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Biomedical subjects

S Lin

Publications and source records attributed to S Lin.

At least 55 records · Page 3Linked to original sources
PubMed2002

A laboratory study of the effect of calcium hydroxide mixed with iodine or electrophoretically activated copper on bacterial viability in dentinal tubules.

AIM: The aim of this laboratory study was to evaluate the ability of calcium hydroxide (CH), CH/iodine-potassium iodide (IKI) and electrophoretically activated copper to kill bacteria in dentinal tubules. METHODOLOGY: In an in vitro model of dentinal tubule infection, 42 cylindrical root specimens, prepared from freshly extracted bovine teeth were used. After removal of the smear layer, intracanal dentinal tubules were infected with Enterococcus faecalis for 3 weeks. CH alone or preparations of CH with copper or IKI were placed in the root canal for 1 week. In specimens containing copper/CH, an electrophoretic current(5 mA/5 min) was applied using two electrodes follow-ing placement of the medicament in the canal. Powder dentine samples obtained from the canal wall using ISO sizes: 025, 027, 029, 031 and 033 burs were examined for the presence of viable bacteria by inoculating agar plates and counting colony forming units (cfu). RESULTS: A significant difference was found between the experimental groups and the positive control group. CH and CH/IKI significantly (P < 0.001)reduced bacterial viability in dentinal tubules to a depth of 200 microm. Specimens with CH/IKI had significantly fewer viable bacteria than CH alone in tubules between the depths of 200-500 microm. Treatment with CH/copper and electrophoresis was most effective: specimens showed no viable bacteria in dentinal tubules to a depth of 500 microm from the root-canal space. CONCLUSIONS: IKI or electrophoretically activated copper additives can significantly improve the antibacterial properties of CH in dentinal tubules.

Animals↗
PubMed2002

Endoscopic cyclophotocoagulation.

Glaucoma surgery can be classified as either cyclodestructive (reducing inflow) or filtering (increasing outflow). Filtration has traditionally been the procedure of first resort because of its efficacy and relative predictability, whereas ciliary destruction has been reserved for more refractory cases of glaucoma and in eyes which have little or no visual potential. Refractory glaucomas include neovascular glaucoma, post-traumatic glaucoma, glaucoma associated with aphakia, severe congenital/developmental glaucoma, post-retinal surgery glaucoma, glaucoma associated with penetrating keratoplasties, and glaucoma in eyes with scarred conjunctiva from surgery or disease processes.

Blindness↗
PubMed2001

[Therapeutic effect of medical therapy upon undifferentiated nasopharyngeal carcinoma: analysis of 149 cases].

OBJECTIVE: To study the therapeutic effect and prognosis of undifferentiated nasopharyngeal carcinoma. METHODS: 149 patients with undifferentiated nasopharyngeal carcinoma, 4 at stage I, 33 at stage II, 73 at stage III, and 39 at stage IV according to the Fuzhou Staging Criteria of Nasopharyngeal Carcinoma 1992, were treated mainly by radiotherapy from 1999 to 2000: 78 of them underwent radiotherapy alone, 32 underwent radiotherapy combined with induced chemotherapy, and 39 underwent radiotherapy combined with synchronized chemotherapy. Relevant clinical data, especially the therapeutic effect upon and prognosis of the type, were analyzed. RESULTS: Undifferentaited nasopharyngeal carcinoma accounts for 3.58% of nasopharyngeal carcinoma and was with a 5-year overall survival rate (OS) of 64.48%, a disease-free survival rate (DFS) of 60.35%, a distance-metastasis-free (DMF) survival rate of 77.05%, and a local recurrence free (LRF) survival rate of 80.13%. The key factors influencing prognosis were the stage of N and stage of international classification of cancer based on TNM. CONCLUSION: Undifferentiated nasopharyngeal carcinoma is a rare type. Its prognosis is influenced mainly by the stage of N and TNM. Treatment maninly on radiotherapy is effective.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2001

Linkage studies between attention-deficit hyperactivity disorder and the monoamine oxidase genes.

