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Background: Treatment of pyogenic flexor tenosynovitis (FTS) historically involved surgical debridement supplemented with antibiotic therapy. No consensus exists on either: (1) the treatment algorithm for this infection; or (2) the clinical definition of “early” FTS. We performed a retrospective study to clarify indications for nonoperative management. Methods: We identified 40 patients with a diagnosis of FTS using Current Procedural Terminology and International Classification of Diseases, Tenth Revision, codes and a keyword search from an electronic medical record between 2011 and 2019. Patients underwent either surgical management (SG) (n = 20) or early antibiotics only (EAG) (n = 20). The surgical group was divided into patients with intraoperative purulence within the tendon sheath (PU) and those without purulence (NP). Results: The number of Kanavel signs and duration of days of symptoms were significantly greater in SG compared with EAG. Subgroup analysis of SG showed a greater number of days of symptoms in the NP group when compared with the PU group. No statistical significance was found with respect to age, smoking, or specific individual Kanavel signs between SG and EAG. Conclusions: Both duration of symptoms and number of Kanavel signs should be considered in suspected early FTS. Patients with shorter duration of symptoms and fewer Kanavel signs were treated successfully with antibiotics alone. Operatively confirmed FTS presented more acutely with fewer days of symptoms and a higher number of Kanavel signs. Patients with subacute presentations may represent inflammatory conditions and hand infections other than FTS.

Prostate cancer (PCa) is a common cancer among men in the United States. While malignancy is a known cause of venous thromboembolism (VTE), little is known about the effect of PCa history on postoperative complications after elective total hip arthroplasty (THA). This study aimed to evaluate the risk of hematologic complications in patients with a history of PCa taking common postoperative anticoagulants.THA patients were identified through the PearlDiver Mariner database. Patients with a history of PCa were placed in one of the following cohorts based on postoperative anticoagulant prescription: aspirin, warfarin, low-molecular-weight heparin, direct Xa inhibitor, or any anticoagulant. PCa cohorts were matched 1:3 to patients without a history of PCa with the same anticoagulant prescription based on age, gender, and Charlson Comorbidity Index. Postoperative complications were evaluated using multivariable logistic regression.A total of 74,744 patients that underwent THA were included. PCa patients taking any anticoagulant were found to have increased risk of postoperative deep vein thrombosis (DVT) (odds ratio: 1.25, lower 99% confidence interval: 1.09, upper 99% confidence interval: 1.43,Our results suggest postoperative aspirin prophylaxis may not increase VTE complication risk when compared to other anticoagulants. Surgeons should be aware that PCa history may be an independent risk factor for VTE, and these patients may benefit from medical optimization.

Purpose\ud Self-compassion has been associated with a set of adaptive coping strategies, which in turn explain better adjustment in individuals with chronic illnesses such as inflammatory bowel disease and arthritis. The aim of this study was to investigate whether self-compassion is associated with adjustment in people with epilepsy (PWE) and people with psychogenic nonepileptic seizures (PWPNES). Adjustment was measured via coping efficacy, quality of life (QoL), anxiety, and depression.\ud \ud Method\ud A cross-sectional questionnaire design was employed. People with epilepsy (N = 74), PWPNES (N = 46), and controls (N = 89), recruited from outpatient seizure clinics and online, completed questionnaires about their self-compassion, coping efficacy, QoL, anxiety, and depression levels.\ud \ud Results\ud Overall, self-compassion was associated with adjustment in PWE and PWPNES. Self-compassion was negatively related to anxiety and depression in PWE, PWPNES, and controls and positively related to coping efficacy in PWE and PWPNES. Self-compassion was also positively related to QoL in PWE and controls; however, this relationship was not significant in PWPNES.\ud \ud Conclusion\ud Self-compassion is associated with better adjustment in PWE and PWPNES. Implications of these findings for psychotherapeutic interventions for individuals with seizure disorders and future research are discussed.

