Small extracellular vesicles secreted by induced pluripotent stem cell-derived mesenchymal stem cells improve postoperative cognitive dysfunction in mice with diabetes.

Postoperative cognitive dysfunction (POCD) is a common surgical complication. Diabetes mellitus (DM) increases risk of developing POCD after surgery. DM patients with POCD seriously threaten the quality of patients' life, however, the intrinsic mechanism is unclear, and the effective treatment is deficiency. Previous studies have demonstrated neuronal loss and reduced neurogenesis in the hippocampus in mouse models of POCD. In this study, we constructed a mouse model of DM by intraperitoneal injection of streptozotocin, and then induced postoperative cognitive dysfunction by transient bilateral common carotid artery occlusion. We found that mouse models of DM-POCD exhibited the most serious cognitive impairment, as well as the most hippocampal neural stem cells (H-NSCs) loss and neurogenesis decline. Subsequently, we hypothesized that small extracellular vesicles secreted by induced pluripotent stem cell-derived mesenchymal stem cells (iMSC-sEVs) might promote neurogenesis and restore cognitive function in patients with DM-POCD. iMSC-sEVs were administered via the tail vein beginning on day 2 after surgery, and then once every 3 days for 1 month thereafter. Our results showed that iMSC-sEVs treatment significantly recovered compromised proliferation and neuronal-differentiation capacity in H-NSCs, and reversed cognitive impairment in mouse models of DM-POCD. Furthermore, miRNA sequencing and qPCR showed miR-21-5p and miR-486-5p were the highest expression in iMSC-sEVs. We found iMSC-sEVs mainly transferred miR-21-5p and miR-486-5p to promote H-NSCs proliferation and neurogenesis. As miR-21-5p was demonstrated to directly targete Epha4 and CDKN2C, while miR-486-5p can inhibit FoxO1 in NSCs. We then demonstrated iMSC-sEVs can transfer miR-21-5p and miR-486-5p to inhibit EphA4, CDKN2C, and FoxO1 expression in H-NSCs. Collectively, these results indicate significant H-NSC loss and neurogenesis reduction lead to DM-POCD, the application of iMSC-sEVs may represent a novel cell-free therapeutic tool for diabetic patients with postoperative cognitive dysfunction.

Efficacy and safety of remimazolam besylate in bronchoscopy for adults: A multicenter, randomized, double-blind, positive-controlled clinical study.

Background: With the development of fiberoptic bronchoscopy in the diagnosis and treatment of various pulmonary diseases, the anesthesia/sedation requirements are becoming more demanding, posing great challenges for patient safety while ensuring a smooth examination/surgery process. Remimazolam, a brand-new ultra-short-acting anesthetic, may compensate for the shortcomings of current anesthetic/sedation strategies in bronchoscopy. Methods: This study was a prospective, multicenter, randomized, double-blind, parallel positive controlled phase 3 clinical trial. Subjects were randomized to receive 0.2 mg/kg remimazolam besylate or 2 mg/kg propofol during bronchoscopy to evaluate the efficacy and safety of remimazolam. Results: A total of 154 subjects were successfully sedated in both the remimazolam group and the propofol group, with a success rate of 99.4% (95%CI of the adjusted difference -6.7 × 10%-6% to -5.1 × 10%-6%). The sedative effect of remimazolam was noninferior to that of propofol based on the prespecified noninferiority margin of -5%. Compared with the propofol group, the time of loss of consciousness in the remimazolam group (median 61 vs. 48s, p < 0.001), the time from the end of study drug administration to complete awakening (median 17.60 vs. 12.80 min, p < 0.001), the time from the end of bronchoscopy to complete awakening (median 11.00 vs. 7.00 min, p < 0.001), the time from the end of study drug administration to removal of monitoring (median 19.50 vs. 14.50 min, p < 0.001), and the time from the end of bronchoscopy to removal of monitoring (median 12.70 vs. 8.60 min, p < 0.001) were slightly longer. The incidence of Adverse Events in the remimazolam group and the propofol group (74.8% vs. 77.4%, p = 0.59) was not statistically significant, and none of them had Serious Adverse Events. The incidence of hypotension (13.5% vs. 29.7%, p < 0.001), hypotension requiring treatment (1.9% vs. 7.7%, p = 0.017), and injection pain (0.6% vs. 16.8%, p < 0.001) were significantly lower in the remimazolam group than in the propofol group. Conclusion: Moderate sedation with 0.2 mg/kg remimazolam besylate is effective and safe during bronchoscopy. The incidence of hypotension and injection pain was less than with propofol, but the time to loss of consciousness and recovery were slightly longer. Clinical Trial Registration: clinicaltrials.gov, ChiCTR2000039753.

Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis.

Evidence suggests circRBMS1 regulates mRNA to mediate cell apoptosis, inflammation, and oxidative stress in different diseases. MST1 is reported to be the target and activator of apoptosis-related molecules and signaling pathways. Hence, the present study aims to investigate the role of circ-RBMS1/miR-2355-3p/MST1 in the development of I/R injury. In vitro experiments showed increased circ-RBMS1 and decreased miR-2355-3p in H/R-induced HCMs. CircRBMS1 served as a sponge for miR-2355-3p and miR-2355-3p targeted MST1. Furthermore, knockout of circRBMS1 attenuated cell apoptosis, oxidized stress, and inflammation in H/R-induced HCMs. In vivo experiments indicated circRBMS1 knockdown attenuated cardiac function damage, cell apoptosis, oxidative stress injury and inflammatory response through miR-2355-3p/MST1 axis in mice. In summary, these results demonstrated circRBMS1 played a protective role in myocardial I/R injury though inhibition of miR-2355-3p/MST1 axis. It might provide a new therapeutic target for cardiac I/R injury.

LncRNA ROR modulates myocardial ischemia-reperfusion injury mediated by the miR-185-5p/CDK6 axis.

LncRNAs and miRNAs are correlated with the pathogenesis of myocardial ischemia-reperfusion injury (MIRI). Whether lncRNA ROR or miR-185-5p plays a crucial role in MIRI is still unclear. In in-vitro, human cardiac myocytes (HCMs) were treated with hypoxia/reoxygenation (H/R). Wistar rats were used to set up an in-vitro I/R model by means of recanalization after ligation. Evaluation of the myocardial injury marker lactate dehydrogenase (LDH) in HCMs cells was performed. The expression of miR-185-5p and ROR, IL-1ß, and IL-18 were detected by qRT-PCR. ELISA was also performed to evaluate the secretion of IL-1ß and IL-18. Western blotting was carried out to determine CDK6, NLRP3, GSDMD-N, ASC, and cleaved-caspase1 protein expression. The relationship between miR-185-5p and CDK6 or ROR was confirmed by a dual-luciferase reporter assay. Our findings revealed that H/R treated HCMs showed a significantly decreased miR-185-5p expression and increased expression of CDK6 and ROR. ROR knockdown reduced H/R induced pyroptosis and inflammation, while knockdown of miR-185-5p accelerated the effect. Furthermore, miR-185-5p was negatively regulated and absorbed by ROR in HCMs. Overexpression of miR-185-5p reversed the H/R-induced cell pyroptosis and upregulation of LDH, IL-1ß, and IL-18. In HCMs, miR-185-5p was also negatively regulated and related to CDK6 expression. Moreover, overexpression of CDK6 significantly inhibited the effects of miR-185-5p mimics on the inflammatory response and pyroptosis of HCMs. Knockdown of ROR alleviated H/R-induced myocardial injury by elevating miR-185-5p and inhibiting CDK6 expression. Taken together, our results show that the ROR/miR-185-5p/CDK6 axis modulates cell pyroptosis induced by H/R and the inflammatory response of HCMs.

Three thiacalix[4]arene-based Cu(i) coordination polymers: catalytic activities for azide-alkyne cycloaddition reactions and luminescence properties.

Three new coordination polymers, [Cu2(CN)(L)(OCH3)]·CH3OH·3H2O (1), [Cu3(Br)3(L)] (2) and [Cu(I)(L)]·1.5H2O (3), have been solvothermally prepared by reacting L (5,11,17,23-tetra-tert-butyl-25,26,27,28-tetra[(3-pyridylmethyl)oxy]-2,8,14,20-tetrathiacalix[4]arene) with Cu(i) halide. 1 and 2 exhibit layers. 3 displays a chain, a supramolecular layer constructed by hydrogen bonds. The performance of 1-3 was examined as heterogeneous catalysts for azide-alkyne cycloaddition reactions. Most strikingly, 1 and 2 show predominant efficiency with high regioselectivity and excellent recyclability. Remarkably, solids 1-3 all have luminescence characteristics under irradiation with a UV lamp.

The lncRNA ROR/miR-124-3p/TRAF6 axis regulated the ischaemia reperfusion injury-induced inflammatory response in human cardiac myocytes.

