Abdominal CT scan were performed on 180 patients with a Philips 256-slices spiral CT.The anterior-posterior dimension (AP) and lateral dimension (LAT) of each patients were measured at the level of left renal vein, and the effective diameter (ED) and SSDE were calculated with recorded CTDIvol Patients were categorized into 3 groups depending on body mass index (BMI): group A, BMI ＜ 20.0 kg/m2;group B, 20.0-24.9 kg/m2;group C, BMI ＞ 24.9 kg/m2.The differences between CTDIvoland SSDE of 180 patients and three different BMI groups were compared respectively.Results There was a significant difference between CTDIvol and SSDE of the 180 patients (t =-13.354, P ＜ 0.01), CTDIvol and SSDE were (9.91 ± 2.91) and (14.01 ± 2.82) mGy, respectively.For group A, CTDIvol and SSDE were (7.96 ± 1.83) and (12.83 ± 2.52) mGy, respectively (t =-8.417, P ＜ 0.01).Group B, CTDIvol and SSDE were (9.28 ± 1.76) and (13.62 ±2.18) mGy, respectively (t =-15.051, P ＜ 0.01).Group C, CTDIvol and SSDE were (12.19 ± 3.65) and (15.39 ± 3.47) mGy, respectively (t =-4.535, P ＜ 0.01).In addition, the mean percentage values of difference between CTDIvol and SSDE for the three groups were 62.83％, 47.80％, 28.40％, respectively, which meant CTDIvol underestimated the radiation dose compared to SSDE.With the BMI increasing, the values of difference between CTDIvol and SSDE decreased.Conclusions SSDE can be used to estimate the radiation dose of abdominal CT scan for a given size person.
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Purpose To investigate 1H-MRS in differentiating intracranial lymphoma from tumor-like demyelinating lesions. Materials and Methods Thirty-three cases of intracranial lymphoma confirmed by pathology and 18 cases of tumor-like demyelinating lesions confirmed by pathology or clinic were recruited in this study. Imaging data including single-voxel (TE=144 ms) 1H-MRS was retrospective analyzed. The Cho/Cr and Cho/NAA area ratios were calculated. The lipid and lactate peak was visually categorized into 5 grades based on the ratio of Lip-Lac peak to the height of the Cr peak. 1H-MRS findings of the intracranial lymphoma and the tumor-like demyelinating lesions were compared. The differentiation of the two diseases diagnosed by 1H-MRS and conventional MR were evaluated by use of receiver operating characteristic curves. Results There were significant difference of Cho/Cr, Cho/NAA ratio and Lip-Lac peak level between the intracranial lymphoma and tumor-like demyelinating lesions (P2.56, Cho/NAA ratio was>1.71, and Lip-Lac peak grade was>3. Cho/Cr, Cho/NAA ratio and Lip-Lac peak grade were found higher in atypical intracranial lymphomas when compared with those of tumor-like demyelinating lesions. The area under the receiver operating characteristic curve of conventional MR was increased from 0.827 to 0.870 when Cho/NAA ratio was added for analysis in the 28 uncertain cases. Conclusion 1H-MRS has great clinical significance for differentiating intracranial lymphoma from tumor-like demyelinating lesions. The values of Cho/Cr ratio>2.56, Cho/NAA ratio>1.71 and Lip-Lac grade >3 suggest intracranial lymphoma rather than TDLs. When the conventional MR imaging features can not do the differentiation, Cho/NAA ratio is a useful complement.
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Objective To explore the neuroprotective role of Genistein (GEN) on hippocampal CA1 neurons and the possible mechanism following global cerebral ischemia ( GCI) in rats.Methods Seventy five rats were subjected to global cerebral ischemia ( GCI ) by four-vessel occlusion and randomly divided into five groups , sham, ischemia/reperfusion (I/R), GEN, ICI 182,780 and vehicle groups.Fluoro-Jade B and neuron-specific nuclear-binding protein ( NeuN) staining was used to observe CA 1 neuronal survival .TUNEL was used to detect apoptotic neurons .Spatial learning and memory function of the rats were evaluated by Morris water maze .Results The best dose of neuroprotective role of GEN was 1.0mg/kg body weight.Compared with sham, TUNEL-positive neurons in the hippocampal CA1 region increased significantly in I/R and vehicle groups (P<0.01), while post-treatment with GEN (1.0mg/kg) at 5min after ischemia by tail vein injection decreased markedly (P<0.01).Treatment of 1.0mg/kg GEN markedly attenuated spatial learning and memory deficits of the rats after ischemic insult compared to I /R group.Furthermore, ICI 182,780 significantly abolished the neuroprotective role of GEN (P <0.01).Conclusion The low-dose (1.0mg/kg) GEN significantly attenuates neuronal damage and cognitive deficits following GCI in rats , and the mechanism may be involved in estrogen receptor activity.
