Production of CA125 with Tn antigens using a glycosylphosphatidylinositol anchoring system.

Cancer antigen 125 (CA125) is a serum marker associated with ovarian cancer. Despite its widespread use, CA125 levels can also be elevated in benign conditions. Recent reports suggest that detecting serum CA125 that carries the Tn antigen, a truncated O-glycan containing only N-acetylgalactosamine on serine or threonine residues, can improve the specificity of ovarian cancer diagnosis. In this study, we engineered cells to express CA125 with a Tn antigen. To achieve this, we knocked out C1GALT1 and SLC35A1, genes encoding Core1 synthase and a transporter for cytidine-5'-monophospho-sialic acid respectively, in human embryonic kidney 293 (HEK293) cells. In ClGALT1-SLC35A1-knockout (KO) cells, the expression of the Tn antigen showed a significant increase, whereas the expression of the T antigen (galactose-ß1,3-N-acetylgalactosamine on serine or threonine residues) was decreased. Due to the inefficient secretion of soluble CA125, we employed a glycosylphosphatidylinositol (GPI) anchoring system. This allowed for the expression of GPI-anchored CA125 on the cell surface of ClGALT1-SLC35A1-KO cells. Cells expressing high levels of GPI-anchored CA125 were then enriched through cell sorting. By knocking out the PGAP2 gene, the GPI-anchored form of CA125 was converted to a secretory form. Through the engineering of O-glycans and the use of a GPI-anchoring system, we successfully produced CA125 with Tn antigen modification.

Exploring the relationship between malnutrition and the systemic immune-inflammation index in older inpatients: a study based on comprehensive geriatric assessment.

BACKGROUND: Malnutrition is a prevalent and major challenge among senior citizens, possibly due to the continual low-grade inflammatory state of the body. A novel inflammatory parameter, the systemic immune-inflammation index (SII), is highly valuable in evaluating and predicting the prognosis of a wide range of diseases. This study aims to explore the significance of the SII in assessing malnutrition in older inpatients. METHODS: This retrospective study included 500 senior hospitalized patients who met the inclusion and exclusion criteria from the Comprehensive Geriatric Assessment database of the First Hospital of Jilin University. The Mini-Nutritional Assessment (MNA) questionnaire was used to evaluate the nutritional status of patients. The SII was calculated using complete blood counts, and we performed natural logarithm transformation of the SII [ln(SII)]. Multivariable logistic regression analysis was used to identify the association between ln(SII) and malnutrition. To ensure the stability of the findings, a sensitivity analysis was conducted. RESULTS: The 500 patients had a mean age of 77.29 ± 9.85 years, and 68.6% were male. In accordance with the MNA, 30.4% of the patients were malnourished or at risk of malnutrition, and patients in this group had considerably greater levels of ln(SII) than patients with adequate nutrition (P < 0.001). The optimum ln(SII) cutoff value for patients with malnutrition or at risk of malnutrition was 6.46 (SII = 635.87) with 46.7% sensitivity and 80.2% specificity [95% CI: 0.613-0.721, AUC: 0.667, P < 0.001]. Multivariable logistic regression demonstrated that ln(SII) was an independent risk factor for the risk of malnutrition or malnutrition in older individuals (OR 3.984, 95% CI: 2.426-6.543, P < 0.001). Other metrics from the geriatric comprehensive assessment, including body mass index, calf circumference, fat ratio, activities of daily living and instrumental activities of daily living, and geriatric depression scale scores, were also independently correlated with nutritional status. CONCLUSIONS: According to our research, a high SII is an independent predictor of older inpatient malnutrition, and the SII aids in screening for malnutrition and may be a potential target for intervention. Comprehensive geriatric assessment parameters such as BMI, calf circumference, fat ratio, activities of daily living and depression were also linked to malnutrition.

Differential reductions in the capillary red-blood-cell flux between retina and brain under chronic global hypoperfusion.

