Acute liver failure with thrombotic microangiopathy due to sodium valproate toxicity: A case report.

BACKGROUND: Sodium valproate is widely used in the treatment of epilepsy in clinical practice. Most adverse reactions to sodium valproate are mild and reversible, while serious idiosyncratic side effects are becoming apparent, particularly hepatotoxicity. Herein, we report a case of fatal acute liver failure (ALF) with thrombotic microangiopathy (TMA) caused by treatment with sodium valproate in a patient following surgery for meningioma. CASE SUMMARY: A 42-year-old man who received antiepileptic treatment with sodium valproate after surgery for meningioma exhibited extreme fatigue, severe jaundice accompanied by oliguria, soy sauce-colored urine, and ecchymosis. His postoperative laboratory values indicated a rapid decreased platelet count and hemoglobin level, severe liver and kidney dysfunction, and disturbance of the coagulation system. He was diagnosed with drug-induced liver failure combined with TMA. After plasma exchange combined with hemoperfusion, pulse therapy with high-dose methylprednisolone, and blood transfusion, his liver function deteriorated, and finally, he died. CONCLUSION: ALF with TMA is a rare and fatal adverse reaction of sodium valproate which needs to be highly valued.

[Cardioprotective mechanism of calreticulin up-regulation induced by hypoxic postconditioning.].

Calreticulin (CRT) is an essential Ca(2+)-binding chaperone existing in endoplasmic reticulum (ER) or sarcoplasmic reticulum (SR), and is involved in intracellular Ca(2+) homeostasis and protein folding. Ischemic postconditioning (I-postC), a newly discovered endogenous protective phenomenon, induces CRT up-regulation. The present study aimed to investigate the cardioprotective mechanism of CRT up-regulation induced by hypoxic postconditioning (H-postC). Primary cultured neonatal rat cardiomyocytes were exposed to 2 h of hypoxia followed by 24 h of reoxygenation. Postconditioning was carried out by two cycles of 10 min of reoxygenation and 20 min of rehypoxia after 2 h of hypoxia. Antisense oligodeoxynucleotides (AS-ODNs) were used to inhibit CRT expression 36 h before hypoxia. Cardiomyocytes were randomly divided into 6 groups as follows (n=4): control, hypoxia/reoxygenation (H/R), H-postC, AS, AS + H/R, and AS + H-postC. Morphological studies, lactate dehydrogenase (LDH) activity assay in culture medium, and flow cytometry were used to detect cardiomyocyte necrosis and apoptosis. Intracellular Ca(2+) concentration was detected by fluorescent Fluo-3/AM staining through laser confocal microscope, and p-nitrophenyl phosphate (PNPP) was used as substrate to measure calcineurin (CaN) activity. The expression of CRT, CaN, nuclear factor kappa B (NFκB) and apoptosis-related proteins, such as Bcl-2, Bax and C/EBP homologous protein (CHOP) were detected by Western blot. The results were as follows. (1) H-postC protected neonatal cardiomyocytes from H/R injury. Compared with H/R group, cell survival rate increased by 17.1%, apoptotic rate and LDH leakage decreased by 6.67% and 27.9% in H-postC group, respectively (P<0.05). (2) H-postC induced mild up-regulation of CRT expression. Inhibition of CRT by AS-ODNs attenuated the cardioprotection of H-postC partly. Compared with H-postC group, cell survival rate decreased by 8.98%, and apoptotic rate and LDH leakage increased by 1.74% and 13.6% in AS + H-postC group, respectively (P<0.05), but intracellular Ca(2+) concentration, CaN activity, and expression of CaN and NFκB did not change significantly (P>0.05), suggesting that CRT participates in endogenous protection, not through Ca(2+)-CaN pathway. (3) H-postC inhibited the expression of pro-apoptosis proteins such as Bax and CHOP, but induced up-regulation of anti-apoptosis protein Bcl-2. Inhibition of CRT by AS-ODNs partly inhibited the changes in apoptosis-related proteins expression induced by H-postC, suggesting that CRT participates in the anti-apoptosis effect of H-postC through regulating expression of apoptosis-related proteins. These results indicate that CRT up-regulation induced by H-postC is involved in the cardioprotection through regulating expression of apoptosis-related proteins, not through Ca(2+)-CaN pathway in neonatal cardiomyocytes.

