Macrophages, which have functions of engulfing and digesting foreign substances, can clear away harmful matter, including cellular debris and tumor cells. Based on the condition of the internal environment, circulating monocytes give rise to mature macrophages, and when they are recruited into the tumor microenvironment and in suitable conditions, they are converted into tumor-associated macrophages (TAMs). Generally, macrophages grow into two main groups called classically activated macrophages (M1) and alternatively activated macrophages (M2). M2 and a small fraction of M1 cells, also known as TAMs, not only lack the function of phagocytizing tumor cells but also help these tumor cells escape from being killed and help them spread to other tissues and organs. In this review, we introduce several mechanisms by which macrophages play a role in the immune regulation of tumor cells, including both killing factors and promoting effects. Furthermore, the targeted therapy for treating tumors based on macrophages is also referred to in our review. We confirm that further studies of macrophage-focused therapeutic strategies and their use in clinical practice are needed to verify their superior efficacy and potential in cancer treatment.

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The synthesis and characterization, including crystallographic analysis, of the bifunctional boranes RCHdC[B(C 6 F 5 ) 2 ] 2 (R ) t-C 4 H 9 , 1a; C 6 H 5 , 1b; C 6 F 5 , 1c) by regioselective hydroboration of the corresponding 1-boraalkynes using HB(C 6 F 5 ) 2 are reported herein. Compounds 1a and 1b have been screened as cocatalysts for ethylene polymerization in the presence of Cp 2 ZrMe 2 (3) under a variety of conditions. NMR spectroscopic studies indicate that Cp 2 -Zr[η 2 -Bu t CtCB(C 6 F 5 ) 2 ] (4a), Cp 2 ZrMe(C 6 F 5 ), the organoborane Me 2 BC 6 F 5 , and methane gas are the final products formed from reaction of 1a with 3 in toluene solution at room temperature. The stoichiometric mechanism for this transformation has been elucidated through variable-temperature NMR studies. Complex 4a and MeB(C 6 F 5 ) 2 (7) were prepared independently and screened as ethylene polymerization catalysts and cocatalysts, respectively. Compound 4a is inactive for ethylene polymerization, either alone or in the presence of additional 1a. However, the combination of Cp 2 ZrMe 2 and 7 gives rise to the species [Cp 2 ZrMe] + [Me 2 B(C 6 F 5 ) 2 ] -(8), which although unstable at room temperature in solution (decomposing over a period of 60 min to give Cp 2 ZrMe(C 6 F 5 ) and the organoborane Me 2 -BC 6 F 5 ), is active for ethylene polymerization. From a comparison of activity and MW data, it is concluded that the putative ion pairs formed from 1a (or 1b) and 3 lack sufficient thermal stability at conventional polymerization temperatures and that the polymerization activity observed can be interpreted as arising from species 8.

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Although it is well known that Cr underlayers sputter deposited on glass or NiP/Al substrates have either the (002) or (110) textures, the mechanism of the formation of the crystallographic textures is not clear. A model is proposed for the formation of the crystallographic texture of sputter-deposited Cr thin films. A systematic set of experiments has been carried out to test the model. It was found that the (110) texture, which is usually found in Cr thin films deposited on substrates without preheating, can form at elevated temperatures (250 °C) when deposited at low Ar pressure or by applying substrate bias. The initial stage of the texture formation was also investigated by using very thin Cr films. It was found that the (002) texture can be initiated directly on the substrate surface, while the (110) texture appears not to form directly on substrate surface, but rather as a result of film growth. The proposed model is consistent with the experimental results.

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Histone deacetylase 6 (HDAC6) contributed to the pathogenesis of rhabdomyolysis-induced acute kidney injury (AKI) and selective inhibition of HDAC6 activity may be a promising strategy for the treatment of AKI. Compound 23BB as a highly selective HDAC6 inhibitor was designed, synthesized by our lab and exhibited therapeutic potential in various cancer models with good safety. However, it remained unknown whether 23BB as a drug candidate could offer renal protective effect against rhabdomyolysis-induced AKI. In the present study, we investigated the effect of 23BB in a murine model of glycerol (GL) injection-induced rhabdomyolysis. Following GL injection, the mice developed severe AKI as indicated by acute renal dysfunction and histologic changes, accompanied by increased HDAC6 expression in the cytoplasm of tubular epithelial cells. Pharmacological inhibition of HDAC6 by 23BB pretreatment significantly reduced serum creatinine and serum blood urea nitrogen (BUN) levels as well as attenuated renal tubular damage in GL-injured kidneys. HDAC6 inhibition also resulted in reduced TdT-mediated dUTP nick-end labeling (TUNEL)-positive tubular cells, suppressed BAX, BAK, cleaved caspase-3 levels, and preserved Bcl-2 expression, indicating that 23BB exerted potent renoprotective effects by the regulation of tubular cell apoptosis. Moreover, GL-induced kidney injury triggered multiple signal mediators of endoplasmic reticulum (ER) stress including GRP78, CHOP, IRE1α, p-eIF2α, ATF4, XBP1, p-JNK, and caspase-12. Oral administration of 23BB improved above-mentioned responses in injured kidney tissues and suggested that 23BB modulated tubular cell apoptosis via the inactivation of ER stress. Overall, these data highlighted that renal protection of novel HDAC6 inhibitor 23BB is substantiated by the reduction of ER stress-mediated apoptosis in tubular epithelial cells of rhabdomyolysis-induced AKI.

Roxithromycin inhibits the pulmonary inflammatory response and airway mucus hypersecretion induced by LPS. The inhibitory effect of roxithromycin on airway mucus hypersecretion may be mediated through reduction of NF-kappaB activation, neutrophil infiltration and release of inflammatory cytokines in the lung.