Identifying postoperative complications after inguinal hernia repair with a smartphone application: a comparative cohort study.

PURPOSE: The Q1.6 Inguinal Hernia application continuously measures patient-reported outcomes (PROs) by sampling experiences through brief, digital and condition-specific questions, utilising micro-moments. This can overcome the limitations of current paper questionnaires and give real-time insight into patient recovery. This exploratory study compares data from the application with retrospective data from electronic medical records (EMRs) to provide information on its accuracy in detecting postoperative complications after inguinal hernia repair. METHODS: Patients were asked to use the application in addition to their usual care. The application employs twitch crowdsourcing to gather PROs. Questions from validated and frequently used questionnaires were integrated. A retrospective assessment of EMRs was combined with an additional telephone interview. The primary endpoints were the sensitivity and specificity of the application in detecting chronic postoperative inguinal pain, recurrence and surgical-site infection (SSI). RESULTS: A total of 215 patients were analysed. The sensitivity and specificity for detecting chronic postoperative inguinal pain were 100% (95% CI [47.8%, 100%]) and 93.7% (95% CI [88.3%, 97.1%]), respectively. For recurrence, the sensitivity was 77.8% (95% CI [40.0%, 97.2%]), and the specificity was 81.3% (95% CI [75.0%, 86.5%]). For SSI, the sensitivity and specificity were 75.0% (95% CI [19.4%, 99.4%]) and 89.8% (95% CI [84.8%, 93.6%]), respectively. CONCLUSION: This study demonstrates satisfactory measurement capabilities of the Q1.6 Inguinal Hernia application for identifying postoperative complications following inguinal hernia repair. However, certain aspects require further improvement, such as addressing error-prone questions, enhancing long-term compliance, and validating (pain) measurements through prospective control data. TRAIL REGISTRATION NUMBER: NL7813 (Dutch Trial Registry), 19 May 2019.

Psychological sweating: a systematic review focused on aetiology and cutaneous response.

Psychological sweating in response to emotive stimuli like stress, anxiety and pain occurs over the whole body surface, but is most evident on the palms, soles, face and axilla. This is primarily a consequence of high eccrine sweat gland densities at these body sites. Cholinergic innervation is the primary effector eliciting activation of eccrine sweat glands during periods of acute psychological stress. A dual innervation pathway for eccrine glands (adrenergic and cholinergic) may augment increased sweat output, but this remains to be substantiated. Circulating catecholamines appear not to mediate eccrine gland activity, but may play a role in the activation of apocrine sweat glands. Apocrine sweating is strongly regulated by psychological stimuli and localised to those body sites hosting apocrine glands, with adrenergic peripheral pathways being the primary effector. Accordingly, in the axilla psychological sweating leads to increased sweat output and malodour formation, although this form of sweating at this body site is not observed until puberty.

Axillary skin: biology and care.

In skin care, the axilla is a biologically unique site requiring specialized attention and care. This area of skin is often subject to hair removal techniques, such as shaving and plucking. These procedures damage the skin leading to erythema and dryness in the short term, and in some cases, post-inflammatory hyperpigmentation (PIHP) in the long term. This study will (i) briefly review the biology and unique properties of axillary skin, and (ii) describe the characteristics of the irritation and damage induced by contemporary skin care habits and resolution of these responses by the use of efficacious skin moisturizing technology. With respect to the latter, we propose that there are five groups of compounds, defined according to their mechanism of action, which are particularly relevant to the care of damaged axillary skin.

The analytical utility of thermally desorbed polydimethylsilicone membranes for in-vivo sampling of volatile organic compounds in and on human skin.