C-banding and AgNOR-staining were still effective complementary methods to indentify chromosomal heteromorphisms and some structural abnormalities in prenatal diagnosis.

BACKGROUND: In prenatal diagnosis, CMA has begun to emerge as a favorable alternative to karyotype analysis, but it could not identify balanced translocations, triploidies, inversion and heteromorphisms. Therefore, conventional cytogenetic and specific staining methods still play an important role in the work-up of chromosome anomaly. This study investigated the application of C-banding and AgNOR-staining techniques in prenatal diagnosis of chromosomal heteromorphisms and some structure abnormalities. RESULTS: Among the 2970 samples, the incidence of chromosomal heteromorphisms was 8.79% (261/2970). The most frequent was found to be chromosome Y (2.93%, 87/2970), followed by chromosome 1 (1.65 %, 49/2970), 9 (1.52 %, 45/2970), 22 (0.77 %, 23/2970) and 15 (0.64 %, 19/2970). We compared the incidence of chromosomal heteromorphisms between recurrent spontaneous abortion (RSA) group and control group. The frequency of autosomal hetermorphisms in RSA group was 7.63% higher than that in control group (5.78%), while the frequency of Y chromosomal heteromorphisms was 4.76% lower than that in control group (5.71%). Here we summarized 4 representative cases, inv (1) (p12q24), psu dic (4;17) (p16.3;p13.3), r(X)(p11; q21) and an isodicentric bisatellited chromosome to illustrate the application of C-banding or AgNOR-staining, CMA or NGS was performed to detect CNVs if necessary. CONCLUSIONS: This study indicated that C-banding and AgNOR-staining were still effective complementary methods to identify chromosomal heteromorphisms and marker chromosomes or some structural rearrangements involving the centromere or acrocentric chromosomes. Our results suggested that there was no evidence for an association between chromosomal heteromorphisms and infertility or recurrent spontaneous abortions. Undoubtedly, sometimes we needed to combine the results of CMA or CNV-seq to comprehensively reflect the structure and aberration of chromosome segments. Thus, accurate karyotype reports and genetic counseling could be provided.

Tenofovir and telbivudine combination therapy rapidly decreases viral loads in immune-tolerant chronic hepatitis B patients awaiting assisted reproduction: an open-label, randomized, controlled study.

BACKGROUND: Immune-tolerant chronic hepatitis B (CHB) patients awaiting assisted reproduction (AR) are required to initiate antiviral therapy because of laboratory safety concerns. The antiviral therapy in this group has not been well assessed. We sought to explore the efficacy and safety of the combination therapy (COM) of tenofovir (TDF) and telbivudine (LdT). PATIENTS AND METHODS: In this open-label, randomized, controlled study, we enrolled and randomized hepatitis B virus e-antigen (HBeAg)-positive CHB patients awaiting AR into the study COM group and the control (TDF) group. The COM group received combination therapy of TDF and LdT, and the TDF group received a single treatment of TDF. The patients were followed up for at least 48 weeks. The primary endpoint was the proportion of patients with undetectable HBV DNA level at week 12. RESULTS: A total of 121 patients were recruited into the COM group (n=60) and the TDF group (n=61). The percentages of patients with undetectable HBV DNA levels were 90.0% (54/60) in the COM group and 67.2% (41/61) (P=0.002) in the TDF group at week 12; the percentages were 96.6% (58/60) in the COM group and 85.2% (52/61) in the TDF group at week 48 (P=0.028), respectively. HBeAg seroconversion occurred in 5/60 (8.3%) patients in the COM group and 2/61 (3.3%) patients in the TDF group at week 48 (P=0.233). CONCLUSION: TDF and LdT combination therapy shows a rapid antivirological response in immune-tolerant CHB patients awaiting AR, which provide an alternative for this group at AR centers. However, the HBeAg seroconversion rate is unsatisfactory in the short term.

High resolution global chromosomal aberrations from spontaneous miscarriages revealed by low coverage whole genome sequencing.

