Experimental study on the effects of different exposure conditions and contrast agent concentrations on spectral computed tomography virtual non-contrast images.

Background: The early diagnosis of thrombosis and fat embolism is important for subsequent treatment regimens. Spectral computed tomography (CT) virtual non-contrast (VNC) scanning can not only accurately diagnose thrombosis and medium fat embolism but can also reduce the radiation dose and scanning time. However, there is a relative paucity of studies on what contrast concentration and exposure conditions are best for the quality of VNC images. To address this issue, this study aimed to investigate the effects of different exposure conditions and contrast concentrations on the quality of VNC images of low-density substances in spectral CT. Methods: Four solution groups [i.e., groups A (15 mgI/mL), B (10 mgI/mL), C (5 mgI/mL), and D (the control group)] were matched with normal saline and contrast agent groups. Four groups of solution, duck blood clots, and fat were injected into four sections of the pig large intestine, respectively. CT scans with different exposure amounts were performed under the condition of 120 KV. Comparing the true non-contrast (TNC) image based on solution D group with the VNC images of the other three solution groups. The differences in the CT values, standard deviation (SD) values, and contrast noise ratio (CNR) values of the duck blood and fat under different iodine concentrations and exposures were compared. The image quality was evaluated using a three-point method and the Kappa consistency test was performed. The consistency of the tissue CT values in the TNC and VNC images was analyzed by drawing Bland-Altman scatter plots. Results: The CT values of the duck blood in the VNC20mAs and VNCC groups were lower than those in the TNC groups (P<0.05). Under different exposures and contrast agent concentrations, the CT value of the fat in the VNC group was higher than that in the TNC group (P<0.05). The SD values of the duck blood and fat in three groups (i.e., groups A, B, and C) were lower than those in the TNC group (P<0.05). The CNR value of the duck blood in the VNC20mAs group was lower than that in the TNC group (Z=-2.10, P=0.04), and the CNR values of the duck blood and fat in the VNC group were higher than those in the TNC groups in the remaining different exposure and concentration groups (P<0.05). The CT values of the lesions in the two groups were consistent, and there were no statistically significant differences between the subjective scores of the TNC and VNC images (z=-1.34, P=0.18); the subjective evaluations of the two physicians had good consistency (K=0.80). Conclusions: Under the conditions of higher contrast agent concentrations and proper exposure conditions, the VNC images were better able to restore the CT values of the blood clots, reduce the SD values of the blood clots and fat. In addition, and improve the CNR values of the blood clots and fat. In addition, the quality of the two images was similar.

CD9 is critical for cutaneous wound healing through JNK signaling.

Cutaneous injury triggers a cascade of signaling events essential for wound re-epithelialization. CD9, a cell-surface protein, has been implicated in a number of cellular processes by coupling to intracellular signaling; however, its exact role in wound healing remains unidentified. We reported that CD9 was downregulated in migrating epidermis, and reelevated to basal level when re-epithelialization was completed. Although low level of CD9 appears to be required for normal wound healing, a significant healing delay was found in CD9-null mice, with wounds gaping wider on day 5 and day 7 post wounding. Further analysis showed that re-epithelialization was adversely affected in CD9-null mice, due to impaired migration of epidermis. Notably, CD9 deficiency caused a persistent enhancement of C-JUN NH2 terminal kinase (JNK) signaling primarily in migrating epidermis with abnormal elevation of matrix metalloproteinase (MMP)-9 detected in CD9-null wounds, leading to excessive degradation of type IV collagen, and thus a defective basement membrane at the wound site. JNK suppression reduced MMP-9 production and therefore ameliorated the healing delay with the appearance of significantly elongated migrating epidermis in CD9-null mice. Our study demonstrated the importance of CD9 in wound re-epithelialization, linking this molecule directly to basement membrane formation and epidermal migration through participating in the regulation of the JNK/MMP-9 pathway.

Improvement of barrier function and stimulation of colonic epithelial anion secretion by Menoease Pills.

AIM: Menoease Pills (MP), a Chinese medicine-based new formula for postmenopausal women, has been shown to modulate the endocrine and immune systems. The present study investigated the effects of MP and one of its active ingredients, ligustrazine, on epithelial barrier and ion transport function in a human colonic cell line, T84. METHODS: Colonic transepithelial electrophysiological characteristics and colonic anion secretion were studied using the short circuit current (ISC) technique. RT-PCR was used to examine the expression of cytoplasmic proteins associated with the tight junctions, ZO-1 (zonula occludens-1) and ZO-2 (zonula occludens-2). RESULTS: Pretreatment of T84 cells with MP (15 microg/mL) for 72 h significantly increased basal potential difference, transepithelial resistance and basal ISC. RT-PCR results showed that the expressions of ZO-1 and ZO-2 were significantly increased after MP treatment, consistent with improved epithelial barrier function. Results of acute stimulation showed that apical addition of MP produced a concentration-dependent (10-5,000 microg/mL, EC50 = 293.9 microg/mL) increase in ISC. MP-induced ISC was inhibited by basolateral treatment with bumetanide (100 micromol/L), an inhibitor of the Na+-K+-2Cl- cotransporter, apical addition of Cl- channel blockers, diphenylamine-2, 2'-dicarboxylic acid (1 mmol/L) or glibenclamide (1 mmol/L), but not 4, 4'-diisothiocyanostilbene-2, 2'-disulfonic acid or epithelial Na+ channel blocker, amiloride. The effect of MP on ZO-1 and ZO-2 was mimicked by Ligustrazine and the ligustrazine-induced ISC was also blocked by basolateral application of bumetanide and apical addition of diphenylamine-2, 2'-dicarboxylic acid or glibenclamide, and reduced by a removal of extracellular Cl-. CONCLUSION: The results of the present study suggest that MP and lligustrazine may improve epithelial barrier function and exert a stimulatory effect on colonic anion secretion, indicating the potential use of MP and its active ingredients for improvement of GI tract host defense and alleviation of constipation often seen in the elderly.

Effect of tetramethylpyrazine on exocrine pancreatic and bile secretion.

AIM: To investigate the effect of tetramethylpyrazine (ligustrazine, TMP) on the secretion of exocrine pancreas (and biliary). METHODS: In in vivo study, we investigated the effect of TMP on the secretion of pancreatic-bile juice (PBJ) in rats. Using human pancreatic duct cell line, CAPAN-1, combined with the short-circuit current (ISC) technique we further studied the effect of TMP on the pancreatic anion secretion. RESULTS: Administration of TMP (80 mg/kg, i.p.) significantly increased the secretion of PBJ (P<0.05), but the pH of PBJ and the secretion of pancreatic protein were not significantly affected. Basolateral addition of TMP produced a dose-dependent increase in ISC (EC50=1.56 mmol/L), which contained a fast transient ISC response followed by a slow decay. Apical application of Cl- channel blockers, DPC (1 mmol/L), decreased the response by about 67.1% (P<0.001), whereas amiloride (100 micromol/L), a epithelial sodium channel blockers, had no effect. Removal of extracellular HCO3- abolished TMP-induced increase in ISC by about 74.4% (P<0.001), but the removal of external Cl- did not. Pretreatment with phosphodiesterase inhibitor, IBMX(0.5 mmol/L), decreased the TMP-induced ISC by 91% (P<0.001). CONCLUSION: TMP could stimulate the secretion of PBJ, especially pancreatic ductal HCO3- secretion via cAMP or cGMP-dependent pathway. It need further study to investigate the roles of cAMP or cGMP in the effect of TMP on the secretion of exocrine pancreas.