Attention-deficit hyperactivity disorder (ADHD) is a prevalent behavioral disorder in children and the etiology of this disorder is not clear. Molecular genetic and pharmacological studies suggest the involvement of dopaminergic and noradrenergic neurotransmitter systems in ADHD, e.g., several reports have found association between ADHD and the dopamine receptor gene DRD-4, the dopamine transporter gene DAT1, and the catecholamine clearance enzyme catechol-O-methyltransferase. Monoamine oxidase (MAO) A and B genes encode enzymes that participate in the metabolism of neurotransmitters of the dopaminergic and noradrenergic systems. MAO inhibitors have been shown to be effective in the treatment of ADHD. Our previous studies showed an association between ADHD and the DXS7 locus, which is located in close vicinity to the MAO genes on chromosome X. These findings suggest that there might be linkage between ADHD and MAO genes. To test this hypothesis, we used the transmission/disequilibrium test (TDT) to test for linkage between a VNTR polymorphism at the MAOA(CA)(n) or MAOB(GT)(n) locus and DSM-III-R-diagnosed ADHD in 82 nuclear families of the Chinese population. The TDT analysis revealed linkage between ADHD and the MAOA(CA)(n) locus (chi-square = 15.25, df = 7, P < 0.05), but not the MAOB(GT)(n) locus (chi-square = 11.18, df = 7, P > 0.05). The data showed that ADHD was in linkage with the MAOA gene and suggested that MAOA might be a susceptibility factor for ADHD.

Alleles↗
PubMed2001

Minocycline prevents nigrostriatal dopaminergic neurodegeneration in the MPTP model of Parkinson's disease.

Parkinson's disease is a chronic neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra, decreased striatal dopamine levels, and consequent extrapyramidal motor dysfunction. We now report that minocycline, a semisynthetic tetracycline, recently shown to have neuroprotective effects in animal models of stroke/ischemic injury and Huntington's disease, prevents nigrostriatal dopaminergic neurodegeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. Minocycline treatment also blocked dopamine depletion in the striatum as well as in the nucleus accumbens after MPTP administration. The neuroprotective effect of minocycline is associated with marked reductions in inducible NO synthase (iNOS) and caspase 1 expression. In vitro studies using primary cultures of mesencephalic and cerebellar granule neurons (CGN) and/or glia demonstrate that minocycline inhibits both 1-methyl-4-phenylpyridinium (MPP(+))-mediated iNOS expression and NO-induced neurotoxicity, but MPP(+)-induced neurotoxicity is inhibited only in the presence of glia. Further, minocycline also inhibits NO-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) in CGN and the p38 MAPK inhibitor, SB203580, blocks NO toxicity of CGN. Our results suggest that minocycline blocks MPTP neurotoxicity in vivo by indirectly inhibiting MPTP/MPP(+)-induced glial iNOS expression and/or directly inhibiting NO-induced neurotoxicity, most likely by inhibiting the phosphorylation of p38 MAPK. Thus, NO appears to play an important role in MPTP neurotoxicity. Neuroprotective tetracyclines may be effective in preventing or slowing the progression of Parkinson's and other neurodegenerative diseases.

Animals↗
PubMed2001

Minocycline blocks nitric oxide-induced neurotoxicity by inhibition p38 MAP kinase in rat cerebellar granule neurons.

Minocycline, a semisynthetic second-generation tetracycline, was reported to have neuroprotective effects in models of global and focal cerebral ischemia, the R6/2 mouse model of Huntington disease, as well as glutamate-induced neurotoxicity in mixed neuronal/glial cultures. It was suggested that neuroprotective effects of minocycline resulted from inhibition of microglial/astroglial activation 'Proc. Natl. Acad. Sci. USA 95 1998 15769'. To determine whether or not minocycline is able to directly protect neurons against injury insults and to delineate its neuroprotective mechanism(s), we treated cultured rat cerebellar granule neurons (CGN) with nitric oxide (NO) in the presence or absence of minocycline. We found that minocycline protected neurons against NO-induced neuronal death in a concentration-dependent fashion. Consistent to other reports, NO was able to induce p38 MAP kinase phosphorylation at 3-6 h and such an induction could be significantly inhibited by minocycline. Furthermore, SB 203580, a p38 MAP kinase inhibitor, almost completely attenuated NO-induced neuronal death of CGN as well. These results suggest that minocycline is able to block NO-induced neurotoxicity in CGN by inhibiting NO-induced phosphorylation of p38 MAP kinase. Our finding may explain the neuroprotective mechanism of minocycline in those neurodegenerative models.

Animals↗
PubMed2001

Blue light drives B-side electron transfer in bacterial photosynthetic reaction centers.