OBJECTIVE: Chromosome aberrations are generally considered as one of the most substantial causative factors contributing to spontaneous miscarriages. Cytogenetic analyses like G-banded karyotype and chromosomal microarray analyses are often performed to further investigate the chromosome status of a miscarried fetus. STUDY DESIGN: Here, we describe a novel method, AnnoCNV, to detect DNA copy number variations (CNVs) using low coverage whole genome sequencing (WGS). We investigated the overall frequency of chromosomal abnormalities in 149 miscarriage specimens using AnnoCNV. RESULTS: Among 149 fetal miscarriage samples, more than two fifths of them (42.95%, 64) carried at least one chromosomal abnormality, and a subset (40) was identified as autosomal trisomy which account for 26.84% of all samples. We have also developed a robust algorithm in AnnoCNV, which is able to differentiate specifically karyotype 69,XXY from sex chromosomal aneuploidy 45,X, and to identify 45,X/46,XX mosaicism. Lastly, across the whole genome AnnoCNV identifies CNVs, which are associated with both reported symptoms and unknown clinical conditions. CONCLUSION: This cost-effective strategy reveals genome wide discovery of chromosome aberrations at higher resolution, which are consistent with parallel investigation conducted by SNP based assay.

Down-regulation of perlecan expression contributes to the inhibition of rat cardiac microvascular endothelial cell proliferation induced by hypoxia.

Exposure of endothelial cells (ECs) to hypoxia leads to a decrease in EC proliferation. However, the mechanism by which hypoxia inhibits EC proliferation is unclear. Perlecan has been reported to play an important role in regulating EC proliferation. We hypothesized that perlecan was involved in the hypoxia-induced inhibition of EC proliferation. To test this hypothesis, rat cardiac microvascular ECs were cultured under normoxic or hypoxic conditions for 12 h and harvested for determination of perlecan mRNA expression using real-time reverse transcription-polymerase chain reaction (RT-PCR). The results showed that exposure of ECs to hypoxia for 12 h induced a decrease in perlecan mRNA expression (61.72%, P<0.05). Concomitantly, the down-regulation of endogenous perlecan induced by hypoxia or the neutralization of endogenous perlecan with anti-perlecan antibody significantly inhibited EC proliferation and responsiveness to basic fibroblast growth factor (bFGF), and decreased focal adhesion kinase (FAK) expression and extracellular signal-regulated kinase 1/2 (ERK1/2) activation. These data indicate that down-regulation of perlecan expression contributes to hypoxia-induced inhibition of rat cardiac microvascular EC proliferation by suppressing FAK-mediated and ERK1/2-dependent growth signals.

[Perlecan participates in the protection of ischemic myocardium induced by basic fibroblast growth factor: experiment with rats].

OBJECTIVE: To investigate if perlecan (PN) is involved in the myocardial protection of basic fibroblast growth factor (bFGF) in acute myocardial infarction. METHODS: Twenty-four Wistar rats were randomized into 3 groups: myocardial infarction group (MI group, n = 8, undergoing ligation of the descending anterior branch of the left coronary artery), bFGF + MI group (n = 10, injected with bFGF into the border myocardium between the infracted and non- infracted areas immediately after the ligation of the descending anterior branch), and sham operation group (n = 6, undergoing sham operation and injection of normal saline). 24 h, 14 days, and 28 days after the operation the hemodynamic parameters, infarct size, and microvessel density (MVD) were observed. The hearts were taken out, RT-PCR was used to detect the mRNA expression of PN, and Western blotting was used to detect the expression of focal adhesion kinase (FAK) and p38 mitogen-activated protein kinase (MAPK) phosphorylation. RESULTS: In the bFGF + MI group, the +dp/dt and -dp/dt were improved markedly, the infarct size was significantly smaller, the MVD value was higher than those of the MI group on day 14 and day 28; the perlecan mRNA expression was higher in the infarct marginal area and interior zone; and the expression of FAK and the p38MAPK phosphorylation were up-regulated in the marginal zone of the bFGF group. CONCLUSION: bFGF is useful in promoting ischemic myocardial angiogenesis; reducing the size of infracted myocardium, and improving the ventricular function in acute myocardial infarction. Perlecan participates in the cardiac protection induced by bFGF. The relevant pathway is related to up-regulation of FAK and p38MAPK.

[Factors influencing tree radial growth of three common species in broad-leaved Korean pine mixed forests in Changbai Mountains, China]. / 长白山阔叶红松林3ä¸ªå¸¸è§æ ‘ç§å¾„å‘ç”Ÿé•¿çš„å½±å“å› ç´ .