Significance: It has been hypothesized that abnormal microcirculation in the retina might predict the risk of ischemic damages in the brain. Direct comparison between the retinal and the cerebral microcirculation using similar animal preparation and under similar experimental conditions would help test this hypothesis. Aim: We investigated capillary red-blood-cell (RBC) flux changes under controlled conditions and bilateral-carotid-artery-stenosis (BCAS)-induced hypoperfusion, and then compared them with our previous measurements performed in the brain. Approach: We measured capillary RBC flux in mouse retina with two-photon microscopy using a fluorescence-labeled RBC-passage approach. Key physiological parameters were monitored during experiments to ensure stable physiology. Results: We found that under the controlled conditions, capillary RBC flux in the retina was much higher than in the brain (i.e., cerebral cortical gray matter and subcortical white matter), and that BCAS induced a much larger decrease in capillary RBC flux in the retina than in the brain. Conclusions: We demonstrated a two-photon microscopy-based technique to efficiently measure capillary RBC flux in the retina. Since cerebral subcortical white matter often exhibits early pathological developments due to global hypoperfusion, our results suggest that retinal microcirculation may be utilized as an early marker of brain diseases involving global hypoperfusion.

Measurements of cerebral microvascular blood flow, oxygenation, and morphology in a mouse model of whole-brain irradiation-induced cognitive impairment by two-photon microscopy and optical coherence tomography: evidence for microvascular injury in the cerebral white matter.

Whole-brain irradiation (WBI, also known as whole-brain radiation therapy) is a mainstay treatment modality for patients with multiple brain metastases. It is also used as a prophylactic treatment for microscopic tumors that cannot be detected by magnetic resonance imaging. WBI induces a progressive cognitive decline in ~ 50% of the patients surviving over 6 months, significantly compromising the quality of life. There is increasing preclinical evidence that radiation-induced injury to the cerebral microvasculature and accelerated neurovascular senescence plays a central role in this side effect of WBI. To better understand this side effect, male C57BL/6 mice were first subjected to a clinically relevant protocol of fractionated WBI (5 Gy, two doses per week, for 4 weeks). Nine months post the WBI treatment, we applied two-photon microscopy and Doppler optical coherence tomography to measure capillary red-blood-cell (RBC) flux, capillary morphology, and microvascular oxygen partial pressure (PO2) in the cerebral somatosensory cortex in the awake, head-restrained, WPI-treated mice and their age-matched controls, through a cover-glass-sealed chronic cranial window. Thanks to the extended penetration depth with the fluorophore - Alexa680, measurements of capillary blood flow properties (e.g., RBC flux, speed, and linear density) in the cerebral subcortical white matter were enabled. We found that the WBI-treated mice exhibited a significantly decreased capillary RBC flux in the white matter. WBI also caused a significant reduction in capillary diameter, as well as a large (although insignificant) reduction in segment density at the deeper cortical layers (e.g., 600-700 µm), while the other morphological properties (e.g., segment length and tortuosity) were not obviously affected. In addition, we found that PO2 measured in the arterioles and venules, as well as the calculated oxygen saturation and oxygen extraction fraction, were not obviously affected by WBI. Lastly, WBI was associated with a significant increase in the erythrocyte-associated transients of PO2, while the changes of other cerebral capillary PO2 properties (e.g., capillary mean-PO2, RBC-PO2, and InterRBC-PO2) were not significant. Collectively, our findings support the notion that WBI results in persistent cerebral white matter microvascular impairment, which likely contributes to the WBI-induced brain injury and cognitive decline. Further studies are warranted to assess the WBI-induced changes in brain tissue oxygenation and malfunction of the white matter microvasculature as well.

Slow magnetic relaxation of mononuclear complexes based on uncommon Kramers lanthanide ions CeIII, SmIII and YbIII.

Based on the uncommon Kramers ions CeIII, SmIII and YbIII, complexes [Ce(dppbO2)2Cl3] (1, dppbO2 = 1,2-bis(diphenylphosphino)benzene dioxide), [Sm(dppbO2)2Cl3] (2) and [Yb(dppbO2)2Cl2]Cl (3) toward single-ion magnets were obtained and fully characterized. Complexes 1 and 2 are isostructural seven-coordinate with distorted geometries between a capped trigonal prism and a capped octahedron, while 3 is six-coordinate with an octahedral geometry. Dynamic magnetic property measurements reveal their field induced slow magnetic relaxation behaviours. Fits to the temperature dependent relaxation time (τ) result in effective barriers of 38(2), 11.7(2) and 20.2(6) cm-1 for 1, 2 and 3, respectively, as well as relatively low Raman exponents (3.4(2) for 1 and 2.1(1) for 3). Ab initio calculations were then performed and they indicated that the first excited Kramers doublets (KDs) for 1, 2 and 3 lie at ca. 291, 63.5 and 137 cm-1, respectively, which are much higher than the fitting results. Combining the significant transverse magnetic moments between the ground state KDs and the first excited KDs, we thus attribute the dominant relaxation pathway of the three compounds to a Raman process, while quantum tunnelling of magnetization and direct relaxation processes may coexist. In this case, the obtained effective barriers in a high temperature region for 1 and 3 are actually the energies of the vibrational modes, which lead to second-order Raman processes with exponential temperature dependence.