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<p><b>OBJECTIVE</b>To investigate the distribution and expression of transforming growth factor beta (TGF-β) receptors I and II, p38 mitogen-activated protein kinase (p38 MAPK), and type I and type III collagen in the lungs of rats with silicosis and cultured pulmonary fibroblasts, and to investigate the relationship of the anti-fibrosis effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) with its inhibition of TGF-β receptor-mediated p38 MAPK pathway activity.</p><p><b>METHODS</b>Rats were randomly divided into control group, silicosis model group, and AcSDKP treatment group (n = 10 for each group). For the model group and AcSDKP treatment group, rats were intratracheally instilled with silica to establish a silicosis model. Cultured pulmonary fibroblasts from neonatal rats were divided into control group, TGF-β1 stimulation group, TGF-β receptor inhibition group, p38 MAPK pathway inhibition group, and AcSDKP treatment group. The protein expression of TGF-β receptors I and II, p38 MAPK, and type I and type III collagen were determined by immunohistochemistry and Western blot. The mRNA expression of TGF-β receptors I and II were determined by real-time PCR. The distribution and nuclear translocation of phospho-p38 MAPK in cultured fibroblasts were determined by laser scanner confocal microscopy.</p><p><b>RESULTS</b>In the AcSDKP treatment group, AcSDKP reduced the expression of TGF-β receptors I and II, phospho-p38 MAPK, and type I and type III collagen to 86.12%, 41.01%, 42.63%, 89.05%, and 52.71%, respectively, of those of the silicosis model group (P < 0.05). In cultured fibroblasts, AcSDKP reduced the mRNA expression of TGF-β receptors I and II to 42.26% and 54.33%, respectively, of those of the TGF-β1 stimulation group; the protein expression of TGF-β receptors I and II, phospho-p38 MAPK, and type 1 and type III collagen was reduced to 58.14%, 51.40%, 45.6%, 58.04%, and 44.74%, respectively, of those of the TGF-β1 stimulation group. The phospho-p38 MAPK translocation from plasma to the nucleus was also inhibited; the nucleus/plasma ratio of p38 MAPK and the protein expression of type I and type III collagen were reduced to 68.60%, 58.04%, and 44.74%, respectively, of those of the TGF-β stimulation group (P < 0.05).</p><p><b>CONCLUSION</b>AcSDKP can inhibit the expression of collagen through inhibition of TGF-β receptor-mediated p38 MAPK pathway activity, and is thus able to exert anti-fibrosis effect in rats with silicosis.</p>
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Animals , Male , Rats , Cells, Cultured , Collagen , Metabolism , Disease Models, Animal , Fibroblasts , Metabolism , MAP Kinase Signaling System , Oligopeptides , Pharmacology , Protein Serine-Threonine Kinases , Metabolism , Rats, Wistar , Receptors, Transforming Growth Factor beta , Metabolism , Silicosis , Metabolism , Transforming Growth Factor beta , Metabolism , p38 Mitogen-Activated Protein Kinases , MetabolismABSTRACT
Objective To assess the validity of transanal local excision for stage Ⅰ low rectal carcinoma.Methods The clinical data of 93 patients with stage Ⅰ low rectal carcinoma who underwent transanal excision (group A,n=45)or radical resection(group B,n=48)were retrospectively analyzed.Twenty-four T1 patients and 21 T2 patients in group A received postoperative adjuvant radiation therapy and adjuvant chemoradiotherapy,respectively.All patients in group B received radical surgery only.The 5-year survival rates,recurrence rates,and postoperative complications between the 2 groups were compared.Results The 5-year survival rates were 100%(24/24)for T1 patients,86%(18/21)for T2 patients in group A,and 100%(18/18)for T1 patients,93%(28/30)for T2 patients in group B,with no significantly statistical difference between the 2 groups(P＞0.05).The recurrence rates were 4%(1/24)for T1 patients,19%(4/21)for T2 patients in group A,and 0(0/18)for T1 patients,7%(2/30)for T2 patients in group B,with no significance between the 2 groups(P＞0.05).The incidence of postoperative complications in group A was 2%(1/45),which was significantly lower than that of 15%(7/48))in group B(P＜0.05).Conclusions Transanal local excision of early low rectal carcinoma,combined with postoperative chemotherapy for T1 patients or chemoradiotherapy for T2 patients, results in a low complication rate and good sphincter function,and provides satisfactory local control and 5-year survival rates.
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Objective To investigate the level of MEF2C phosphorylation (activation) and protein expression, and to further clarify the possible mechanism following ischemia-reperfusion in hippocampal CA1 region of rat. MethodsBrain ischemia was induced by four-vessel occlusion in SD rats. Protein level was determined by Western blotting. Results MEF2C was significantly activated with a peak at 6 h of reperfusion, but its protein expression decreased in late phase of reperfusion (3～5 d). The elevation of activated (17 ku) and the inactivated forms (32 ku) of caspase-3 proteases were remarkable during 1～5 d of reperfusion. In addition, Ac-DEVD-CHO, a specific inhibitor of caspase-3, up-regulated MEF2C protein level of 3 d reperfusion. SB202190 (an inhibitor of P38), but not ERK5-antisense oligonucleotides, not only inhibited MEF2C activation of 6 h reperfusion but also apparently prevented the increase of caspase-3 activation caused by 3 d reperfusion. Conclusion P38/caspase-3 mediated MEF2C pathway may function in the injuries of hippocampal CA1 region of rats following ischemia/reperfusion.