To understand the factors influencing tree radial growth, we analyzed the seasonal dynamics of tree growth of 3 common species (Pinus koraiensis, Tilia amurensis, Quercus mongolica), compared interspecific growth rates and explored the effects of size, neighborhood competition, soil and topography based on five years dendrometer bands monitoring data of the 3 common species in a broad-leaved Korean pine (P. koraiensis) mixed forest plot in Changbai Mountain, Northeast China. The results showed that the growth dynamics of 3 species were consistent. Trees began to grow in late May, thrived in July, grew at declining rates from late August and stopped growing in late October. Annual relative growth rates were significantly different among the species. Q. mongolica tended to grow faster than the other two species, and the differences of growth rates among the 3 species were especially large for small and medium trees. Tree growth rates of P. koraiensis and Q. mongolica were strongly decreased by neighborhood competition, while tree growth rate of T. amurensis was significantly related to tree size, soil and topography.

[Hypoxic preconditioning induces endoplasmic reticulum stress-related cardioprotection mediated by p38 mitogen-activated protein kinase].

Calreticulin (CRT), an important Ca(2+)-binding molecular chaperone in the endoplasmic reticulum (ER), and caspase-12, a pivotal molecule mediating ER-initiated apoptosis, are involved in the ER stress (ERS). Using primary cultured neonatal cardiomyocytes, CRT and caspase-12 expression and activation during hypoxic preconditioning (HPC) and hypoxia/reoxygenation (H/R) were studied to explore the role of ERS in cardioprotection by HPC. And by using SB203580 and SP600125 [the specific inhibitors of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK)] separately, the role of p38 MAPK in HPC-induced ERS was also detected. Neonatal cardiomyocytes were prepared from Sprague-Dawley rats aged 24 h, and cultured in DMEM medium containing 10% fetal bovine serum, and then randomly divided into six groups as follows: H/R, HPC+H/R, SB203580+HPC+H/R, SP600125+HPC+H/R, HPC and control groups. H/R was produced by 2-hour hypoxia/14-hour reoxygenation, and HPC by 20-minute hypoxia/24-hour reoxygenation. Morphological studies, estimation of lactate dehydrogenase (LDH) leakage and flow cytometry were employed to assess cell apoptosis and necrosis. CRT and caspase-12 expression and activation, levels of phospho-p38 MAPK and phospho-JNK were detected by Western blot. All experiments were repeated at least four separate times. The results obtained are as follows: (1) HPC relieved the cell injury caused by H/R. Compared with that in H/R group, cellso survival rate in HPC+H/R group increased by 6.4%, and the apoptosis rate and LDH leakage in the cell culture medium decreased by 6.6% and 70.0%, respectively. (2) H/R induced caspase-12 activation (33.2-fold increase in comparison with control) and CRT expression (8.1-fold increase in comparison with control). HPC itself resulted in mild CRT up-regulation (2.6-fold increase in comparison with control), but the extent of up-regulation was lower than that induced by H/R. HPC before H/R was found to relieve the over-expression of CRT induced by H/R (72.4% decrease), and to inhibit the activation of caspase-12 (59.6% decrease). (3) The protection of HPC and HPC-induced up-expression of CRT and inhibition of caspase-12 activation were almost eliminated when the inhibitor of p38 MAPK, not of JNK, was present before HPC. These results suggest that HPC protects the neonatal cardiomyocytes from severe ERS-induced apoptosis during sustained H/R through pre-invoking proper ERS response. Mild up-expression of CRT and inhibition of caspase-12 activation induced by HPC, which are important protection factors, are mediated by p38 MAPK, not by JNK.

Complete mitochondrial genome sequence and mutations of the hepatocellular carcinoma model inbred Sprague-Dawley strain.

In the present work we undertook the complete mitochondrial genome sequencing of an important hepatocellular carcinoma model inbred Sprague-Dawley strain for the first time. The total length of the mitogenome was 16,308 bp. It harbored 13 protein-coding genes, two ribosomal RNA genes, 22 transfer RNA genes and one non-coding control region (D-loop region). The mutation events were also reported.

[Role of hypoxia-inducible factor-1alpha in the prevention of cardiomyocyte injury induced by hypoxic preconditioning].