Background: Cultural competence is key to high-quality mental health care and is a required competency for professionals. However, there is little to guide practitioners on the content, format, implementation or effectiveness of cultural competence training. Aims: This review aimed to identify the evidence base for cultural competence training in UK mental health settings and to summarise definitions, theoretical models, contents and measures of effectiveness used in such training. Methods: A systematic search and narrative synthesis of the literature on cultural competence training was conducted. Results: A literature search generated seven articles that met the inclusion criteria, which reported five original studies. There were no randomised controlled trials. Only two studies described training that was underpinned by an explicit definition or model of cultural competence. Three studies reported service user involvement. Conclusions: There literature on cultural competence training in mental health settings in the UK is surprisingly limited. There is insufficient evidence on which to base recommendations for clinical practice. Research is required to develop theoretically informed cultural competence training and evaluate its effectiveness

Summary Two polytopic membrane proteins, NarK and NarU, are assumed to transport nitrite out of the Escherichia coli cytoplasm, but how nitrate enters enteric bacteria is unknown. We report the construction and use of four isogenic strains that lack nitrate reductase Z and the periplasmic nitrate reductase, but express all combinations of narK and narU. The active site of the only functional nitrate reductase, nitrate reductase A, is located in the cytoplasm, so nitrate reduction by these four strains is totally dependent upon a mechanism for importing nitrate. These strains were exploited to determine the roles of NarK and NarU in both nitrate and nitrite transport. Single mutants that lack either NarK or NarU were competent for nitrate-dependent anaerobic growth on a non-fermentable carbon source, glycerol. They transported and reduced nitrate almost as rapidly as the parental strain. In contrast, the narK–narU double mutant was defective in nitrate-dependent growth unless nitrate transport was facilitated by the nitrate ionophore, reduced benzyl viologen (BV). It was also unable to catalyse nitrate reduction in the presence of physiological electron donors. Synthesis of active nitrate reductase A and the cytoplasmic, NADH-dependent nitrite reductase were unaffected by the narK and narU mutations. The rate of nitrite reduction catalysed by the cytoplasmic, NADH-dependent nitrite reductase by the double mutant was almost as rapid as that of the NarK+-NarU+ strain, indicating that there is a mechanism for nitrite uptake by E. coli that is in-dependent of either NarK or NarU. The nir operon encodes a soluble, cytoplasmic nitrite reductase that catalyses NADH-dependent reduction of nitrite to ammonia. One additional component that contributes to nitrite uptake was shown to be NirC, the hydrophobic product of the third gene of the nir operon, which is predicted to be a polytopic membrane protein with six membrane-spanning helices. Deletion of both NarK and NirC decreased nitrite uptake and reduction to a basal rate that was fully restored by a single chromosomal copy of either narK or nirC. A multicopy plasmid encoding NarU complemented a narK mutation for nitrite excretion, but not for nitrite uptake. We conclude that, in contrast to NirC, which transports only nitrite, NarK and NarU provide alternative mechanisms for both nitrate and nitrite transport. However, NarU might selectively promote nitrite ex-cretion, not nitrite uptake.

Two related polytopic membrane proteins of the major facilitator family, NarK and NarU, catalyse nitrate uptake, nitrite export and nitrite uptake across the Escherichia coli cytoplasmic membrane by an unknown mechanism. A 12-helix model of NarU was constructed based upon six alkaline phosphatase and β-galactosidase fusions to NarK and the predicted hydropathy for the NarK family. Fifteen residues conserved in the NarK-NarU protein family were substituted by site-directed mutagenesis, including four residues that are essential for nitrate uptake by Aspergillus nidulans : arginines Arg 87 and Arg 303 in helices 2 and 8, and two glycines in a nitrate signature motif. Despite the wide range of substitutions studied, in no case did mutation result in loss of one biochemical function without simultaneous loss of all other functions. A NarU + NirC + strain grew more rapidly and accumulated nitrite more rapidly than the isogenic NarU + NirC − strain. Only the NirC + strain consumed nitrite rapidly during the later stages of growth. Under conditions in which the rate of nitrite reduction was limited by the rate of nitrite uptake, NirC + strains reduced nitrite up to 10 times more rapidly than isogenic NarU + strains, indicating that both nitrite efflux and nitrite uptake are largely dependent on NirC. Isotope tracer experiments with [ 15 N]nitrate and [ 14 N]nitrite revealed that [ 15 N]nitrite accumulated in the extracellular medium even when there was a net rate of nitrite uptake and reduction. We propose that NarU functions as a single channel for nitrate uptake and nitrite expulsion, either as a nitrate–nitrite antiporter, or more likely as a nitrate/H + or nitrite/H + channel.

