N′-(2-Bromo-5-hy­droxy-4-meth­oxy­benzyl­idene)-3,5-dihy­droxy­benzo­hydrazide methanol monosolvate

In the crystal structure of the title compound, C15H13BrN2O5·CH3OH, the methanol solvent mol­ecule links symmetry-related mol­ecules through O—H⋯O and N—H⋯O hydrogen bonds. Further inter­molecular O—H⋯O hydrogen bonds link symmetry-related mol­ecules, leading to the formation of a three-dimensional network. Two of the H atoms involved in hydrogen bonding are disordered. The dihedral angle between the rings is 5.64 (14)°

Curcumin Blocks Small Cell Lung Cancer Cells Migration, Invasion, Angiogenesis, Cell Cycle and Neoplasia through Janus Kinase-STAT3 Signalling Pathway

Curcumin, the active component of turmeric, has been shown to protect against carcinogenesis and prevent tumor development. However, little is known about its anti-tumor mechanism in small cell lung cancer (SCLC). In this study, we found that curcumin can inhibit SCLC cell proliferation, cell cycle, migration, invasion and angiogenesis through suppression of the STAT3. SCLC cells were treated with curcumin (15 µmol/L) and the results showed that curcumin was effective in inhibiting STAT3 phosphorylation to downregulate of an array of STAT3 downstream targets ,which contributed to suppression of cell proliferation, loss of colony formation, depression of cell migration and invasion. Curcumin also suppressed the expression of proliferative proteins (Survivin, Bcl-XL and Cyclin B1), and invasive proteins (VEGF, MMP-2, MMP-7 and ICAM-1).Knockdown of STAT3 expression by siRNA was able to induce anti-invasive effects in vitro. In contrast, activation of STAT3 upstream of interleukin 6 (IL-6) leads to the increased cell proliferation ,cell survival, angiogenesis, invasion, migration and tumor growth. Our findings illustrate the biologic significance of IL-6/JAK/STAT3 signaling in SCLC progression and providenovel evidence that the pathway may be a new potential target for therapy of SCLC. It was concluded that curcumin is a potent agent in the inhibition of STAT3 with favorable pharmacological activity,and curcumin may have translational potential as an effective cancer therapeutic or preventive agent for SCLC

Decreased Dicer expression elicits DNA damage and up-regulation of MICA and MICB

RNA interference (RNAi) acts constitutively to silence the innate immune response, and innate immunity genes are misregulated in Dicer-deficient Caenorhabditis elegans. Here, we show that inhibition of Dicer expression by RNAi in human cells up-regulates major histocompatibility complex class I–related molecules A and B (MICA and MICB). MICA and MICB are innate immune system ligands for the NKG2D receptor expressed by natural killer cells and activated CD8(+)T cells. We reveal that knockdown of Dicer elicits DNA damage. Up-regulation of MICA and MICB by Dicer knockdown is prevented by pharmacologic or genetic inhibition of DNA damage pathway components, including ataxia telangiectasia mutated (ATM) kinase, ATM- and Rad3-related kinase, or checkpoint kinase 1. Therefore we conclude that up-regulation of MICA and MICB is the result of DNA damage response activation caused by Dicer knockdown. Our results suggest that RNAi is indirectly linked to the human innate immune system via the DNA damage pathway

Effect of lens opacity on retinal oxygen saturation in patients with diabetic cataract

AIM: To investigate the effect of crystal turbidity on retinal oxygen saturation in patients with diabetic cataract. METHODS:This was a cross-sectional study. Totally 68 patients with 68 eyes of diabetic cataract admitted to our hospital from June 2017 to December 2017 were selected as subjects. Retinal oximetry was used to measure the blood oxygen saturation of the retinal veins, veins, and their supraorbital, nasal, subnasal, and infraorbital branches. The objective scatter index(OSI)of the eye was measured by Visual Quality Analysis System II, and the degree of opacity of the lens was graded according to OSI. RESULTS:The blood oxygen saturation of the retinal artery and its branches in this group were 101.39%±10.84%, 106.19%±11.40%, 103.22%±10.91%, 102.36%±20.31%, and 101.29%±13.88%, respectively. The oxygen saturation of the retinal vein and its branches were 62.51%±8.95%, 66.37%±10.74%, 64.81%±8.97%, 58.37%±13.85%, and 58.66%±19.94%, respectively. The difference between arteriovenous oxygen saturation was 40.72%±12.08%. In this group of patients, 68 patients with 68 eyes had an OSI value of 4.21±3.14. Among them, 15 eyes were turbid at the first stage, 14 eyes were turbid at level 2, 23 eyes were turbid at level 3, and 16 eyes were turbid at level 4. Pearson correlation analysis showed that the retinal veins, veins and their branches were negatively correlated with OSI(both PPPPP>0.05). There was no significant difference in the difference of arteriovenous oxygen saturation between the patients with different degrees of lens opacity(P>0.05).CONCLUSION: In patients with diabetic cataract, when the degree of lens opacity is 1 to 3, the degree of abnormality of retinal blood oxygen metabolism is not obvious. When the degree of lens opacity reaches 4, the blood oxygen saturation of the retinal veins, veins and their branches will decrease

4-[5-(4-Pyrid­yl)-1,3,4-oxadiazol-2-yl]pyridine N-oxide–isophthalic acid (1/1)

The title compound, C12H8N4O2·C8H6O4, was synthesized from 4-[5-(4-pyrid­yl)-1,3,4-oxadiazol-2-yl]pyridine N-oxide and isophthalic acid. The two mol­ecules are linked through O—H⋯O and O—H⋯N hydrogen bonds. Weak intra­molecular π–π inter­actions between the two hydrogen-bonded chains result in the formation a one-dimensional supra­molecular curved tape (the face-to-face distance between the pyridine N-oxide ring and the benzene ring is 3.7 Å)