In order to understand the intracellular mechanism of preconditioning, we investigated the relationship among activities of extracellular signal-regulated protein kinases (ERKs), the expression of hypoxia-inducible factor -1alpha (HIF-1alpha) and the effect of hypoxic preconditioning (HPC) on cell injury induced by hypoxia-reoxygenation in cultured neonatal rat cardiomyocytes 24 h after brief hypoxia. Cultured cardiomyocytes of neonatal Sprague-Dawley rats were divided into four groups: hypoxia/reoxygenation (H/R), hypoxia preconditioning (HPC), hypoxia preconditioning + mitogen-activated protein kinase (MAPK) inhibitor PD98059 (HPC+PD98059), and control (C). We measured the survival rate and apoptosis rate of cardiomyocytes at 6 or 12 h after hypoxia/reoxygenation, activities of extracellular signal-regulated protein kinases (ERKs), and expression of hypoxia-inducible factor-1alpha (HIF-1alpha). We found that the survival rate of cardiomyocytes in hypoxic preconditioning group increased by 6.08% and 7.91% at 6 and 12 h after hypoxia/reoxygenation (n=6, P<0.05), respectively, and the apoptotic rate decreased by 10.92% and 14.34% (n=6, P<0.05) respectively. Hypoxic preconditioning increased the abundance of phospho-ERK1/2 by 3-folds and expression of HIF-1alpha by 1-fold in whole cell extracts from hypoxic preconditioned cardiomyocytes. PD98059, an inhibitor of the upstream kinase of ERKs, abolished the anti-injury effect, ERKs activation, and expression of HIF-1alpha induced by hypoxic preconditioning. Statistical analysis indicated that there was negative correlation between apoptotic rate and activities of ERKs or expression of HIF-1alpha, and positive correlation between activities of ERKs and expression of HIF-1alpha. It is concluded that hypoxic preconditioning protects cardiomyocytes from hypoxia/reoxygenation-induced injury and that upregulation of HIF-1alpha through ERKs pathway mediates the cardioprotection of hypoxic preconditioning.

[C3d molecular adjuvant increases the immunity of human chorionic gonadotropin beta DNA contraceptive vaccination and changes its immune response from Th1 to Th2].

OBJECTIVE: To testify the effect of C3d molecular adjuvant on the immunogenicity of human chorionic gonadotropin beta (hCG beta) DNA vaccination as well as the mode of immune response. METHODS: BALB/c mice aged 6 weeks were immunized intramuscularly two times at an interval of 3 weeks with by the plasmid pcDNA3 (A1-3 groups), pcDNA3-hCG beta (B-3 groups), pcDNA3-hCG beta-C3d3 (C1-3 groups), or pCMV4-hCG beta-C3d3 (D1-3 groups), at dosage of 5 pmol, 10 pmol, and 20 pmol, respectively. Three weeks after the second vaccination the animals were killed, specimens of their peripheral blood were extracted to determine the anti-hCG beta antibody titer by indirect ELISA. Their spleen cells were harvested and stimulated in vitro by hCG antigen for 24 hours. The Th1/Th2 cytokines in the culture supernatant were determined by ELISA. RESULTS: At the dosage of 20 pmol, C3d molecular adjuvant significantly enhanced the anti-hCG beta antibody titer. The utmost anti-hCG beta antibody titer of C3 group was 1:450, 9 times higher than that of B3 group, and the utmost anti-hCG beta antibody titer of D3 group was 1:12 150, 243 times higher than that of B3 group. Stimulated in vitro by 5,000 IU hCG beta antigen, the splenic cells of the C3 and D3 immunization group produced significantly lower IL-2, INF-gamma and TNF-alpha than those of the B3 immunization group (P < 0.01 or P < 0.05). The IL-4 level of the C3 group was higher than that of the B3 group while the IL-10 level of the D3 group was significantly higher than that of the B3 group (P < 0.01). CONCLUSIONS: The C3d molecular adjuvant increases significantly the hCG beta immunogenicity of hCG beta DNA vaccination; meanwhile decreases the secretion of Th1 cytokines (IL-2, INF-gamma, and TNF-alpha), and increases the expression of Th2 cytokines (IL-4 and IL-10) in response to hCG antigen. So C3d changes the anti-hCG immune response from Th1 type to Th2 type.

ARC contributes to the inhibitory effect of preconditioning on cardiomyocyte apoptosis.