Stereoisomeric coordination polymers based on facial and meridional six-coordinate dysprosium(III ).

Due to the small differences in the chemical properties of facial (fac) and meridional (mer) stereoisomers, selective synthesis of one of the isomers is challenging, especially for lanthanide complexes. By using a flexible bidentate phosphine oxide ligand, we managed to isolate three stereoisomeric 2D and 3D coordination polymers, in which six-coordinate Dy(III) ions possess fac- or mer-Cl3O3 coordination environments. Structural studies indicate that the stereochemistry differences result from their various supramolecular interactions (e.g., hydrogen bonding and π⋯π stacking). Magnetic property measurements reveal the different static and dynamic magnetic behaviours of the three stereoisomers. Ab initio CASSCF calculations were then performed which indicated that their distinct magnetic behaviours arise from their fac/mer configurations. Compared to fac-Dy(III), mer-Dy(III) possesses more axial ground-state KDs and higher first excited KDs.

Case Report: Successful Outcome for Refractory Diabetic Peripheral Neuropathy in Patients With Ultrasound-Guided Injection Treatment.

Diabetic peripheral neuropathy is the most prevalent chronic complication of diabetes and is based on sensory and autonomic nerve symptoms. Generally, intensive glucose control and nerve nourishment are the main treatments. However, it is difficult to improve the symptoms for some patients; such cases are defined as refractory diabetic peripheral neuropathy (RDPN). In this paper, we present five patients treated with saline and mecobalamin by ultrasound-guided injection. The Visual Analog Scale and Toronto Clinical Scoring System were used to evaluate the symptoms, and the neuro-ultrasound scoring system and electrophysiological severity scale were evaluated by ultrasound and electrophysiological examination. In brief, ultrasound-guided hydrodissection may be a safe way to treat RDPN.

Multi-spectral intravascular photoacoustic/ultrasound/optical coherence tomography tri-modality system with a fully-integrated 0.9-mm full field-of-view catheter for plaque vulnerability imaging.

Myocardial infarctions are most often caused by the so-called vulnerable plaques, usually featured as non-obstructive lesions with a lipid-rich necrotic core, thin-cap fibroatheroma, and large plaque size. The identification and quantification of these characteristics are the keys to evaluate plaque vulnerability. However, single modality intravascular methods, such as intravascular ultrasound, optical coherence tomography and photoacoustic, can hardly achieve all the comprehensive information to satisfy clinical needs. In this paper, for the first time, we developed a novel multi-spectral intravascular tri-modality (MS-IVTM) imaging system, which can perform 360° continuous rotation and pull-backing with a 0.9-mm miniature catheter and achieve simultaneous acquisition of both morphological characteristics and pathological compositions. Intravascular tri-modality imaging demonstrates the ability of our MS-IVTM system to provide macroscopic and microscopic structural information of the vessel wall, with identity and quantification of lipids with multi-wavelength excitation. This study offers clinicians and researchers a novel imaging tool to facilitate the accurate diagnosis of vulnerable atherosclerotic plaques. It also has the potential of clinical translations to help better identify and evaluate high-risk plaques during coronary interventions.

The significance of detecting glucose transporter 1 and calretinin in serous effusions to differentiate between carcinoma cells and reactive mesothelial cells.

BACKGROUND: The cytologic evaluation of serous effusions to distinguish malignant cells from reactive mesothelial cells (RMCs)was an enormous challenge. The purpose of this study was to investigate the diagnostic value of glucose transporter 1 (GLUT1) and calretinin (CR) in serous effusions of patients with malignant and in order to significantly ameliorate the diagnostic accuracy. METHODS: The expressions of GLUT1 and CR were measured by streptavidin-peroxidase (S-P) immunocytochemical technique in serous effusions of 183 patients with malignant and in 95 patients with benign diseases. RESULTS: The positive ratio of GLUT1 was 91.8% (168/183) in serous effusions from patients with malignant and 5.3% (5/95) in benign diseases, they had a significant difference (P < .01). CR was expressed 89.5% (85/95) in benign diseases and 6.6% (12/183) in malignant, it also showed an important difference (P < 0.01). The combination of GLUT1 + CR revealed the best efficiency: the sensitivity and specificity were 100% and 98.9%, respectively. CONCLUSION: Immunocytochemical staining for GLUT1 and CR may be used as a complementary tool for the detection of malignant effusions and help to make a distinction between cancer cells and RMCs. The combination of GLUT1 and CR with immunocytochemistry stained can be achieved a higher diagnostic performance.