The core of the photosynthetic reaction center from the purple non-sulfur bacterium Rhodobacter sphaeroides is a quasi-symmetric heterodimer, providing two potential pathways for transmembrane electron transfer. Past measurements have demonstrated that only one of the two pathways (the A-side) is used to any significant extent upon excitation with red or near-infrared light. Here, it is shown that excitation with blue light into the Soret band of the reaction center gives rise to electron transfer along the alternate or B-side pathway, resulting in a charge-separated state involving the anion of the B-side bacteriopheophytin. This electron transfer is much faster than normal A-side transfer, apparently occurring within a few hundred femtoseconds. At low temperatures, the B-side charge-separated state is stable for at least 1 ns, but at room temperature, the B-side bacteriopheophytin anion is short-lived, decaying within approximately 15 ps. One possible physiological role for B-side electron transfer is photoprotection, rapidly quenching higher excited states of the reaction center.

Bacteriochlorophylls↗
PubMed2001

[A randomized case-control study on the influence of percutaneous estradiol and progestin in cyclic combined regimen on endometrium and vaginal bleeding pattern in Chinese early postmenopausal women].

OBJECTIVE: To observe the influence of percutaneous estradiol + micronized progesterone or medroxyprogesterone on endometrium and vaginal bleeding in Chinese post-menopausal women. METHODS: A 3-year open randomized clinical study was designed. The estrogen and progestin were used continuous-combined together in a cyclic regimen. The percutaneous estradiol was regarded as estrogen. The microprogesterone (MP) and medroxyprogesterone (MPA) were served as progestin. Sixty healthy women (naturally menopausal for 1 to 5 years) were recruited and divided into four groups. The regimen as follows: (1) percutaneous estradiol gel (gel) containing 1.5 mg of 17 beta-estradiol (E2)/d plus micronized progesterone (MP) 100 mg/d in group 1 (G1, E2 1.5 + MP); (2) gel, 1.5 mg E2/d plus medroxyprogesterone acetate (MPA), 2 mg/d in group 2 (G2, E2 1.5 + MPA); (3) gel, 0.75 mg E2/d plus MP, 100 mg/d in group 3 (G3, E2 0.75 + MP); and (4) gel, 0.75 mg E2/d plus MPA, 2 mg/d in group 4 (G4, E2 0.75 + MPA). All were given for 25 d/month, and 5 days free. The transvaginal sonography was performed 0, 12, 24 and 36 months. The thickness of endometrium were measured. The endometrium biopsy by Pipelle tube was conducted at 24th or 36th months. The vaginal bleeding was recorded. RESULTS: Fifty-nine patients (98.3%) finished 1 year and 56 patients (93.3%) for 2 years, 51 (85%) for 3 years. There was no significant changes of endometrium. The thickness of endometrium before treatment in four groups were 0.25 cm, 0.27 cm, 0.22 cm, 0.28 cm and after treatment 0.37 cm, 0.30 cm, 0.326 7 cm and 0.3 cm respectively. No significant differences was found in four groups (P > 0. 05). Fifty -three patients had the Pipelle biopsy. The pathological result showed: 16 cases (25.8%) proliferated, 1 case (1.6%) secretary; 11 cases (17.7%) atrophy; 23 cases (37.1%) mixed cell; tendency to hyperplasia in 2 cases (3.2%). During the treatment, the vaginal irregular bleeding rate was highest in G2 and lowest in G3. CONCLUSIONS: Daily estrogen containing 0.75 mg and 1.5 mg E2 combined with 100 mg progesterone and 2 mg medroxyprogesterone do not increase the thickness of endometrium significantly. The vaginal bleeding rate was low when combined with 100 mg micronized progesterone. Addition of natural progesterone will low down the bleeding rate and improve the HRT compliance.

Adult↗
PubMed2001

The cellular metabolism and systemic toxicity of arsenic.