A thermally-desorbed polydimethylsilicone (PDMS) membrane approach with analysis by gas chromatography-mass spectrometry has been developed and characterised, to enable the VOC arising in, and on skin, from glandular secretions, exogenous materials, products of perfusion from blood, and microbiological metabolites to be sampled in a single procedure. In-vitro studies using a series of volatile fatty acid standards indicated that the recovery efficiency of the technique increased with decreasing volatility; for example, the recovery of hexanoic acid was 3.3 times greater than that for 2-methylpropanoic acid. The relative standard deviation of the methodology decreased with decreasing volatility; RSD = 19% for 2-methylpropanoic acid and RSD = 7% for hexanoic acid. Sampled-mass vs. response relationships were modelled satisfactorily using linear regression analysis with regression coefficients in the range 0.95 to 0.998. In-vivo reproducibility was assessed though the analysis of the responses of 1-dodecane, 3,7-dimethyloct-1-ene, 2-propenoic acid, 2-ethylhexyl ester, 2-ethylhexan-1-ol, butanoic, 2-ethylhexylester, and junipen (1,4-methanoazulene, decahydro-4,8,8-trimethyl-9-methylene-); six compounds selected at random retention times from a GC-MS chromatographic VOC profile of human skin containing several hundred resolved and partially resolved compounds. Five samples were obtained simultaneously from the forearm of a healthy male participant. The in-vivo sample masses were estimated to be in the range 50 pg to 100 ng per sample with observed RSD falling between 15% and 32%; in line with a Horwitz trend. Increasing the sample time from 5 min to 120 min generally resulted in an enrichment of the VOC recovered, and for many VOC substantial increases in sensitivity (x7) were observed over this time range as the PDMS sampling-patch approached equilibrium with the underlying skin. Nevertheless, more volatile components, 2,4,6-trimethylcarbazole for instance, were observed to be lost from the analysis with increasing sample time, in a manner analogous with breakthrough behaviour in adsorbent traps. Finally, a 10 day storage study at 4 degrees C suggested that micro-biological factors were significant in their effect on sample stability. Significant changes (up to x8) were observed in the masses of compounds recovered post storage. These studies confirmed that polydimethylsilicone membrane sampling patches of human skin provide rich and analytical useful data. It is important to note that care in experimental design is needed to avoid sampling artefacts being introduced through sampling selectivity, and/or, sample instability where samples are stored for longer than 24 h at 4 degrees C or higher.

Innervation and receptor profiles of the human apocrine (epitrichial) sweat gland: routes for intervention in bromhidrosis.

BACKGROUND: Human apocrine (epitrichial) sweat glands secrete in response to local or systemic administration of catecholamines and cholinergic agonists. As the process of secretion in human apocrine glands is not fully understood and no literature detailing the expression of adrenergic, cholinergic and purinergic receptors is available, there is a need to know the receptor types. Such data could provide new approaches for the treatment of axillary bromhidrosis. OBJECTIVES: To investigate the localization of nerve fibres, adrenergic, cholinergic and purinergic receptors in human axillary apocrine sweat glands by immunohistochemistry. METHODS: Human axillary apocrine sweat glands were investigated by serial sectioning of paraffin wax-embedded skin samples from volunteers. Sections were examined by light microscopy and immunohistochemistry, using antibodies against neurofilament, alpha- and beta-adrenoceptors, P2Y(1), P2Y(2) and P2Y(4) purinoceptors, and M(3) cholinoceptors. RESULTS: Neurofilaments were found near the eccrine but not the apocrine gland. Apocrine glands demonstrated the presence of beta-2 and beta-3 adrenoceptors in the secretory coil of the gland, but not alpha-1, beta-1 or M(3) receptors. Glandular purinergic staining (P2Y(1), P2Y(2) and P2Y(4)) was found in what looked like myoepithelial cells, while P2Y(1) and P2Y(2) staining was found on apical membranes and diffusely throughout secretory cells. Eccrine gland staining acted as internal positive controls. CONCLUSIONS: No nerve fibres were found near the apocrine gland, suggesting that any catecholamine influence is through humoral effects and that glands could be influenced by beta-adrenoceptor subtypes and purinoceptors. Blockage of both these types of receptors offers a route to controlling apocrine secretion from axillary glands and reducing the opportunity for the development of bromhidrosis.

Development of a web-based, specialty specific portfolio.

BACKGROUND: This article illustrates the creation of a specialty specific portfolio that can be used by several different residency programs to document resident competence during a given rotation. METHODS: Three different disciplines (anesthesiology, surgery and medicine) worked together to create a critical care medicine portfolio. We began by reviewing the curriculum requirements for critical care medicine and organized these requirements into the six ACGME core competencies. We then developed learner led exercises in each core competency that were specific to critical care. Each exercise includes assessment of resident knowledge and application, an evaluation of the exercise, a learner self-assessment of skill, and a review of performance by a faculty member. Portfolio entries are highlighted in a multi-disciplinary weekly conference and posted on a critical care web site at our University. CONCLUSIONS: Creation of specialty specific portfolio reduces redundancy between disciplines, allows for increased time to be spent on the development of exercises specific to rotation objectives, and aids program directors in the collection of portfolio entries for each resident over the course of a residency.