Myocardial ischaemia reperfusion injury (MIRI) is considered the primary cause of death in patients with cardiovascular diseases. Recently, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been found to be involved in the pathogenesis of MIRI. However, whether lncRNA ROR and miR-124-3p play roles in MIRI and the underlying mechanism remain undetermined. HCMs were exposed to hypoxic conditions for 2 h followed by re-oxygenation (H/R) treatment. Expression of miR-124-3p and lncRNA ROR in HCMs was measured by qRT-PCR. TRAF6 expression was evaluated by qRT-PCR and western blotting. ELISA and qRT-PCR were conducted to assess the production of TNF-α, IL-6, and IL-1ß. The interaction between miR-124-3p and TRAF6, as well as between miR-124-3p and lncRNA ROR, was verified by dual-luciferase reporter assay. Cell apoptosis was detected by flow cytometry analysis. Our data revealed that miR-124-3p was significantly downregulated, while TRAF6 and lncRNA ROR were upregulated in both MIRI rat model and H/R treated HCMs. Overexpression of miR-124-3p reversed the H/R-induced cell apoptosis and upregulation of TNF-α, IL-6, and IL-1ß. Mechanistically, miR-124-3p bound and negatively regulated TRAF6 expression in HCMs. Moreover, TRAF6 overexpression significantly blocked the effects of miR-124-3p mimics on cell apoptosis and inflammatory response of HCMs, which involved the NF-κB pathway. Further analysis showed that lncRNA ROR sponged and negatively regulated miR-124-3p in HCMs. Overexpression of IL-1ß was demonstrated to promote H/R induced cell apoptosis in HCMs. In addition, overexpression of ROR further enhanced the H/R-induced inflammation and cell apoptosis through its action on miR-124-3p. The lncRNA ROR/miR-124-3p/TRAF6 axis regulated the H/R-induced cell apoptosis and inflammatory response of HCMs.

[Effect of triptolide on cognitive dysfunction in vascular dementia rats through SIRT1/NF-κB signaling pathway].

To investigate the effect of triptolide on cognitive dysfunction in vascular dementia rats and its effect on SIRT1/NF-κB pathway,fifty healthy male Sprague-Dawley rats were randomly divided into 5 groups: Sham operation group( Sham group),vascular dementia model group( 2 VO group),triptolide intraperitoneal injection group( TR group),triptolide intraperitoneal injection + EX527 intracerebroventricular administration group( T+E group),EX527 intracerebroventricular administration group( EX527 group). After 4 weeks of modeling,Morris water maze test and object recognition test were used to evaluate the learning and memory ability of rats. The morphological changes of hippocampus in each group were observed in brain tissue. The chemical colorimetry was used to detect the activities of SOD and MDA in hippocampus. IL-6 and TNF-α levels were detected by ELISA. Western blot was used to detect the expression of SIRT1,NF-κB,IκBα and caspase 3 in hippocampus. The results showed that compared with the Sham group,the learning and memory ability of the vascular dementia model rats was reduced,the SOD activity in the hippocampus was decreased,the MDA activity and IL-6 level were increased,the neuronal degeneration changed significantly,the expression of SIRT1 and IκBα was decreased and the expression of caspase 3 and NF-κB was significantly increased. After intervention by triptolide,the level of oxidative stress and the degenerative changes in hippocampus were significantly slowed down. The expression of SIRT1 and IκBα protein was increased and the expression of caspase 3 and NF-κB was significantly decreased. While,after intervention by triptolide and EX527,the expression of SIRT1 was decreased,the levels of oxidative stress and neuronal degeneration in the hippocampus were aggravated,and the learning and memory ability was reduced. The results showed that triptolide could improve cognitive impairment in vascular dementia rats and its mechanism may be related to SIRT1/NF-κB signaling pathway.

Glioma cells enhance angiogenesis and inhibit endothelial cell apoptosis through the release of exosomes that contain long non-coding RNA CCAT2.

