Preparation of high-performance monoazo disperse dyes bearing ester groups based on benzisothiazole and their dyeing performance on polyester fabrics.

To obtain high-performance disperse dyes, a series of azo disperse dyes containing different kinds of ester groups based on benzisothiazole were synthesized by the coupling reaction of diazotization of 3-amino-5-nitro [2,1] benzisothiazole with N-substituted aniline compounds bearing different ester moieties. The structures of the synthesized dyes were evaluated using Fourier transform infrared spectroscopy (FT-IR), nuclear magnetic resonance techniques (1H-NMR), and MS analysis. UV-Vis spectrophotometry methods were applied to study absorption maxima, molar extinction coefficients, and solvatochromic behaviors of the dyes, and time-dependent density functional theory (TD-DFT) simulations were applied to reveal the nature of the absorption spectrum properties. Polyester fabrics were colored using a high-temperature dyeing method under pressure, and the dyed fabrics exhibited deep and bright intense blue hues. In addition, excellent fastness properties, including washing fastness, sublimation fastness, rubbing fastness, and light fastness, were achieved.

An Innovative Preauricular Free Flap Pedicled with Retrograde Vascular (PFFPRV) for Pediatric Nasal Reconstruction.

SUMMARY: Nasal reconstruction in pediatric patient is very challenging and it requires consideration of later nasal development. Herein, we introduce an innovative preauricular free flap pedicled with retrograde vascular (PFFPRV) for pediatric nasal reconstruction. In this PFFPRV technique, the retrograde superficial temporal vessels were used as the flap pedicle. The lateral alar artery and angular vein were used as vessels of the nasal recipient zone. The flap vessels were anastomosed directly to the recipient area vessels without additional vessel transplantation. Eight pediatric patients with nasal defects underwent this operation. All patients were followed up for more than 2 years. Patients' medical history data were retrospectively analyzed. Preoperative and postoperative facial photos were compared and analyzed. The satisfaction of patient's parents with the aesthetic results was assessed. All patients were successfully operated without intraoperative complications. None of the procedures required additional blood vessel grafts. One patient developed a vascular crisis the next day after the surgery and underwent vascular exploration operation. The free flaps of all patients survived without wound infection or necrosis. The color difference of flap gradually became unobvious. The transplanted flap did not show obvious contracture or retraction, and the nose was symmetrical and developed well. The parents of all patients were satisfied with the surgical results. We think this PFFPRV technique can be a reasonable alternative strategy for reconstruction of pediatric nasal defect, with no adverse effect on nasal development and no need of vascular transplantation. LEVEL OF EVIDENCE: Level IV, therapeutic study.

PFKFB3 Increases IL-1ß and TNF-α in Intestinal Epithelial Cells to Promote Tumorigenesis in Colitis-Associated Colorectal Cancer.

Colorectal cancer (CRC) is significantly correlated with inflammatory bowel disease, which usually manifests as chronic relapsing-remitting colitis. Phosphofructo-2-kinase/fructose-2,6-biophosphatase 3 (PFKFB3) can catalyze to produce fructose-2,6-bisphosphate and function as an oncogene. In this study, we revealed the function of PFKFB3 in colitis-associated CRC (CAC) and the potential mechanism. RT-qPCR and Western blot were utilized to detect the level of PFKFB3 expression. Increased PFKFB3 expression was observed in the mouse CAC model and CAC patient samples. We identified that overexpression of PFKFB3 in intestinal epithelial cells (IECs) could increase the proliferation, migration, and invasion of CRC cells by the coculture system. Mechanistically, overexpression of PFKFB3 induced phospho-p65 and promoted the expression of IL-1ß and tumor necrosis factor alpha (TNF-α) in the development of colitis and CAC. In addition, PFK158, the PFKFB3 inhibitor, could reduce the CRC cell viability, migration, and invasion caused by PFKFB3 overexpression. In conclusion, overexpression of PFKFB3 promoted tumorigenesis in CAC by inducing phospho-p65 and expression of IL-1ß and TNF-α. Our study suggested that PFKFB3 acted as a potential treatment target for CAC.

Comprehensive transcriptome analysis of colorectal cancer risk of hyperglycemia in humans.