The absence of apoeccrine glands in the human axilla has disease pathogenetic implications, including axillary hyperhidrosis.

BACKGROUND: The existence of a third type of sweat gland in human axillary skin, the apoeccrine gland, with a capacity to produce much higher sweat output than the eccrine gland, was proposed from examination of microdissected glands. However, previous studies of axillary skin glands did not examine the entire individual glandular structure via serial sections and the markers used to identify the different glands gave conflicting results and, hence, the existence of the apoeccrine gland remains controversial. OBJECTIVES: To investigate human axillary sweat glands by serial section histology and immunofluorescence. METHODS: Human axillary sweat glands were investigated by serial sectioning of paraffin wax-embedded skin samples taken by biopsy from four male and six female volunteers (age range 20-35 years). Sections were examined by light microscopy and immunofluorescence, using antibodies to antigens reported to be markers for discriminating between eccrine and apocrine gland cells: CD15, CD44, S100 and human milk fat globulin. RESULTS: Light microscopy demonstrated that there were hair follicles and a mean +/- SD of 76 +/- 14 sweat glands cm(-2). Eccrine and apocrine glands were found to be present; however, no glands resembling the apoeccrine glands were detected. Both types of sweat gland exhibited signs of being active, with segments of the secretory coils displaying flattened cells and dilated glandular lumina; however, this dilation did not extend to obvious changes in the width of the gland. None of the eccrine glands exhibited evidence of the presence of apocrine cells or vice versa. Immunofluorescence markers were found not to be specific and did not discriminate between the different types of glands or demonstrate the presence of apoeccrine glands. CONCLUSIONS: This is the first time that serial sections of axillary skin have been examined by histology and immunofluorescence. The markers reported to discriminate between apocrine and eccrine glands were found to be nonspecific. No evidence of apoeccrine glands was found either by histology or by immunofluorescence.

Metabolic engineering of astaxanthin production in tobacco flowers.

Using metabolic engineering, we have modified the carotenoid biosynthesis pathway in tobacco (Nicotiana tabacum) to produce astaxanthin, a red pigment of considerable economic value. To alter the carotenoid pathway in chromoplasts of higher plants, the cDNA of the gene CrtO from the alga Haematococcus pluvialis, encoding beta-carotene ketolase, was transferred to tobacco under the regulation of the tomato Pds (phytoene desaturase) promoter. The transit peptide of PDS from tomato was used to target the CRTO polypeptide to the plastids. Chromoplasts in the nectary tissue of transgenic plants accumulated (3S,3'S) astaxanthin and other ketocarotenoids, changing the color of the nectary from yellow to red. This accomplishment demonstrates that plants can be used as a source of novel carotenoid pigments such as astaxanthin. The procedures described in this work can serve as a platform technology for future genetic manipulations of pigmentation of fruits and flowers of horticultural and floricultural importance.

Expression of prokaryotic 1-deoxy-D-xylulose-5-phosphatases in Escherichia coli increases carotenoid and ubiquinone biosynthesis.

Isopentenyl diphosphate (IPP) acts as the common, five-carbon building block in the biosynthesis of all isoprenoids. The first reaction of IPP biosynthesis in Escherichia coli is the formation of 1-deoxy-D-xylulose-5-phosphate, catalysed by 1-deoxy-D-xylulose-5-phosphate synthase (DXPS). E. coli engineered to produce lycopene, was transformed with dxps genes cloned from Bacillus subtilis and Synechocystis sp. 6803. Increases in lycopene levels were observed in strains expressing exogenous DXPS compared to controls. The recombinant strains also exhibited elevated levels of ubiquinone-8. These increases corresponded with enhanced DXP synthase activity in the recombinant E. coli strains.

Paracoccus marcusii sp. nov., an orange gram-negative coccus.

Phenotypic, chemotaxonomic and 16S rDNA sequence analysis of an orange Gram-negative coccus that appeared as a contaminant on a nutrient agar plate delineated a new species of the genus Paracoccus. Phenotypic features of the strain that differ from all or most of the previously described Paracoccus species include its bright orange colour, caused by the synthesis of large amounts of carotenoids (mainly astaxanthin), and its inability to use nitrate as an electron acceptor in respiration. The name Paracoccus marcusii is proposed for this organism. The type strain is DSM 11574T.