Angiogenesis is a key event in the progression of gliomas. Exosomes, as signaling extracellular organelles, modulate the tumor microenvironment and promote angiogenesis and tumor progression. We previously demonstrated that long intergenic non-coding RNA CCAT2 (linc-CCAT2) was overexpressed in glioma tissues and functioned to promote glioma progression. Therefore, this study aimed to explore an underlying mechanism of glioma cell-affected angiogenesis. First, qRT-PCR was used to determine the expression level of linc-CCAT2 in 4 glioma cell lines and 293T cells, and the results revealed that the U87-MG cells exhibited the highest expression level. Subsequently, the pro-angiogenesis function of exosomes that were derived from negative control shRNA-treated U87-MG cells (ncU87-Exo) and linc-CCAT2 shRNA-treated U87-MG cells (shU87-Exo) was evaluated in vitro and in vivo. We found that ncU87-Exo, which was enriched in linc-CCAT2, could be taken up by HUVECs. ncU87-Exo improved the linc-CCAT2 expression level in HUVECs and more strongly promoted HUVEC migration, proliferation, tubular-like structure formation in vitro and arteriole formation in vivo as well as inhibited HUVEC apoptosis induced by hypoxia. Further mechanistic studies revealed that ncU87-Exo could upregulate VEGFA and TGFß expression in HUVECs as well as promote Bcl-2 expression and inhibit Bax and caspase-3 expression. Finally, gain-/loss-of-function studies revealed that the overexpression of linc-CCAT2 in HUVECs activated VEGFA and TGFß, promoted angiogenesis, promoted Bcl-2 expression and inhibited Bax and caspase-3 expression, thus decreasing apoptosis. Downregulation of linc-CCAT2 revealed the opposite effect. Thus, our results revealed a new exosome­mediated mechanism by which glioma cells could promote angiogenesis through the transfer of linc-CCAT2 by exosomes to endothelial cells. Moreover, we suggest that exosomes and linc-CCAT2 are putative therapeutic targets in glioma.

Intrathecal Administration of Flavopiridol Promotes Regeneration in Experimental Model of Spinal Cord Injury.

AIM: Spinal cord injury (SCI) is a serious condition of the central nervous system and it affects the quality of life and even hampers the day-to-day activity of the patient. In the current study, we investigated the efficacy of intrathecal administration of flavopiridol in an experimental animal model of SCI. The study also aimed at exploring the physiological effects of flavopiridol on neurons, astrocytes and cell cycle regulatory proteins. MATERIAL AND METHODS: In vitro scratch wound experiments were performed on female Sprague-Dawley rats (n=23). A complete hemisection to the right of T10 was made, and flavopiridol solution (200 mM, 0.8 nmol flavopiridol/animal) was delivered topically to the lesion site. Cell viability assay, in vitro scratch injury assay, cell cycle analysis using flow cytometry and behavioural assessments were performed. RESULTS: The local delivery of flavopiridol reduced cavity formation and improved regeneration of neurons with improvement in physiological performance. Flavopiridol also inhibited the migration and proliferation of astrocytes, and at the same time, promoted the survival of neurons. CONCLUSION: Intrathecal administration of flavopiridol can be a promising treatment strategy in patients with SCI and it needs to be validated in patient setting.

Naringenin pre-treatment inhibits neuroapoptosis and ameliorates cognitive impairment in rats exposed to isoflurane anesthesia by regulating the PI3/Akt/PTEN signalling pathway and suppressing NF-κB-mediated inflammation.

The volatile anaesthetic isoflurane is one of the most frequently employed general anaesthetics in neonates, children and adults. Accumulating evidence demonstrated that exposure to anaesthetics is associated with widespread neurodegeneration and cognitive impairment. Thus, the identification and development of compounds capable of preventing or reducing these adverse effects is of great clinical importance. For this purpose, the present study aimed to assess the effects of a flavonoid, naringenin, on isoflurane-induced neuroapoptosis and cognitive impairment. Separate groups of neonatal rat pups were administered naringenin at 25, 50 or 100 mg/kg body weight from postnatal day 1 (P1) to P21. On P7, the pups were exposed to 6 h of isoflurane (0.75%) anaesthesia. Neuroapoptosis was examined using the TUNEL assay. The expression of cleaved caspase-3, the apoptotic pathway proteins (Bad, Bax, Bcl-2 and Bcl-xL), the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway proteins [Akt, phosphorylated (-)Akt, glycogen synthase kinase 3ß (GSK­3ß), p­GSK-3ß, phosphatase and tensin homolog (PTEN)] and nuclear factor-κB (NF-κB)­mediated signalling proteins were determined by western blot analysis. General behaviour, as well as the learning ability and memory of the pups were assessed. Naringenin significantly inhibited isoflurane­induced neuroapoptosis and markedly decreased the protein expression of caspase-3, Bad, Bax, NF-κB, tumor necrosis factor-α, interleukin (IL)-6 and IL-1ß. Furthermore, naringenin increased the expression of Bcl-xL and Bcl-2 and activated the PI3K/Akt pathway. Significant improvements in learning capacity and memory retention were observed following naringenin treatment. Naringenin effectively ameliorated cognitive dysfunction and reduced isoflurane­induced apoptosis as well as modulating the PI3/Akt/PTEN and NF-κB signalling pathways.