Although it has been known for decades that humans and many other species convert inorganic arsenic to mono- and dimethylated metabolites, relatively little attention has been given to the biological effects of these methylated products. It has been widely held that inorganic arsenicals were the species that accounted for the toxic and carcinogenic effects of this metalloid and that methylation was properly regarded as a mechanism for detoxification of arsenic. Elucidation of the metabolic pathway for arsenic has changed our understanding of the significance of methylation. Both methylated and dimethylated arsenicals that contain arsenic in the trivalent oxidation state have been identified as intermediates in the metabolic pathway. These compounds have been detected in human cells cultured in the presence of inorganic arsenic and in urine of individuals who were chronically exposed to inorganic arsenic. Methylated and dimethylated arsenicals that contain arsenic in the trivalent oxidation state are more cytotoxic, more genotoxic, and more potent inhibitors of the activities of some enzymes than are inorganic arsenicals that contain arsenic in the trivalent oxidation state. Hence, it is reasonable to describe the methylation of arsenic as a pathway for its activation, not as a mode of detoxification. This review summarizes the current knowledge of the processes that control the formation and fate of the methylated metabolites of arsenic and of the biological effects of these compounds. Given the considerable interest in the dose-response relationships for arsenic as a toxin and a carcinogen, understanding the metabolism of arsenic may be critical to assessing the risk associated with chronic exposure to this element.

Animals↗
PubMed2001

In vitro and in vivo evaluations of biodegradable implants for hormone replacement therapy: effect of system design and PK-PD relationship.

This investigation evaluated the feasibility of using subdermally implantable devices fabricated by nonconventional 3-dimensional printing technology for controlled delivery of ethinyl estradiol (EE2). In vitro release kinetics of EE2 and in vivo pharmacokinetics/pharmacodynamics in ovariectomized New Zealand White rabbits were carried out to study 3 implant prototypes: implant I (single-channel EE2 distribution in polycaprolactone polymer core), implant II (homogeneous EE2 distribution in polycaprolactone polymer matrix), and implant III (concentration-gradient EE2 distribution in polycaprolactone and poly(dl-lactide-co-glycolide) (50:50 matrix). EE2 was found to be released from all the implants in a nonlinear pattern with an order of implant III > implant II > implant I. The noncompartmental pharmacokinetic analysis of plasma EE2 profiles in rabbits indicated a significant difference (p < .05) in Cmax, tmax, and mean residence time between implant I and implants II and III, but no difference in the area under the plasma concentration time curves calculated by trapezoidal rule (AUC) among the implants. For pharmacodynamic studies, endogenous follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were observed to be suppressed following implantation of all implants, which demonstrated that a therapeutically effective dose of EE2 had been delivered. Furthermore, the noncompartmental analysis of plasma FSH and LH profiles in rabbits showed a significant difference (p < .05) in AUC and the mean residence time between implant III and implants I and II. A good in vivo/in vitro relationship was observed between daily amounts of EE2 released and plasma profiles of EE2 for all implants. This relationship suggests that plasma profiles of EE2 could be predicted from in vitro measurement of daily amount of EE2 released. Therefore, performing in vitro drug release studies may aid in the development of an EE2 implant with the desired in vivo release rate.

Absorbable Implants↗
PubMed2001

An agrin minigene rescues dystrophic symptoms in a mouse model for congenital muscular dystrophy.

Congenital muscular dystrophy is a heterogeneous and severe, progressive muscle-wasting disease that frequently leads to death in early childhood. Most cases of congenital muscular dystrophy are caused by mutations in LAMA2, the gene encoding the alpha2 chain of the main laminin isoforms expressed by muscle fibres. Muscle fibre deterioration in this disease is thought to be caused by the failure to form the primary laminin scaffold, which is necessary for basement membrane structure, and the missing interaction between muscle basement membrane and the dystrophin-glycoprotein complex (DGC) or the integrins. With the aim to restore muscle function in a mouse model for this disease, we have designed a minigene of agrin, a protein known for its role in the formation of the neuromuscular junction. Here we show that this mini-agrin-which binds to basement membrane and to alpha-dystroglycan, a member of the DGC-amends muscle pathology by a mechanism that includes agrin-mediated stabilization of alpha-dystroglycan and the laminin alpha5 chain. Our data provides in vivo evidence that a non-homologous protein in combination with rational protein design can be used to devise therapeutic tools that may restore muscle function in human muscular dystrophies.

Agrin↗
PubMed2001

Reduced levels of amyloid beta-peptide antibody in Alzheimer disease.