UNLABELLED: Inhibition of cardiomyocyte apoptosis plays a key role in preconditioning-triggered cardioprotection. However, the molecular mechanism(s) by which preconditioning inhibits apoptosis is not fully understood. Apoptosis repressor with caspase recruitment domain (ARC) possesses the ability to block hypoxia-induced cardiomyocyte apoptosis. We tested whether ARC contributes to the inhibitory effect of preconditioning on cardiomyocyte apoptosis. Cardiomyocytes from 1-day-old male Sprague-Dawley rats were preconditioned by exposing to 10 min of hypoxia, followed by 30 min of reoxygenation. Then, the preconditioned and non-preconditioned cardiomyocytes were exposed to 90 min of hypoxia followed by 120 min of reoxygenation. The results showed that preconditioning inhibited cell death induced by hypoxia and reoxygenation. Hypoxia and reoxygenation could induce a decrease of ARC protein levels. Intriguingly, preconditioning could maintain ARC protein levels. Inhibition of endogenous ARC expression by ARC antisense oligonucleotides reduced the inhibitory effect of preconditioning on apoptosis. Furthermore, preconditioning-induced suppression of the release of mitochondrial cytochrome c to cytosol and caspase-3 activation could be abolished by the inhibition of endogenous ARC expression using ARC antisense oligonucleotides. CONCLUSION: These data indicate that ARC participates in preconditioning-triggered cardioprotection by interfering with cytochrome c release and caspase-3 activation.

[Effects of human urotensin II on pia mater microcirculation in rats].

AIM: To investigate the effects of human urotensin II (hUII) on in vivo pia mater microcirculation in rats. METHODS: Adult SD rats were randomly assigned to the following groups: control, sodium chloride injection (NS), UII(10(-6) mol/L), noradrenaline (NA, 10(-6) mol/L), and UII (10(-6) mol/L) + NA (10(-6) mol/L) groups. For recording of microcirculation images in pia mater, skull windows were performed and mounted on the stage of an intravital microscope equipped with a TV camera. Video images of microcirculation were stored by a video cassette recorder. Temporal changes in internal diameter and microcirculatory velocity of microvessels were measured by computer using the Image Pro software. The blood flow in cerebral tissues were measured with PIMII laser Doppler perfusion Imager (Lisca, Sweden). RESULTS: The internal diameters of arterioles and venules in control group were (35.4 +/- 3.6) microm and (40.6 +/- 8.5) microm, respectively. In UII group, the arterioles and venules contracted immediately after treated with UII and up to the peak at 1 min, the internal diameters of arterioles and venules were (25.6 +/- 3.4) microm and (23.4 +/- 3.3) microm, respectively (P < 0.05). Both microcirculatory velocity in arterioles and venules had no significant changes in UII group (P > 0.05). The blood flow in meninges increased 1 min after treated with UII and up to high peak at 5 min (3.5 +/- 0.4 perfusion unit vs. control 2.3 +/- 0.6, P < 0.05). CONCLUSION: hUII can contract microvessels in pia mater of rats and increase microcirculatory blood perfusion to cerebral tissue involved.

Mono-, di-, and tetranuclear ruthenium(II) complexes containing 3-(pyridin-2-yl)-as-triazino[5,6-f]1,10-phenanthroline: synthesis, characterization, and electrochemical and photophysical properties.

Mono-, di-, and tetranuclear Ru(II) polypyridine complexes based on the bridging ligand pdtp, where pdtp is 3-(pyridin-2-yl)-as-triazino[5,6-f]1,10-phenanthroline, have been synthesized and characterizated. This asymmetric bridging ligand is composed of two nonequivalent coordinating sites: one involves the phenanthroline moiety, and the other one involves the pyridyltriazine moiety. Electrochemical data show that the first redox process in these complexes is pdtp based and the metal-metal interaction in di- and tetranuclear complexes is very weak. The two oxidations (+1.41 and +1.56 V vs SCE) observed in dinuclear complex 2 are mainly ascribed to the different coordination environments of two metal centers. Absorption spectra are essentially the sum of the spectra of the component monometallic species. The emission spectra are measured both at room temperature and at 80 K in a 4:1 (v/v) EtOH/MeOH matrix. The complexes all display luminescence properties which are close to that featured by the parent [Ru(phen)(3)](2+) species. It is also noted that center-to-periphery energy transfer occurs in the dendritic tetranuclear complex 3.