Cell engineering for the production of hybrid-type N-glycans in HEK293 cells.

Glycoprotein therapeutics are among the leading products in the biopharmaceutical industry. The heterogeneity of glycans in therapeutic proteins is an issue for maintaining quality, activity and safety during bioprocessing. In this study, we knocked out genes encoding Golgi α-mannosidase-II, MAN2A1 and MAN2A2 in human embryonic kidney 293 (HEK293) cells, establishing an M2D-KO cell line that can produce recombinant proteins mainly with hybrid-type N-glycans. Furthermore, FUT8, which encodes α1,6-fucosyltransferase, was knocked out in the M2D-KO cell line, establishing a DF-KO cell line that can express noncore fucosylated hybrid-type N-glycans. Two recombinant proteins, lysosomal acid lipase and constant fragment of human IgG1, were expressed in the M2D-KO and DF-KO cell lines. Glycan structural analysis revealed that complex-type N-glycans were removed in both M2D-KO and DF-KO cells. Our results suggest that these cell lines are suitable for the production of therapeutic proteins with hybrid-type N-glycans. Moreover, KO cell lines would be useful as models for researching the mechanism of antimetastatic effects in human tumours by swainsonine treatment.

Zinc as a countermeasure for cadmium toxicity.

Cadmium (Cd) is an important environmental pollutant and long-term Cd exposure is closely related to autoimmune diseases, cancer, cardiovascular diseases (CVD), and hepatic dysfunction. Zinc (Zn) is an essential metal that plays key roles in protein structure, catalysis, and regulation of their function. Numerous studies have shown that Zn can reduce Cd toxicity; however, the underlying mechanisms have not been extensively explored. Preclinical studies have revealed direct competition for sarcolemmal uptake between these two metals. Multiple sarcolemmal transporters participate in Cd uptake, including Zn transporters, calcium channels, and DMT1 (divalent metal transporter 1). Zn also induces several protective mechanisms, including MT (metallothionein) induction and favorable redox homeostasis. This review summarizes current knowledge related to the role of Zn and metal transporters in reducing Cd toxicity and discusses potential future directions of related research.

Zinc protects against cadmium-induced toxicity in neonatal murine engineered cardiac tissues via metallothionein-dependent and independent mechanisms.

Cadmium (Cd) is a nonessential heavy metal and a prevalent environmental toxin that has been shown to induce significant cardiomyocyte apoptosis in neonatal murine engineered cardiac tissues (ECTs). In contrast, zinc (Zn) is a potent metallothionein (MT) inducer, which plays an important role in protection against Cd toxicity. In this study, we investigated the protective effects of Zn against Cd toxicity in ECTs and explore the underlying mechanisms. ECTs were constructed from neonatal ventricular cells of wild-type (WT) mice and mice with global MT gene deletion (MT-KO). In WT-ECTs, Cd (5-20 µM) caused a dose-dependent toxicity that was detected within 8 h evidenced by suppressed beating, apoptosis, and LDH release; Zn (50-200 µM) dose-dependently induced MT expression in ECTs without causing ECT toxicity; co-treatment of ECT with Zn (50 µM) prevented Cd-induced toxicity. In MT-KO ECTs, Cd toxicity was enhanced; but unexpectedly, cotreatment with Zn provided partial protection against Cd toxicity. Furthermore, Cd, but not Zn, significantly activated Nrf2 and its downstream targets, including HO-1; inhibition of HO-1 by a specific HO-1 inhibitor, ZnPP (10 µM), significantly increased Cd-induced toxicity, but did not inhibit Zn protection against Cd injury, suggesting that Nrf2-mediated HO-1 activation was not required for Zn protective effect. Finally, the ability of Zn to reduce Cd uptake provided an additional MT-independent mechanism for reducing Cd toxicity. Thus, Zn exerts protective effects against Cd toxicity for murine ECTs that are partially MT-mediated. Further studies are required to translate these findings towards clinical trials.