OBJECTIVE: To investigate whether it was possible to detect the presence and different levels of naturally occurring anti-beta-amyloid (Abeta) antibodies in the CSF of patients with AD and age-matched controls by employing a sensitive ELISA. BACKGROUND: Immunization with preaggregated amyloid beta-peptide (Abeta(1-42)) and administration of antibodies against Abeta into amyloid precursor protein APP(V717F)- transgenic mice (an animal model of AD) have recently been reported to dramatically reduce amyloid plaque deposition, neuritic dystrophy, and astrogliosis, most likely by enhancing Abeta clearance from brain. METHODS: A sensitive ELISA was performed to detect levels of naturally occurring anti-Abeta antibodies in the CSF of patients with AD and age-matched controls. Additionally, an immunoprecipitation assay was performed to confirm that naturally occurring anti-Abeta antibodies also exist in the human blood. RESULT: - Naturally occurring antibodies directed against Abeta were found in the CSF and plasma of patients with AD and healthy control subjects. Moreover, CSF anti-Abeta antibody titers are significantly lower in patients with AD compared with healthy control subjects. CONCLUSION: Naturally occurring antibodies directed against Abeta exist in human CSF and plasma. The CSF anti-Abeta antibody titers may be helpful in better understanding the effects of future immunologic therapies for AD.

Aged↗
PubMed2001

Lipid A modifications in polymyxin-resistant Salmonella typhimurium: PMRA-dependent 4-amino-4-deoxy-L-arabinose, and phosphoethanolamine incorporation.

Lipid A of Salmonella typhimurium can be resolved into multiple molecular species. Many of these substances are more polar than the predominant hexa-acylated lipid A 1,4'-bisphosphate of Escherichia coli K-12. By using new isolation methods, we have purified six lipid A subtypes (St1 to St6) from wild type S. typhimurium. We demonstrate that these lipid A variants are covalently modified with one or two 4-amino-4-deoxy-l-arabinose (l-Ara4N) moieties. Each lipid A species with a defined set of polar modifications can be further derivatized with a palmitoyl moiety and/or a 2-hydroxymyristoyl residue in place of the secondary myristoyl chain at position 3'. The unexpected finding that St5 and St6 contain two l-Ara4N residues accounts for the anomalous structures of lipid A precursors seen in S. typhimurium mutants defective in 3-deoxy-d-manno-octulosonic acid biosynthesis in which only the 1-phosphate group is modified with the l-Ara4N moiety (Strain, S. M., Armitage, I. M., Anderson, L., Takayama, K., Quershi, N., and Raetz, C. R. H. (1985) J. Biol. Chem. 260, 16089-16098). Phosphoethanolamine (pEtN)-modified lipid A species are much less abundant than l-Ara4N containing forms in wild type S. typhimurium grown in broth but accumulate to high levels when l-Ara4N synthesis is blocked in pmrA(C)pmrE(-) and pmrA(C)pmrF(-) mutants. Purification and analysis of selected compounds demonstrate that one or two pEtN moieties may be present. Our findings show that S. typhimurium contains versatile enzymes capable of modifying both the 1- and 4'-phosphates of lipid A with l-Ara4N and/or pEtN groups. PmrA null mutants of S. typhimurium produce lipid A species without any pEtN or l-Ara4N substituents. However, PmrA is not needed for the incorporation of 2-hydroxymyristate or palmitate.

Amino Sugars↗
PubMed2001

An inner membrane enzyme in Salmonella and Escherichia coli that transfers 4-amino-4-deoxy-L-arabinose to lipid A: induction on polymyxin-resistant mutants and role of a novel lipid-linked donor.

Attachment of the cationic sugar 4-amino-4-deoxy-l-arabinose (l-Ara4N) to lipid A is required for the maintenance of polymyxin resistance in Escherichia coli and Salmonella typhimurium. The enzymes that synthesize l-Ara4N and transfer it to lipid A have not been identified. We now report an inner membrane enzyme, expressed in polymyxin-resistant mutants, that adds one or two l-Ara4N moieties to lipid A or its immediate precursors. No soluble factors are required. A gene located near minute 51 on the S. typhimurium and E. coli chromosomes (previously termed orf5, pmrK, or yfbI) encodes the l-Ara4N transferase. The enzyme, renamed ArnT, consists of 548 amino acid residues in S. typhimurium with 12 possible membrane-spanning regions. ArnT displays distant similarity to yeast protein mannosyltransferases. ArnT adds two l-Ara4N units to lipid A precursors containing a Kdo disaccharide. However, as shown by mass spectrometry and NMR spectroscopy, it transfers only a single l-Ara4N residue to the 1-phosphate moiety of lipid IV(A), a precursor lacking Kdo. Proteins with full-length sequence similarity to ArnT are present in genomes of other bacteria thought to synthesize l-Ara4N-modified lipid A, including Pseudomonas aeruginosa and Yersinia pestis. As shown in the following article (Trent, M. S., Ribeiro, A. A., Doerrler, W. T., Lin, S., Cotter, R. J., and Raetz, C. R. H. (2001) J. Biol. Chem. 276, 43132-43144), ArnT utilizes the novel lipid undecaprenyl phosphate-alpha-l-Ara4N as its sugar donor, suggesting that l-Ara4N transfer to lipid A occurs on the periplasmic side of the inner membrane.