Escherichia coli K-12 strains expressing either NarU or NarK as the only nitrate transport protein are both able to support nitrate-dependent anaerobic growth. The narK gene is highly expressed during anaerobic growth in the presence of nitrate, consistent with a role for NarK in nitrate transport coupled to nitrate reduction by the most active nitrate reductase encoded by the adjacent narGHJI operon. The physiological role of NarU is unknown. Reverse transcriptase PCR experiments established that, unlike the monocistronic narK gene, narU is co-transcribed with narZ as the first gene of a five-gene narUZYWV operon. The narK and narU genes were fused in-frame to a myc tag: the encoded fusion proteins complemented the nitrate-dependent growth defect of chromosomal narK and narU mutations. A commercial anti-Myc antibody was used to detect NarK and NarU in membrane fractions. During anaerobic growth in the presence of nitrate, the quantity of NarU-Myc accumulated during exponential growth was far less than that of NarK-Myc, but NarU was more abundant than NarK in stationary-phase cultures in the absence of nitrate. Although the concentration of NarU-Myc increased considerably during the post-exponential phase of growth, NarK-Myc was still more abundant than NarU-Myc in stationary-phase bacteria in the presence of nitrate. In chemostat competition experiments, a strain expressing only narU had a selective advantage relative to a strain expressing only narK during nutrient starvation or very slow growth, but NarK+ bacteria had a much greater selective advantage during rapid growth. The data suggest that NarU confers a selective advantage during severe nutrient starvation or slow growth, conditions similar to those encountered in vivo.

Two polytopic membrane proteins, NarK and NarU, are assumed to transport nitrite out of the Escherichia coli cytoplasm, but how nitrate enters enteric bacteria is unknown. We report the construction and use of four isogenic strains that lack nitrate reductase Z and the periplasmic nitrate reductase, but express all combinations of narK and narU. The active site of the only functional nitrate reductase, nitrate reductase A, is located in the cytoplasm, so nitrate reduction by these four strains is totally dependent upon a mechanism for importing nitrate. These strains were exploited to determine the roles of NarK and NarU in both nitrate and nitrite transport. Single mutants that lack either NarK or NarU were competent for nitrate-dependent anaerobic growth on a non-fermentable carbon source, glycerol. They transported and reduced nitrate almost as rapidly as the parental strain. In contrast, the narK-narU double mutant was defective in nitrate-dependent growth unless nitrate transport was facilitated by the nitrate ionophore, reduced benzyl viologen (BV). It was also unable to catalyse nitrate reduction in the presence of physiological electron donors. Synthesis of active nitrate reductase A and the cytoplasmic, NADH-dependent nitrite reductase were unaffected by the narK and narU mutations. The rate of nitrite reduction catalysed by the cytoplasmic, NADH-dependent nitrite reductase by the double mutant was almost as rapid as that of the NarK+-NarU+ strain, indicating that there is a mechanism for nitrite uptake by E. coli that is in-dependent of either NarK or NarU. The nir operon encodes a soluble, cytoplasmic nitrite reductase that catalyses NADH-dependent reduction of nitrite to ammonia. One additional component that contributes to nitrite uptake was shown to be NirC, the hydrophobic product of the third gene of the nir operon, which is predicted to be a polytopic membrane protein with six membrane-spanning helices. Deletion of both NarK and NirC decreased nitrite uptake and reduction to a basal rate that was fully restored by a single chromosomal copy of either narK or nirC. A multicopy plasmid encoding NarU complemented a narK mutation for nitrite excretion, but not for nitrite uptake. We conclude that, in contrast to NirC, which transports only nitrite, NarK and NarU provide alternative mechanisms for both nitrate and nitrite transport. However, NarU might selectively promote nitrite ex-cretion, not nitrite uptake.