How do information and physiotherapy affect health-related quality of life among patients with spinal stenosis undergoing decompression surgery: A qualitative study.

BACKGROUND: There is a lack of qualitative research on how patients with lumbar spinal stenosis (LSS) undergoing surgery perceive their health-related quality of life (HRQOL). Research that increases our understanding in this area could facilitate a biopsychosocial approach to care. AIM: We aimed to investigate the experiences of patients with LSS undergoing decompression surgery regarding their pre- and post-surgery perceptions of HRQOL and the pre-and post-operative information and physiotherapy. METHOD: We used a qualitative design with semi-structured interviews to perform content analysis using an inductive approach. Twelve patients (7 female, 5 male) were included post-surgery and interviewed by phone. The interviews were recorded and transcribed verbatim. RESULTS: Four distinct categories with nine associated subcategories were identified: Patients' feelings of safety and empowerment are enhanced by healthcare professionals; Divided perceptions of information and physiotherapy in a group context; Health-related quality of life is associated with patients' perceived physical capacity; Patients' optimism and concerns influence health-related quality of life. CONCLUSION: Both physical and psychological factors pre- and post-surgery appear to influence patients' HRQOL. Inherent optimism and feelings of empowerment in the care process appear to be important factors, regardless of physical health status. A strong patient-provider relationship is important to promote self-efficacy, which may positively affect perceived HRQOL and is in line with the generally recommended biopsychosocial approach in the treatment of people with low back pain. As qualitative studies in this area are scarce, there is a need for further studies to validate our findings.

Ethylene signaling modulates Arabidopsis thaliana nitrate metabolism.

MAIN CONCLUSION: Genetic analysis reveals a previously unknown role for ethylene signaling in regulating Arabidopsis thaliana nitrogen metabolism. Nitrogen (N) is essential for plant growth, and assimilation of soil nitrate (NO3-) and ammonium ions is an important route of N acquisition. Although N import and assimilation are subject to multiple regulatory inputs, the extent to which ethylene signaling contributes to this regulation remains poorly understood. Here, our analysis of Arabidopsis thaliana ethylene signaling mutants advances that understanding. We show that the loss of CTR1 function ctr1-1 mutation confers resistance to the toxic effects of the NO3- analogue chlorate (ClO3-), and reduces the activity of the nitrate reductase (NR) enzyme of NO3- assimilation. Our further analysis indicates that the lack of the downstream EIN2 component (conferred by novel ein2 mutations) suppresses the effect of ctr1-1, restoring ClO3- sensitivity and NR activity to normal. Collectively, our observations indicate an important role for ethylene signaling in regulating Arabidopsis thaliana NO3- metabolism. We conclude that ethylene signaling enables environmentally responsive coordination of plant growth and N metabolism.

Impairment in karrikin but not strigolactone sensing enhances root skewing in Arabidopsis thaliana.

Roots form highly complex systems varying in growth direction and branching pattern to forage for nutrients efficiently. Here mutations in the KAI2 (KARRIKIN INSENSITIVE) α/ß-fold hydrolase and the MAX2 (MORE AXILLARY GROWTH 2) F-box leucine-rich protein, which together perceive karrikins (smoke-derived butenolides), caused alteration in root skewing in Arabidopsis thaliana. This phenotype was independent of endogenous strigolactones perception by the D14 α/ß-fold hydrolase and MAX2. Thus, KAI2/MAX2 effect on root growth may be through the perception of endogenous KAI2-ligands (KLs), which have yet to be identified. Upon perception of a ligand, a KAI2/MAX2 complex is formed together with additional target proteins before ubiquitination and degradation through the 26S proteasome. Using a genetic approach, we show that SMAX1 (SUPPRESSOR OF MAX2-1)/SMXL2 and SMXL6,7,8 (SUPPRESSOR OF MAX2-1-LIKE) are also likely degradation targets for the KAI2/MAX2 complex in the context of root skewing. In A. thaliana therefore, KAI2 and MAX2 act to limit root skewing, while kai2's gravitropic and mechano-sensing responses remained largely unaffected. Many proteins are involved in root skewing, and we investigated the link between MAX2 and two members of the SKS/SKU family. Though KLs are yet to be identified in plants, our data support the hypothesis that they are present and can affect root skewing.

DNA mismatch repair preferentially protects genes from mutation.

Mutation is the source of genetic variation and fuels biological evolution. Many mutations first arise as DNA replication errors. These errors subsequently evade correction by cellular DNA repair, for example, by the well-known DNA mismatch repair (MMR) mechanism. Here, we determine the genome-wide effects of MMR on mutation. We first identify almost 9000 mutations accumulated over five generations in eight MMR-deficient mutation accumulation (MA) lines of the model plant species, Arabidopsis thaliana We then show that MMR deficiency greatly increases the frequency of both smaller-scale insertions and deletions (indels) and of single-nucleotide variant (SNV) mutations. Most indels involve A or T nucleotides and occur preferentially in homopolymeric (poly A or poly T) genomic stretches. In addition, we find that the likelihood of occurrence of indels in homopolymeric stretches is strongly related to stretch length, and that this relationship causes ultrahigh localized mutation rates in specific homopolymeric stretch regions. For SNVs, we show that MMR deficiency both increases their frequency and changes their molecular mutational spectrum, causing further enhancement of the GC to AT bias characteristic of organisms with normal MMR function. Our final genome-wide analyses show that MMR deficiency disproportionately increases the numbers of SNVs in genes, rather than in nongenic regions of the genome. This latter observation indicates that MMR preferentially protects genes from mutation and has important consequences for understanding the evolution of genomes during both natural selection and human tumor growth.