BACKGROUND: Epidemiological studies have found that hyperglycemia, is an independent risk factor for colorectal cancer (CRC), increasing colon cancer incidence and affecting the recurrence, metastasis, and prognosis in colon cancer patients. However, the intercorrelation between hyperglycemia and CRC risk is still unknown, In the present study, we sought to determine whether gene markers, which act in CRC with hyperglycemia, are silenced in CRC without hyperglycemia. METHODS: In order to characterize the mechanism of functional genes associated with CRC with hyperglycemia, A total 24 CRC and matched controls were sequenced. Through bioinformatics analysis includes differential expression analysis, functional enrichment, new isoform prediction and alternative splicing event identification to found biomarker genes related to CRC development. RESULTS: CRC patients with hyperglycemia were compared with patients without hyperglycemia, and we found that 21 genes were upregulated and 27 were downregulated. Further study showed that these genes are possibly of key genes involved in CRC development with hyperglycemia, such as mannan-binding lectin-associated serine protease 3 (MASP3), which has an immunological role in the activation of the complement system. Based on our comprehensive analysis, a cis-regulatory network for hyperglycemic CRC was reconstructed. CONCLUSIONS: Protein-protein interactions revealed the mechanisms of molecules involved in the interaction of hyperglycemia and cancer development. Our results provide further information on the metabolic pathway interaction with cancer pathways and elucidated the mechanisms of hyperglycemic factors function in cancer development from a transcriptomic perspective.

Role of glucose metabolism related gene GLUT1 in the occurrence and prognosis of colorectal cancer.

Colorectal cancer (CRC) ranks the third most commonly diagnosed cancer in males and the second in females worldwide. However, the functional and causal SNPs for CRC remain to be mined. Glucose transporter 1 (GLUT1), a pivotal rate-limiting element in the transport of glucose in malignancy cells, has been identified to be associated with many cancers. Here, we aim to explore the role of GLUT1 in the occurrence and prognosis of colorectal cancer in a Chinese population. We found that GLUT1 expression levels in CRC tumor tissues were significantly higher than those in the corresponding adjacent normal tissues, and Cox multivariate analysis demonstrated that the GLUT1 expression was an independent prognostic factor for CRC (HR = 2.11, 95% CI = 1.33-3.34, P=0.001). For a functional polymorphism of GLUT1 (rs710218), we found that individuals with TT genotype (OR = 1.68, 95% CI = 1.02-2.75, P = 0.041) or AT genotype (OR = 1.47, 95% CI = 1.09-1.99, P = 0.012) of rs710218 had a significantly increased risk of CRC compared to those with AA homozygote. These findings strongly suggest that glucose metabolism related gene GLUT1, and its functional SNP, rs710218 might contribute to CRC susceptibility and prognosis, and the exact biological mechanism awaits further research.

Platelet activation and the protective effect of aprotinin in hepatolithiasis patients.

OBJECTIVE: To explore platelet activation and the protective effect of aprotinin in patients with hepatolithiasis. METHODS: The count of platelets and levels of CD62P and CD63 were measured by flow cytometry in 38 patients with hepatolithiasis. Several measurements were carried out after treatment with aprotinin. RESULTS: The levels of CD62P, CD63 in patients with hepatolithiasis were higher than those in patients with cholecystolithiasis (P<0.05), but the count of platelets was lower (P<0.05). After operation, the levels of CD62P, CD63 were significantly increased in patients with hepatolithiasis, but the count of platelets was lower (P<0.05). Postoperative levels of CD62P, CD63 were significantly lower in patients treated with aprotinin than in normal controls (P<0.05); but there was no significant change in the count of platelets in the two groups. CONCLUSION: Platelet activation occurs in patients with hepatolithiasis, and may be inhibited by aprotinin.

[Study of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptotic and inflammatory gene expressions in colon cancer cell line].

OBJECTIVE: To study the effect of recombinant tumor necrosis factor-related apoptosis-inducing ligand(TRAIL) on the expression of apoptosis and inflammatory related genes in human colon cancer cell line HCT-116. METHODS: After 24-hour treatment with recombinant human TRAIL protein, the expressions of apoptosis-related genes(Bcl-2, Bad, caspase-3, and caspase-8) and inflammation-related genes(TNF-α, IL-1ß, and COX-2) were measured by real-time PCR and appropriate kits in HCT-116. RESULTS: After treatments of 10 µg/L and 100 µg/L recombinant human TRAIL proteins, the apoptotic rates of HCT-116 cells were 27.4% and 45.9%, respectively. Expressions of anti-apoptosis gene Bcl-2, pro-apoptosis gene Bad and apoptotic markers caspase-3 and caspase-8 were significantly up-regulated, which was more significant in the group of 100 µg/L treatment(P<0.05). Moreover, after TRAIL treatments, expressions of inflammation-related genes TNF-α, IL-1ß, COX-2 were also dramatically increased, and 100 µg/L treatment group showed higher up-regulation(P<0.05). CONCLUSIONS: Recombinant TRAIL protein induces both apoptosis and inflammation of human colon cancer cells.