The use of anti-biofouling polymers has widespread potential for counteracting marine, medical, and industrial biofouling. The anti-biofouling action is usually related to the degree of surface wettability. This review is focusing on anti-biofouling polymers with special surface wettability, and it will provide a new perspective to promote the development of anti-biofouling polymers for biomedical applications. Firstly, current anti-biofouling strategies are discussed followed by a comprehensive review of anti-biofouling polymers with specific types of surface wettability, including superhydrophilicity, hydrophilicity, and hydrophobicity. We then summarize the applications of anti-biofouling polymers with specific surface wettability in typical biomedical fields both in vivo and in vitro, such as cardiology, ophthalmology, and nephrology. Finally, the challenges and directions of the development of anti-biofouling polymers with special surface wettability are discussed. It is helpful for future researchers to choose suitable anti-biofouling polymers with special surface wettability for specific biomedical applications.

Background: The nephrotoxicity induced by cisplatin (DDP) has been a severe obstacle for its clinical use in anticancer treatment. The apoptosis and inflammation induced by DDP are the main causes of the nephrotoxicity. Transient receptor potential ankyrin 1 (TRPA1) is a non-selective cation ligand-gated channel that is involved in the inflammation progress. Methods: The apoptosis, inflammation, MAPK/NF-κB signaling pathway, and TRPA1 expression were assessed after HEK293 cells had been induced by DDP, and the role of TRPA1 in apoptosis and inflammation of DDP-induced HEK293 cells treated with TRPA1 antagonist HC-030031 was also evaluated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), flow cytometry, and western blot assays. Results: The cell viability was reduced by DDP in both a time-dependent and dose-dependent manner with a minimal cytotoxic concentration of 10 μM. Moreover, DDP induced an enhancement of the apoptosis and inflammation in a dose-dependent manner, as indicated by the increase of the relative protein level of cleaved-caspase3 (cleaved-cas3), the cleavage product of caspase-3 substrate poly-ADP-ribose polymerase (cleaved-PARP) and inducible nitric oxide synthase (iNOS), and the messenger RNA (mRNA) expression level of interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), and interferon-γ (INF-γ). Additionally, DDP treatment increased the protein phosphorylation expression of IKKβ, JNK, ERK, and p38 in a dose-dependent manner, which was antagonized by the treatment of NF-κB-specific inhibitor BAY 11-7082 and pan-MAPK inhibitor U0126. It was also found that DDP upregulated the expression of TRPA1 at both the mRNA and protein levels in a dose-dependent manner. Besides, block of TRPA1 with HC-030031 relieved the apoptosis, diminished the level of IL-1β, IL-6, TNF-α, and INF-γ, reduced the level of cleaved-cas3, cleaved-PARP, and iNOS, decreased the p-IKKβ, p-JNK, p-ERK, and p-p38 expression, and enhanced the expression of IκBα. Conclusions: Taken together, these results indicate that TRPA1 regulates DDP-induced nephrotoxicity via inflammation mediated by the MAPK/NF-κB signaling pathway in HEK293 cells.

Background: Isoniazid (INH), rifampicin (RMP), pyrazinamide (PZA), and ethambutol (EMB) are the four most common drugs for the first-line treatment of tuberculosis (TB). Although chemotherapy drugs are widely used in the treatment of TB, and achieved good results, but the side effects, especially anti-tuberculosis drug-induced liver injury (ATDILI), cannot be overlooked. Many researchers have made efforts to uncover the association of cytochrome P450 (CYP) enzyme genetic polymorphisms with ATDILI. In this study, we systematically reviewed and meta-analyzed the relationship between CYP polymorphism and susceptibility to ATDILI. Methods: We carried out literature searches of PubMed, Ovid, the Cochrane Library, Web of Science and Chinese National Knowledge Infrastructure (CNKI). Medical Subject Headings (MeSH) terms including “cytochrome P450 enzyme”, “drug-induced liver injury”, “polymorphism”, “tuberculosis”, and “hepatotoxicity” were used as keywords for our searches. Results: The pooled odds ratio (OR) of all studies for CYP2E1 to the risk of ATDILI was 1.18 [95% confidence interval (CI): 0.82–1.71]. The articles in this meta-analysis were observed to be mildly heterogeneous. Further subgroup analysis revealed that the patients who receiving a four-drug protocol (INH + RIF + PZA + EMB) or three-drug protocol (INH + RIF + PZA) regimens showed a higher risk of ATDILI than those who receiving INH alone. However, subgroup analyses according to participants’ ethnic origin, study type, and the definition of ATDILI produced no statistically significant results. Associations between other genes in the CYP family and ATDILI were indistinct and equivocal. Discussion: Our meta-analysis has uncovered an association between CYP2E1 RsaI/PstI polymorphisms and ATDILI, especially among patients who receive a four-drug (INH + RIF + PZA + EMB) or three-drug (INH + RIF + PZA) anti-TB treatment regimen.