Biosynthesis of ketocarotenoids in transgenic cyanobacteria expressing the algal gene for beta-C-4-oxygenase, crtO.

The ketocarotenoid astaxanthin is produced by a number of marine bacteria and microalgae. It is synthesized from beta-carotene by the addition of two keto groups to carbons C4 and C4' and two hydroxyl groups to C3 and C3'. The gene, crtO, encoding beta-C-4-oxygenase which converts beta-carotene to canthaxanthin was cloned from the green alga Haematococcus plurialis. We transferred crtO to the cyanobacterium Synechococcus PCC7942, which contains a beta-carotene hydroxylase gene and normally accumulates beta-carotene and zeaxanthin. The genetically engineered cyanobacterium produced astaxanthin as well as other ketocarotenoids. The results confirm that crtO can function in cyanobacteria in conjunction with the intrinsic carotenoid enzymes to produce astaxanthin. Specifically, this finding indicates that beta-carotene hydroxylase, which normally converts beta-carotene to zeaxanthin, can also function in the biosynthesis of astaxanthin. These results provide the first evidence of genetic manipulation of a plant-type carotenoid biosynthesis pathway toward the production of novel carotenoids.

Insulinlike growth factor 1 regulates mRNA levels of osteonectin and pro-alpha 1(I)-collagen in clonal preosteoblastic calvarial cells.

A nontransformed rat clonal cell line (UMR-201) with phenotypic characteristics of osteoblastic precursor cells was found to respond to insulinlike growth factor 1 (IGF-1) by increased osteonectin and pro-alpha 1(I)-collagen mRNA expression. Cells were treated for 24 h with insulin, growth hormone, or IGF-1 to study the regulation of messenger RNA for osteonectin and pro-alpha 1(I)-collagen using Northern blot hybridization. UMR-201 cells possess specific high-affinity receptors for growth hormone, although there were no significant effects of growth hormone (10(-9)-10(-7) M) or insulin (10(-9)-10(-6) M) on mRNA species for osteonectin or pro-alpha 1(I)-collagen. However, IGF-1 increased both mRNA species from a concentration of 10(-9) M. The effect on osteonectin mRNA expression was likely due to increased transcription; when 5' flanking osteonectin (ON) genomic fragments were linked to the bacterial reporter gene chloramphenicol acetyltransferase (CAT) and introduced by transfection into UMR-201 cells, the transcriptional activity of the ON-CAT construct was increased 235 and 270% by 10(-8) and 10(-7) M IGF-1, respectively. In contrast, growth hormone did not change the transcriptional activity of the ON-CAT construct. In confirmation of other work, transforming growth factor beta (TGF-beta, 0.1-2.5 ng/ml) increased mRNA for osteonectin and pro-alpha 1(I)-collagen in a dose-dependent manner. Transforming growth factor alpha (TGF-alpha) at 0.1-10 ng/ml had no consistent effects in repeated experiments on osteonectin and pro-alpha 1(I)-collagen mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Cellular sodium influx is low in type 1 (insulin dependent) diabetes.

Leucocyte sodium influx was studied in 29 type 1 (insulin dependent) diabetic subjects and compared to 24 non diabetic controls matched for age, body mass index and blood pressure. Total sodium influx from a low external concentration ((Na+) = 10 mmol/l) was reduced in type 1 diabetes (0.23 vs 0.31 mmol/l/min, p less than 0.05) as was amiloride insensitive sodium influx (0.09 vs 0.13 mmol/l/min, p less than 0.01). No difference was found in amiloride sensitive flux. No ionic flux was correlated with plasma glucose or insulin concentrations or with HbA1 levels. Intracellular sodium accumulation in type 1 diabetes is not due to an increase in total sodium influx, as judged from an external concentration of 10 mmol/l.

Leukocyte isotopically exchangeable intracellular sodium fractions in lean and overweight hypertensives.

Leukocyte intracellular sodium, as measured by flame photometry, is increased in essential hypertension, especially when associated with a body mass index greater than 27 kg.m-2. A triple isotope method for measuring the isotopically exchangeable pool of intracellular sodium was used to assess if this pool was increased in hypertension. No significant differences in the isotopically exchangeable intracellular sodium concentration were found between lean and overweight hypertensives compared with normotensive controls. Lean hypertensives with systolic blood pressures below the median had significantly lower exchangeable intracellular sodium concentrations than lean normotensives, whereas those with systolic blood pressures above the median had raised exchangeable intracellular sodium concentrations. The obese hypertensives did not show this trend. The exchangeable intracellular sodium concentration was correlated to systolic (r = .53, P less than .001) and diastolic (r = 0.39, P less than .01) blood pressure in hypertensives. We conclude that the increase in total cellular sodium content (as measured by flame photometry) in hypertensives described in previous studies is not associated with any increase in the isotopically exchangeable pool of intracellular Na+, except in those lean hypertensives with systolic blood pressures above the median. By implication, there may be an increased slowly exchangeable pool of intracellular Na+ in leukocytes from most hypertensives.