Limits on the Fill Factor in Organic Photovoltaics: Distinguishing Nongeminate and Geminate Recombination Mechanisms.

In this Letter, we present transient optoelectronic experimental studies of the recombination processes limiting the fill factor (FF) in three conjugated polymer:fullerene systems, poly(3-hexylthiophene) (P3HT) and two lower-band-gap polymers that exhibit lower FFs poly[2,6-(4,4-bis-(2-ethylhexyl)-4H-cyclopenta[2,1-b;3,4-b']dithiophene)-alt-4,7-(2,1,3-benzothiadiazole) (PCPDTBT) and poly(2,7-(9,9-dioctylfluorene)-alt-5,5-(4',7'-di-2-thienyl-2',1',3'-benzothiadiazole)) (APFO-3). Using transient absorption spectroscopy, charge extraction, and transient photovoltage experiments, we show that the lower FF observed for the PCPDTBT-based device results from enhanced nongeminate recombination even at short circuit, In contrast, we show that for APFO-3 devices, the FF is primarily limited by a voltage-dependent free charge generation, which we assign to a geminate recombination process.

Quantification of geminate and non-geminate recombination losses within a solution-processed small-molecule bulk heterojunction solar cell.

Direct measurements of the field-dependent efficiency with which electron-hole pairs are dissociated (1) can be combined with direct measurement of the carrier-density dependent rate at which they subsequently recombine (2) to determine the proportion of carriers which may be usefully extracted (3) for a class of solution-processed organic small-molecule bulk-heterojunction solar cells.

Sequential mutations associated with adaptation of human cytomegalovirus to growth in cell culture.

Mutations that occurred during adaptation of human cytomegalovirus to cell culture were monitored by isolating four strains from clinical samples, passaging them in various cell types and sequencing ten complete virus genomes from the final passages. Mutational dynamics were assessed by targeted sequencing of intermediate passages and the original clinical samples. Gene RL13 and the UL128 locus (UL128L, consisting of genes UL128, UL130 and UL131A) mutated in all strains. Mutations in RL13 occurred in fibroblast, epithelial and endothelial cells, whereas those in UL128L were limited to fibroblasts and detected later than those in RL13. In addition, a region containing genes UL145, UL144, UL142, UL141 and UL140 mutated in three strains. All strains exhibited numerous mutations in other regions of the genome, with a preponderance in parts of the inverted repeats. An investigation was carried out on the kinetic growth yields of viruses derived from selected passages that were predominantly non-mutated in RL13 and UL128L (RL13+UL128L+), or that were largely mutated in RL13 (RL13-UL128L+) or both RL13 and UL128L (RL13-UL128L-). RL13-UL128L- viruses produced greater yields of infectious progeny than RL13-UL128L+ viruses, and RL13-UL128L+ viruses produced greater yields than RL13+UL128L+ viruses. These results suggest strongly that RL13 and UL128L exert at least partially independent suppressive effects on growth in fibroblasts. As all isolates proved genetically unstable in all cell types tested, caution is advised in choosing and monitoring strains for experimental studies of vulnerable functions, particularly those involved in cell tropism, immune evasion or growth temperance.

Transient absorption spectroscopy of charge photogeneration yields and lifetimes in a low bandgap polymer/fullerene film.

Charge photogeneration yields and energetics are determined for a low band gap co-polymer, PCPDTBT blended with PC(70)BM; the increase in charge photogeneration with dithiol is correlated with an increase in the free energy of charge separation.

The products of human cytomegalovirus genes UL23, UL24, UL43 and US22 are tegument components.

We have investigated the human cytomegalovirus (HCMV) US22 gene family members UL23, UL24, UL43 and US22. Specific antibodies were generated to identify pUL23 (33 kDa), pUL24 (40 kDa) and pUL43 (48 kDa), while pUS22 was identified by monoclonal antibody HWLF1. A C-terminally truncated UL43 product (pUL43t; 21 kDa) produced by a deletion mutant was also investigated. The UL24 and UL43 genes were expressed with early-late (gamma1) and true-late (gamma2) kinetics, respectively. Immunoblot and immuno-EM studies demonstrated that pUL23, pUL24, pUL43 and pUS22 were virion tegument components. Immunofluorescence and immuno-EM studies showed that pUL23, pUL24, pUL43 and pUL43t were located in cytoplasmic protein aggregates, manifesting two forms: complex juxtanuclear structures and smaller, membrane-bound aggregates resembling dense bodies. The complex-type aggregate is a putative site of particle maturation. Because pUL43t was present in protein aggregates, but under-represented in virus particles compared to pUL43, it was concluded that N-terminal sequences target pUL43 to protein aggregates and that C-terminal sequences are important for incorporation into particles. Since three other US22 family products (pUL36, pTRS1 and pIRS1) are documented tegument components, at least seven of the twelve US22 family genes encode tegument proteins, suggesting that the products of the remaining five genes might be similarly located. These findings demonstrate a common biological feature among most, if not all, US22 family proteins and implicate the family in events occurring immediately after virus penetration.