RETRACTED: Astragaloside IV protects cardiomyocytes from hypoxia-induced injury by down-regulation of lncRNA GAS5.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. Concerns were raised about the background pattern of the Western Blots from Figures 1B and 1E. Given the comments of Dr Elisabeth Bik regarding this article "This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels", the journal requested the authors to provide the raw data. However, the authors were not able to provide raw data of sufficient quality and detail for the journal to independently audit the provenance and validity of the data, and therefore the Editor-in-Chief decided to retract the article.

Silence of LncRNA GAS5 Protects Cardiomyocytes H9c2 against Hypoxic Injury via Sponging miR-142-5p.

The regulatory role of long noncoding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) in both cancerous and noncancerous cells have been widely reported. This study aimed to evaluate the role of lncRNA GAS5 in heart failure caused by myocardial infarction. We reported that silence of lncRNA GAS5 attenuated hypoxia-triggered cell death, as cell viability was increased and apoptosis rate was decreased. This phenomenon was coupled with the down-regulated expression of p53, Bax and cleaved caspase-3, as well as the up-regulated expression of CyclinD1, CDK4 and Bcl-2. At the meantime, the expression of four heart failure-related miRNAs was altered when lncRNA GAS5 was silenced (miR-21 and miR-142-5p were up-regulated; miR-30b and miR-93 were down-regulated). RNA immunoprecipitation assay results showed that lncRNA GAS5 worked as a molecular sponge for miR-142-5p. More interestingly, the protective actions of lncRNA GAS5 silence on hypoxia-stimulated cells were attenuated by miR-142-5p suppression. Besides, TP53INP1 was a target gene for miR-142-5p. Silence of lncRNA GAS5 promoted the activation of PI3K/AKT and MEK/ERK signaling pathways in a miR-142-5p-dependent manner. Collectively, this study demonstrated that silence of lncRNA GAS5 protected H9c2 cells against hypoxia-induced injury possibly via sponging miR-142-5p, functionally releasing TP53INP1 mRNA transcripts that are normally targeted by miR-142-5p.

Phosphine Oxide Ligand Based Tetrahedral CoII Complexes with Field-induced Slow Magnetic Relaxation Behavior Modified by Terminal Ligands.

Two isostructural mononuclear CoII complexes, [Co(xantpo)(NCE)2 ] (E=S (1) and O (2); xantpo=9,9-dimethyl-4,5-bis(diphenylphosphoryl) xanthene), supported by a bidentate phosphine oxide ligand are reported. The cobalt complexes exhibit characteristic tetrahedral structures coordinated with two oxygen and two nitrogen atoms. Magnetic property measurements show their similar static magnetic behaviours but very different dynamic magnetic behaviours. Both complexes show field-induced slow magnetic relaxation behaviours, but the relaxation of 2 is much slower than that of 1. Fittings to the magnetic data and ab initio CASSCF calculations reveal significant changes in the zero field splitting (ZFS) parameters (D and E), which can be attributed to the small geometrical changes of the Co ions and the different ligand field strength of the two terminal ligands.

Functional analysis of gene expression profiling-based prediction in bladder cancer.

The present study aimed to analyze the modification of gene expression in bladder cancer (BC) by identifying significant differentially expressed genes (DEGs) and functionally assess them using bioinformatics analysis. To achieve this, two microarray datasets, GSE24152 (which included 10 fresh tumor tissue samples from urothelial bladder carcinoma patients and 7 benign mucosa samples from the bladder), and GSE42089 (which included 10 tissues samples from urothelial cell carcinoma patients and 8 tissues samples from the normal bladder), were downloaded from the Gene Expression Omnibus database for further analysis. Differentially expressed genes (DEGs) were screened between benign the mucosa and control groups in GSE24152 and GSE42089 datasets. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) analysis were performed on overlapping DEGs identified in GSE24152 and GSE42089. Protein-protein interaction (PPI) networks and sub-networks were then constructed to identify key genes and main pathways. GO terms analysis was also performed for the selected clusters. In total, 1,325 DEGs in GSE24152 and 647 DEGs in GSE42089 were screened, in which 619 common DEGs were identified. The DEGs were mainly enriched in pathways and GO terms associated with mitotic and chromosome assembly, including nucleosome assembly, spindle checkpoint and DNA replication. In the interaction network, progesterone receptor (PGR), MAF bZIP transcription factor G (MAFG), cell division cycle 6 (CDC6) and members of the minichromosome maintenance family (MCMs) were identified as key genes. Histones were also considered to be significant factors in BC. Nucleosome assembly and sequence-specific DNA binding were the most significant clustered GO terms. In conclusion, the DEGs, including PGR, MAFG, CDC6 and MCMs, and those encoding the core histone family were closely associated with the development of BC via pathways associated with mitotic and chromosome assembly.