Posterior pericardiotomy for the prevention of atrial fibrillation after coronary artery bypass grafting: A meta-analysis of randomized controlled trials.

BACKGROUND: Posterior pericardiotomy (PP) has been shown to be effective in patients after cardiac surgery complicated by a reduced the incidence of atrial fibrillation (AF). However, the role of PP in patients following coronary artery bypass graft (CABG) remains ambiguous. We aimed to systematically evaluate the efficacy of PP in preventing postoperative AF in adult patients after CABG. METHODS: Studies were identified by searching multiple electronic databases (PubMed, Embase, and the Cochrane Library) through February, 2016, and by reviewing reference lists of obtained articles. The outcome measure was the incidence of postoperative AF. The meta-analysis was performed with the fixed-effect model or random-effect model according to heterogeneity. RESULTS: Ten randomized trials incorporating 1648 patients were included in this meta-analysis (822 in the PP group and 826 in the control group). The cumulative incidence of AF was 10.6% in the PP group and 24.9% in the control group. Meta-analysis with all studies using a random-effects model suggested that PP had significant effect on the prevention of postoperative AF (I(2) 55%; P<0.00001; OR, 0.36; 95% CI, 0.23-0.56; RR, 0.45; 95% CI, 0.31-0.64). Sensitivity analyses by methodological quality and surgical technique yields similar results. CONCLUSIONS: This meta-analysis indicates that PP shows beneficial efficacy in preventing postoperative AF in adult patients after CABG. This finding encourages the use of PP to prevent postoperative AF after CABG, but, more high quality randomized controlled trials are still warranted to confirm the safety.

Effect of TRPV1 combined with lidocaine on cell state and apoptosis of U87-MG glioma cell lines.

OBJECTIVE: To study the effects of Transient receptor potential cation channel, subfamily V, member 1 (TRPV1) combined with lidocaine on status and apoptosis of U87-MG glioma cell line, and explore whether local anesthetic produces neurotoxicity by TRPV1. METHODS: U87-MG cells were divided into control group, gene silencing group, empty vector group and TRPV gene up-regulation group. For cells in each group, flow cytometry was employed to detect the intracellular calcium ion concentration and mitochondrial membrane potential at different time point from cellular perspective. Cell apoptosis of U87-MG was assayed by flow cytometry and MTT from a holistic perspective. RESULTS: Calcium ion concentration increased along with time. The concentration in TRPV1 gene up-regulation group was significantly higher than those in other groups at each time point (P < 0.05). After adding lidocaine, mitochondrial membrane potential in U87-MG significantly increased (P < 0.05). This increasing trend in TRPV1 gene up-regulation group was more significant than other groups (P < 0.05), while in TRPV1 gene silencing group, the trend significantly decreased (P < 0.05). Flow cytometry result and MTT result both showed that cell apoptosis in each group significantly increased after lidocaine was added (P < 0.05). This increasing trend in TRPV1 gene up-regulation group was more significant than other groups (P < 0.05), while in TRPV1 gene silencing group, the trend significantly decreased (P < 0.05). Moreover, apoptosis was more severe along with the increasing concentration of lidocaine (P < 0.05). CONCLUSIONS: In this study, it was proved that lidocaine could dose-dependently induce the increase of intracellular calcium ion concentration, mitochondrial membrane potential and apoptosis in U87-MG glioma cell line. The up-regulation of TRPV1 enhanced cytotoxicity of lidocaine, which revealed the correlations between them. Lidocaine might have increased intracellular calcium ion concentration by activating TRPV1 gene and induced apoptosis of U87-GM glioma cell line by up-regulating mitochondrial membrane potential.

Bis(triethanolamine)bis(µ2-trimesato)dicobalt(II): a Co(II) dimer with an unreported two-dimensional supramolecular topology formed from triethanolamine and trimesic acid ligands.