Three-dimensional structure of a light chain dimer crystallized in water. Conformational flexibility of a molecule in two crystal forms.

The three-dimensional structure of an immunoglobulin light chain dimer (Mcg) crystallized in deionized water (orthorhombic form) was determined at 2.0 A resolution by phase extension and crystallographic refinement. This structure was refined side-by-side with that of the same molecule crystallized in ammonium sulfate (trigonal form). The dimer adopted markedly different structures in the two solvents. "Elbow bend" angles between pseudo 2-fold axes of rotation relating pairs of "variable" (V) and "constant" (C) domains were found to be 132 degrees in the orthorhombic form and 115 degrees in the trigonal form. Modes of association of the V domains and, to a lesser extent, the pairing interactions of the C domains were different in the two structures. Alterations in the V domain pairing were reflected in the shapes of the binding regions and in the orientations of the side-chains lining the walls of the binding sites. In the trigonal form, for instance, the V domain interface was compartmentalized into a main binding cavity and a deep pocket, whereas these spaces were continuous in the orthorhombic structure. Patterns of ordered water molecules were quite distinct in the two crystal types. In some cases, the solvent structures could be correlated with conformational changes in the proteins. For example, close contacts between V and C domains of monomer 1 of the trigonal form were not retained in orthorhombic crystals. Ordered water molecules filled the space created when the two domains moved apart.

Skeletal muscle metabolism: effect of age, obesity, thyroid and nutritional status.

To investigate the potential role of skeletal muscle metabolism in the determination of whole body energy balance, the rate of oxygen consumption was measured in soleus muscles isolated from mice of differing age, sex, strain (thin and obese), thyroid and nutritional status. As expected, T3-induced hyperthyroidism resulted in an increase in the intrinsic rate of energy utilization by the muscles; qualitatively similar changes were noted in both younger animals and mice induced to increase their energy intake by sucrose-overfeeding. In contrast, soleus muscle oxygen consumption was significantly reduced in genetically obese NZO mice. Parallel changes in the activity of the Na-K pump were observed in all groups of animals, with a good correlation (r greater than 0.6, P less than 0.01) noted between these two independently measured aspects of muscle metabolism. The results suggest that the intrinsic metabolic rate of the skeletal muscle mass plays an important role in the control of overall energy balance, with changes in this rate being potentially partly responsible for the altered energetic efficiency of genetic obesity and adaptive thermogenesis models. In addition, measurement of the activity of the Na-K-pump may provide a convenient marker for such observed changes in energy utilization.

Leucocyte sodium content and sodium pump activity in overweight and lean hypertensives.

Leucocyte sodium content and sodium pump activity was studied in overweight and lean hypertensive subjects and normotensive controls, all in the fasting state. In lean subjects (body mass index less than 27 kg m-2), hypertensives did not have altered leucocyte sodium content or pump activity. In the overweight (mostly obese) subjects, the leucocyte sodium content was higher in hypertensive than in normotensive subjects (median (range) 56.1 (42.0-84.1) vs 32.0 (18.2-59.4) mmol kg-1, P less than 0.001). This raised sodium content in overweight hypertensives was associated with a lower (ouabain-sensitive) 22Na efflux rate constant (2.25 (1.15-3.01) vs 2.64 (1.98-3.61) h-1, P less than 0.05) and a higher passive (or ouabain-insensitive) 22Na efflux rate constant (0.90(0.53-1.18) vs 0.63 (0.21-1.09) h-1, P less than 0.01). The systolic and diastolic blood pressures were significantly correlated to intracellular Na+ in the overweight group (r = 0.41 and 0.56, P less than 0.02 and 0.001 respectively). Thus, hypertension in the overweight subjects is associated with accumulation of intracellular sodium that may be due to abnormalities of the active sodium pump, though changes in ouabain-insensitive mechanisms also occur.