Photon energy-dependent ultrafast exciton transfer in chlorosomes of Chlorobium tepidum and the role of supramolecular dynamics

The antenna complex of green sulfur bacteria, the chlorosome, is one of the most efficient supramolecular systems for efficient long-range exciton transfer in nature. Femtosecond transient absorption experiments provide new insight into how vibrationally induced quantum overlap between exciton states supports highly efficient long-range exciton transfer in the chlorosome of Chlorobium tepidum. Our work shows that excitation energy is delocalized over the chlorosome in <1 ps at room temperature. The following exciton transfer to the baseplate occurs in ∼3 to 5 ps, in line with earlier work also performed at room temperature, but significantly faster than at the cryogenic temperatures used in previous studies. This difference can be attributed to the increased vibrational motion at room temperature. We observe a so far unknown impact of the excitation photon energy on the efficiency of this process. This dependency can be assigned to distinct optical domains due to structural disorder, combined with an exciton trapping channel competing with exciton transfer toward the baseplate. An oscillatory transient signal damped in <1 ps has the highest intensity in the case of the most efficient exciton transfer to the baseplate. These results agree well with an earlier computational finding of exciton transfer driven by low-frequency rotational motion of molecules in the chlorosome. Such an exciton transfer process belongs to the quantum coherent regime, for which the Förster theory for intermolecular exciton transfer does not apply. Our work hence strongly indicates that structural flexibility is important for efficient long-range exciton transfer in chlorosomes.NWO715.018.001Solid state NMR/Biophysical Organic Chemistr

Sub-alar batten grafts as treatment for nasal valve incompetence; description of technique and functional evaluation.

Item does not contain fulltextOBJECTIVE: To describe and evaluate the functional results of a surgical technique for treating nasal valve incompetence, in which a cartilage graft called a sub-alar batten graft is placed along the undersurface of the lateral crus of the lower lateral cartilage. METHODS: The functional outcomes of 27 patients who had sub-alar batten grafts placed on 39 sides were evaluated by means of clinical examination and subjective self-assessment. RESULTS: Of a total of 39 sides operated upon, 10 (26%) were rated as optimal, 15 (39%) as improved, 13 (33%) as equal and 1 (2%) as worse. Overall on 25 sides (65%) the post-operative situation was considered to be better than pre-operatively. In all cases in which there was a wish for cosmetic improvement, besides the functional indication, this was obtained, and in no case did the grafts give cause to cosmetic grievances or other complications. CONCLUSION: Placement of sub-alar battens had a positive effect on nasal valve function in roughly two thirds of cases in this series. Although in our opinion this result was slightly disappointing from a purely functional point of view, they can improve the cosmetic result and continue to be considered in cases in which avoidance of surface irregularities is a primary concern or as a preventative measure in rhinoplasty patients at risk for post-operative valve collapse

Exploring the Perceptions of Anal Cancer Screening and Behaviors among Gay and Bisexual Men Infected with HIV

BACKGROUND: The incidence of anal cancer is on the rise among HIV-infected men who have sex with men (MSM). Given the increasing availability of screening, this study explored anal cancer screening awareness and behaviors among MSM infected with HIV. METHODS: In-depth interviews were conducted with 58 MSM infected with HIV. RESULTS: Other than 2 participants treated for anal cancer and 3 treated for precancerous anal lesions, the majority of participants had never heard of anal cancer. Men reported lack of awareness and recommendations from their health care professionals as the greatest barriers to screening. Upon learning about their risk for anal cancer and the availability of screening, the men were eager to discuss screening with their physicians. Participants provided numerous recommendations for future interventions, including training health care professionals to promote screening, disseminating information pertaining to anal cancer through social networks, and creating media campaigns to raise awareness about the need to screen for this type of cancer. CONCLUSIONS: Future intervention work should focus on ensuring that health care professionals, particularly among HIV/primary care specialists, promote screening for anal dysplasia. It is critical that intervention methods use a community-based approach to raise awareness about the need to screen for anal cancer, especially among MSM infected with HIV

Manifestation of hydrogen bonding and exciton delocalization on the absorption and two-dimensional electronic spectra of chlorosomes

NWO715.018.001Solid state NMR/Biophysical Organic Chemistr

Defective mitochondrial rRNA methyltransferase MRM2 causes MELAS-like clinical syndrome

Defects in nuclear-encoded proteins of themitochondrial translationmachinery cause early-onset and tissue-specific deficiency of one ormore OXPHOS complexes. Here, we report a 7-year-old Italian boy with childhood-onset rapidly progressive encephalomyopathy and stroke-like episodes. Multiple OXPHOS defects and decreasedmtDNA copy number (40%) were detected in muscle homogenate. Clinical features combined with low level of plasma citrulline were highly suggestive ofmitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome, however, the commonm.3243A &gt; Gmutation was excluded. Targeted exome sequencing of genes encoding themitochondrial proteome identified a damagingmutation, c.567G &gt; A, affecting a highly conserved amino acid residue (p.Gly189Arg) of the MRM2 protein. MRM2 has never before been linked to a human disease and encodes an enzyme responsible for 2'-O-methylmodification at position U1369 in the humanmitochondrial 16S rRNA.We generated a knockout yeastmodel for the orthologous gene that showed a defect in respiration and the reduction of the 2'-O-methylmodification at the equivalent position (U2791) in the yeastmitochondrial 21S rRNA. Complementation with the mrm2 allele carrying the equivalent yeastmutation failed to rescue the respiratory phenotype, which was instead completely rescued by expressing the wild-type allele. Our findings establish that defective MRM2 causes a MELAS-like phenotype, and suggests the genetic screening of the MRM2 gene in patients with am.3243A &gt; G negative MELAS-like presentation

TRMT5 Mutations Cause a Defect in Post-transcriptional Modification of Mitochondrial tRNA Associated with Multiple Respiratory-Chain Deficiencies

Contains fulltext : 154074.pdf (Publisher’s version ) (Open Access)Deficiencies in respiratory-chain complexes lead to a variety of clinical phenotypes resulting from inadequate energy production by the mitochondrial oxidative phosphorylation system. Defective expression of mtDNA-encoded genes, caused by mutations in either the mitochondrial or nuclear genome, represents a rapidly growing group of human disorders. By whole-exome sequencing, we identified two unrelated individuals carrying compound heterozygous variants in TRMT5 (tRNA methyltransferase 5). TRMT5 encodes a mitochondrial protein with strong homology to members of the class I-like methyltransferase superfamily. Both affected individuals presented with lactic acidosis and evidence of multiple mitochondrial respiratory-chain-complex deficiencies in skeletal muscle, although the clinical presentation of the two affected subjects was remarkably different; one presented in childhood with failure to thrive and hypertrophic cardiomyopathy, and the other was an adult with a life-long history of exercise intolerance. Mutations in TRMT5 were associated with the hypomodification of a guanosine residue at position 37 (G37) of mitochondrial tRNA; this hypomodification was particularly prominent in skeletal muscle. Deficiency of the G37 modification was also detected in human cells subjected to TRMT5 RNAi. The pathogenicity of the detected variants was further confirmed in a heterologous yeast model and by the rescue of the molecular phenotype after re-expression of wild-type TRMT5 cDNA in cells derived from the affected individuals. Our study highlights the importance of post-transcriptional modification of mitochondrial tRNAs for faithful mitochondrial function