Supramolecular networks are an important subset in the field of coordination polymer (CP) frameworks and are widely encountered in crystal engineering research. The search for novel topologies continues to be a significant goal in CP chemistry. The dimeric compound bis(µ-5-carboxybenzene-1,3-dicarboxylato-κ(2)O(1):O(3))bis[(triethanolamine-κ(4)N,O,O',O'')cobalt(II)], [Co2(C9H4O6)2(C6H15NO3)2], formed from the coligands 5-carboxybenzene-1,3-dicarboxylate (tmaH(2-)) and triethanolamine (teaH3), namely [Co(µ2-tmaH)(teaH3)]2, was synthesized and characterized by single-crystal and powder X-ray diffraction analyses, IR spectroscopy, thermogravimetric analysis (TGA) and magnetic measurements. The crystal structure features a zero-dimensional molecular structure consisting of centrosymmetric macrocyclic dinuclear complexes. Four classical hydrogen bonds between carboxylate groups and hydroxyethyl arms stabilize and extend the molecules into a two-dimensional supramolecular network. The topological analysis indicates that an unreported (3,5)-binodal supramolecular topology with a short Schläfli symbol of (4.5.6)(4.5(5).6(3).7) can be achieved by means of intermolecular hydrogen bonds. The crystal structure accounts for the potential to obtain unique topological types from two excellent hydrogen-bonding candidates, i.e. tmaH3 and teaH3. A variable-temperature magnetic study shows the existence of antiferromagnetic behaviour in the complex.

Poly[diaquabis(mu(3)-hexamethylenetetramine)[mu(2)-2,2'-(piperazine-1,4-diyl)bis(ethanesulfonato)]disilver(I)]: a three-dimensional pillared-layer framework encapsulating a water chain of (H(2)O)(12) clusters.

The title compound, {[Ag(2)(C(8)H(16)N(2)O(6)S(2))(C(6)H(12)N(4))(2)(H(2)O)(2)].12H(2)O}(n), consists of a two-dimensional Ag(I)-hexamethylenetetramine (6,3) net pillared by the 2,2'-(piperazine-1,4-diyl)bis(ethanesulfonate) ligand, which lies across a centre of inversion. This compound can also be viewed as a (3,4)-connected topology by considering the hexamethylenetetramine ligand and the Ag(I) ion as the three- and four-connected nodes, respectively. There is a one-dimensional channel along the a axis accommodating a water chain assembled by the (H(2)O)(12) clusters.

Poly[[(pentaethylenehexamine)manganese(II)] [hepta-mu-selenido-tritin(IV)]]: a tin-selenium net with remarkable flexibility.

The title compound, {[Mn(C(10)H(28)N(6))][Sn(3)Se(7)]}(n), consists of anionic (infinity){[Sn(3)Se(7)](2-)} layers interspersed by [Mn(peha)](2+) complex cations (peha is pentaethylenehexamine). Pseudocubic (Sn(3)Se(4)) cluster units within each layer are held together to form a 6(3) net with a hole size of 8.74 x 13.87 A. Weak N-H...Se interactions between the host inorganic frameworks and metal complexes extend the components into a three-dimensional network. The incorporation of metal complexes into the flexible anion layer dictates the distortion of the holes.

Chloro(mu-6-methylpyridine-2-carboxylato)bis(6-methylpyridine-2-carboxylato)triphenylchromium(III)tin(IV) chlorotriphenyltin(IV).

The title compound, [CrSn(C6H5)3(C7H6NO2)3Cl][Sn(C6H5)3Cl(CH4O)], was obtained from the reaction of Ph3SnCl with the complex [Cr(C7H6NO2)3] in methanol. The structure contains [Ph3SnCl(MeOH)] (A) and [Ph3SnClCr(C7H6NO2)3] (B) molecules. In molecule A, the Sn atom of Ph3SnCl is coordinated by one methanol molecule. In molecule B, the Sn atom of Ph3SnCl is coordinated by one carboxylate O atom of [Cr(C7H6NO2)3]. Molecules A and B are connected through an O-H...O hydrogen bond between a carboxylate O atom and the methanol OH group. Weak C-H...Cl interactions and O-H...O hydrogen bonds extend the components of (I) into a two-dimensional network.

7-Hydroxy-6-methoxy-3-[(2-oxo-2H-1-benzopyran-7-yl)oxy]-2H-1-benzopyran-2-one.

The title compound, daphnoretin, C19H12O7, was isolated from the leaves of Stellera chamaejasme L. Two independent molecules are present in the asymmetric unit, with similar conformations. Each of the independent molecules is composed of two chromene systems connected by an ether bridge. The dihedral angles between the mean planes of the two chromene systems are 86.9 (2) and 81.9 (3) degrees. Molecules form chains via hydrogen bonds and adjacent chains are parallel to each other.