Salt metathesis routes to homoleptic near-linear Mg(ii) and Ca(ii) bulky bis(silyl)amide complexes.

Herein we investigate salt metathesis reactions of bulky bis(silyl)amide potassium salts [K{N(SiMe2tBu)2}]n, [K{N(SiMe2tBu)(SiiPr3)}]n, [K{N(SiiPr3)2}]n and [K{N(SiPh3)2}]n (1) with AeI2 (Ae = Mg, Ca, Sr) in an effort to synthesise rare homoleptic two-coordinate complexes. Recrystallization of 1 from THF provided structural authentication of the solvated adduct [K{N(SiPh3)2}(THF)3] (1-THF). For Ae = Mg we were able to identify products for three of the four bis(silyl)amides investigated: [Mg{N(SiMe2tBu)2}2(THF)] (2), [Mg{N(SiMe2tBu)(SiiPr3)}2] (3) and [Mg{N(SiPh3)2}2] (4). Complexes 2-4 were isolated in good yields, and on one occasion during recrystallization of 2 a crystal of the heteroleptic complex [Mg{N(SiMe2tBu)2}(I)(THF)2] (5) was identified by XRD. We found that these methodologies were not widely applicable for larger Ae = Ca and Sr, as large quantities of the parent bis(silyl)amines formed in reaction mixtures; however, we were able to isolate the first near-linear Ca(ii) amide [Ca{N(SiiPr3)2}2] (6) from these studies. No Ae-containing products could be isolated from KC8/crown ether reductions of 3, 4 and 6. Complexes 1-4 and 6 were characterised by single crystal XRD, multinuclear NMR and FTIR spectroscopy and elemental analysis, whereas complex 5 was identified by single crystal XRD only.

Chromium chains as polydentate fluoride ligands for actinides and group IV metals.

The reactions of {Cr6} horseshoe chains {[nPr2NH2]3[Cr6F11(O2CtBu)10]}2, 1 and precursors of actinides and group IV metals led to a series of ring complexes [nPr2NH2][Cr7TiF6O2(O2CtBu)16], 2, [nPr2NH2][Cr6Ti2F5O3(O2CtBu)16], 3, [Cr6ThF7(O2CtBu)15 (Me2SO)], 4, [(nPr2NH2)2(Cr6Th2F12(O2CtBu)16)], 5 and [nPr2NH2][Cr6U2O2F8(O2CtBu)16(Me2SO)], 6. X-ray structure studies indicate that the {Cr6} chains maintain their structures in these complexes, acting as polydentate fluoride ligands. Their static magnetic properties were measured and fitted by isotropic exchange Hamiltonian. In accordance with 1, the magnetic exchanges between CrIII are antiferromagnetic, while the exchange interactions can be modified by the tetravalent metals. For compound 6, ferromagnetic exchanges JCr-U and JU-U are obtained. EPR spectra of compounds 2-5 were measured at Q band and were simulated. The spectrum of 2 has the same profile as {Cr7Cd} and {Cr7Zn} rings with a ground state S = 3/2. 3, 4 and 5 give similar EPR spectra with S = 0 ground states.

Reversible crystal-to-crystal transformation from a trinuclear cluster to a 1D chain and the corresponding spin crossover (SCO) behaviour change.

Reversible crystal-to-crystal transformation between a linear trinuclear Fe(ii) complex [Fe3(NH2-trz)6(SCN)5(H2O)] (SCN)·4H2O (1, NH2-trz = 4-amino-1,2,4-triazole) and a 1D chain [Fe3(NH2-trz)6(SCN)5]n(SCN)n (1a) and the SCO behaviour change have been studied by X-ray single-crystal diffraction, magnetic measurements and DSC. Complex 1a exhibits one more SCO step at a low temperature.