Antifouling technologies have attracted considerable attention in recent years, as numerous fouling phenomena pertaining to inorganic, organic, bio-, and composite foulants substantially affect daily life. Poly(dimethyl siloxane) (PDMS) has several practical applications; however, it possesses limited resistance to inorganic, organic, or biofoulants such as proteins or bacteria. Among the antifouling strategies reported thus far, antifouling induced by surface wettability (AFISW) is an exceptional strategy with considerable potential. It presents numerous advantages such as a physical working mechanism, eco-friendliness, and facile material fabrication process. To achieve AFISW, PDMS can be modified with several nanomaterials to tune its surface wettability to meet antifouling requirements. This article presents a systematic review of the existing research on AFISW in PDMS to achieve improved antifouling performance. Specifically, we first provide a background on fouling, focusing on the different types of fouling and antifouling mechanisms. Then, we provide a comprehensive review of AFISW based on four types of surface wettability, namely, superhydrophilicity, hydrophilicity, hydrophobicity, and superhydrophobicity. Finally, we discuss suitable AFISW strategies for different types of fouling mechanisms based on PDMS and its nanocomposites. This review will help researchers design and fabricate various polymeric materials and their nanocomposites with tailored surface wettability for AFISW applications.

Background: Cisplatin has been a vital drug used for tumor treatment because of its excellent effect on numerous malignant solid cancers. Nonetheless, its nephrotoxicity is non-negligible in clinical practice. This study aims to provide a new understanding of the molecular mechanism of transient receptor potential ankyrin 1 (TRPA1) in cisplatin-induced renal apoptosis. Methods: We evaluated the effect on apoptosis, TRPA1 expression, and intracellular calcium concentration of human kidney 2 (HK-2) cells induced by diamminedichloroplatinum (DDP). Additionally, we also assessed DDP-induced apoptosis, the expression of Bax, caspase3, cleaved-cas3, p53, Bcl-2 and intracellular calcium concentration combined with HC-030031 and/or pifithrin-α. The effect of FK506 on apoptosis of HK-2 cells induced by DDP and the expression of the nuclear factor of activated T cells (NFAT) protein treated with HC-030031, pifithrin-α, and/or FK506 were also explored. Results: The results showed that apoptosis, TRPA1 expression, and intracellular calcium concentration of HK-2 cell induced by DDP were enhanced in a dose-dependent manner. HC-030031 and pifithrin-α relieved apoptosis, and intracellular calcium concentration and the expression of NFAT and phospho-NFAT (p-NFAT) were induced by DDP. HC-030031 combined with pifithrin-α further aggravated the above-mentioned tendency, including relieved apoptosis, intracellular calcium concentration, and NFAT and p-NFAT expression. HC-030031 and FK506 decelerated the apoptosis, and NFAT and p-NFAT expression of HK-2 cells was induced by DDP, while simultaneous treatment with HC-030031 and FK506 further decreased apoptosis and protein expression. However, the expression of Bcl-2 increased when HC-030031, pifithrin-α, or FK506 was used alone, and HC-030031 combined with pifithrin-α or FK506 further improved the expression of Bcl-2. Conclusions: TRPA1 mediates cisplatin-induced apoptosis in renal tubular cells via the calcineurin-nuclear factor of activated T-cells-p53 signaling pathway.

Background: The most serious and common complication of the medication recommended by World Health Organization (WHO) for tuberculosis (TB) is anti-tuberculosis drugs-induced hepatotoxicity (ATDH). Pregnane X receptor (PXR) is a key factor of ATDH, while Hepatocyte nuclear factor 4α (HNF4α) and hepatocyte nuclear factor 4 alpha-antisense-1 (HNF4α-AS1) may have co-regulating relationship with PXR. This study aimed to explore whether the genetic variants of HNF4α and HNF4α-AS1 are associated with the predisposition of ATDH. Methods: TB patients diagnosed in West China Hospital between December 2014 and April 2018 were enrolled. TagSNPs in HNF4α and HNF4α-AS1 gene from the samples of the patients were genotyped with a custom-designed 2×48-plex SNP Scan^TM Kit. The frequencies of the alleles, genotypes, genetic models and haplotype distribution of the variants were compared between the case and control groups. The association between SNP and ATDH risk was assessed by single factor logistic regression. Results: Logistic regression analysis showed that none of the 15 genetic variants in HNF4α and HNF4α-AS1 genes were significantly associated with susceptibility to ATDH in the Chinese Han population after Bonferroni correction. Conclusions: A challenge has arisen to the promising application of SNPs in the HNF4α and HNF4α-AS1 genes as genetic markers for ATDH, and further study is needed with a larger sample size.