Amino Sugars↗
PubMed2001

Accumulation of a polyisoprene-linked amino sugar in polymyxin-resistant Salmonella typhimurium and Escherichia coli: structural characterization and transfer to lipid A in the periplasm.

Polymyxin-resistant mutants of Escherichia coli and Salmonella typhimurium accumulate a novel minor lipid that can donate 4-amino-4-deoxy-l-arabinose units (l-Ara4N) to lipid A. We now report the purification of this lipid from a pss(-) pmrA(C) mutant of E. coli and assign its structure as undecaprenyl phosphate-alpha-l-Ara4N. Approximately 0.2 mg of homogeneous material was isolated from an 8-liter culture by solvent extraction, followed by chromatography on DEAE-cellulose, C18 reverse phase resin, and silicic acid. Matrix-assisted laser desorption ionization/time of flight mass spectrometry in the negative mode yielded a single species [M - H](-) at m/z 977.5, consistent with undecaprenyl phosphate-alpha-l-Ara4N (M(r) = 978.41). (31)P NMR spectroscopy showed a single phosphorus atom at -0.44 ppm characteristic of a phosphodiester linkage. Selective inverse decoupling difference spectroscopy demonstrated that the undecaprenyl phosphate group is attached to the anomeric carbon of the l-Ara4N unit. One- and two-dimensional (1)H NMR studies confirmed the presence of a polyisoprene chain and a sugar moiety with chemical shifts and coupling constants expected for an equatorially substituted arabinopyranoside. Heteronuclear multiple-quantum coherence spectroscopy analysis demonstrated that a nitrogen atom is attached to C-4 of the sugar residue. The purified donor supports in vitro conversion of lipid IV(A) to lipid II(A), which is substituted with a single l-Ara4N moiety. The identification of undecaprenyl phosphate-alpha-l-Ara4N implies that l-Ara4N transfer to lipid A occurs in the periplasm of polymyxin-resistant strains, and establishes a new enzymatic pathway by which Gram-negative bacteria acquire antibiotic resistance.

Amino Sugars↗
PubMed2001

Piperazine-based CCR5 antagonists as HIV-1 inhibitors. I: 2(S)-methyl piperazine as a key pharmacophore element.

Optimization of the piperidino-piperazines 1 and 2 provided early leads 3 and 4, which showed good activity in the CCR5-RANTES binding assay and in antiviral assays. A systematic study around these structures showed that the 2(S)-methyl piperazine is essential for CCR5 affinity, which is further enhanced by forming the 2,6-dimethyl benzamide of the piperidine.

Anti-HIV Agents↗
PubMed2001

Photoswitched singlet energy transfer in a porphyrin-spiropyran dyad.

A photochromic nitrospiropyran moiety (Sp) has been covalently linked to a zinc (PZn) and to a free-base (P(H2)) porphyrin. In the resulting dyads (P(Zn)-Sp(c) and P(H2)-Sp(c)), the porphyrin first excited singlet states are unperturbed by the closed form of the attached spiropyran. Excitation of the spiropyran moiety of either dyad in the near-UV region results in ring opening to a merocyanine form (P-Sp(o)) that absorbs at 600 nm. The open form re-closes thermally in 2-methyltetrahydrofuran with a time constant of 20 s, or following irradiation into the 600 nm band. Excitation of the zinc porphyrin moiety in the merocyanine form of the dyad yields 1PZn-Sp(o). The lifetime of the zinc porphyrin excited state is reduced from its usual value of 1.8 ns to 130 ps by singlet-singlet energy transfer to the merocyanine moiety to give PZn-1Sp(o). The quantum yield of energy transfer is 0.93. Quenching is also observed in the free base dyad, where 1P(H2)-Sp(o) and P(H2)-1Sp(o) exchange singlet excitation energy. This photoswitchable quenching phenomenon provides light-activated control of the porphyrin excited states, and consequently control of any subsequent energy or electron-transfer processes that might be initiated by these excited states in more complex molecular photonic or optoelectronic devices.

Benzopyrans↗