Exploring adults' experiences of sedentary behaviour and participation in non-workplace interventions designed to reduce sedentary behaviour: a thematic synthesis of qualitative studies.

BACKGROUND: Sedentary behaviour is any waking behaviour characterised by an energy expenditure of ≤1.5 metabolic equivalent of task while in a sitting or reclining posture. Prolonged bouts of sedentary behaviour have been associated with negative health outcomes in all age groups. We examined qualitative research investigating perceptions and experiences of sedentary behaviour and of participation in non-workplace interventions designed to reduce sedentary behaviour in adult populations. METHOD: A systematic search of seven databases (MEDLINE, AMED, Cochrane, PsychINFO, SPORTDiscus, CINAHL and Web of Science) was conducted in September 2017. Studies were assessed for methodological quality and a thematic synthesis was conducted. Prospero database ID: CRD42017083436. RESULTS: Thirty individual studies capturing the experiences of 918 individuals were included. Eleven studies examined experiences and/or perceptions of sedentary behaviour in older adults (typically ≥60 years); ten studies focused on sedentary behaviour in people experiencing a clinical condition, four explored influences on sedentary behaviour in adults living in socio-economically disadvantaged communities, two examined university students' experiences of sedentary behaviour, two on those of working-age adults, and one focused on cultural influences on sedentary behaviour. Three analytical themes were identified: 1) the impact of different life stages on sedentary behaviour 2) lifestyle factors influencing sedentary behaviour and 3) barriers and facilitators to changing sedentary behaviour. CONCLUSIONS: Sedentary behaviour is multifaceted and influenced by a complex interaction between individual, environmental and socio-cultural factors. Micro and macro pressures are experienced at different life stages and in the context of illness; these shape individuals' beliefs and behaviour related to sedentariness. Knowledge of sedentary behaviour and the associated health consequences appears limited in adult populations, therefore there is a need for provision of accessible information about ways in which sedentary behaviour reduction can be integrated in people's daily lives. Interventions targeting a reduction in sedentary behaviour need to consider the multiple influences on sedentariness when designing and implementing interventions.

Skin conductance rises in preparation and recovery to psychosocial stress and its relationship with impulsivity and testosterone in intimate partner violence perpetrators.

Intimate partner violence (IPV) perpetrators were categorized into 2 groups using Gottman et al.'s (1995) typology depending on their skin conductance (SC) reactivity to stress. Overall, type I perpetrators tend to show autonomic underarousal, whereas type II perpetrators present a preparatory hyperreactivity to confront stress. Moreover, impulsivity traits and testosterone (T) levels may modulate SC responses to increase the risk of proneness to violence. In this study, SC response to stress was assessed by comparing IPV perpetrators with non-violent controls while performing a modified version of the Trier Social Stress Test (TSST). Subjects with a history of IPV demonstrated higher non-specific SC responses during the recovery period than the non-violent controls. Nonetheless, there were no differences between groups in the case of mean SC levels. Furthermore, impulsivity and baseline T levels were associated with higher SC level reactivity during a preparation period only in IPV perpetrators, with both relationships being mediated by anger expression. Our results confirm that the IPV perpetrators correspond physiologically to type II and support the validity of SC as a diagnostic indicator for IPV classification. Our findings contribute to the development of effective treatment and prevention programs that could benefit from the use of biological indicators for analyzing the risk of recidivism in IPV perpetrators.

Studies on plant-mediated fate of the explosives RDX and HMX.

The fate of the explosives RDX and HMX on exposure to plants was investigated in 'natural' aquatic systems of Myriophyllum aquaticum for 16 days, and in axenic hairy root cultures of Catharanthus roseus for > or = 9 weeks. Exposure levels were: HMX, 5 mg/l; and RDX, approximately 8 mg/l. Exposure outcomes observed include: HMX, no transformation by aquatic plants, and minimal biological activity by axenic roots; and RDX, removal by both plant systems. In the case of RDX exposure to axenic roots, since 14C-RDX was included, removal was confirmed by the accumulation of 14C-label in the biomass. The intracellular 14C-label in these RDX studies was detected in two forms: intact RDX and bound unknown(s).

Increases in circulating and lymphoid tissue interleukin-10 in autoimmune lymphoproliferative syndrome are associated with disease expression.

Autoimmune lymphoproliferative syndrome (ALPS) is an inherited disorder in which genetic defects in proteins that mediate lymphocyte apoptosis, most often Fas, are associated with enlargement of lymph nodes and the spleen and a variety of autoimmune manifestations. Some patients with ALPS have relatives with these same apoptotic defects, however, who are clinically well. This study showed that the circulating levels of interleukin 10 (IL-10) were significantly higher (P <.001) in 21 patients with ALPS than in healthy controls. Moreover, the peripheral blood mononuclear cells (PBMCs) and lymphoid tissues of these patients with ALPS contained significantly higher levels of IL-10 messenger RNA (mRNA; P <.001 and P <.01, respectively). By fractionating PBMC populations, disproportionately high concentrations of IL-10 mRNA were found in the CD4(-)CD8(-) T-cell population, expansion of which is virtually pathognomonic for ALPS. Immunohistochemical staining showed intense IL-10 protein signals in lymph node regions known to contain CD4(-)CD8(-) T cells. Nonetheless, in vitro studies showed no influence of IL-10 on the survival of CD4(-)CD8(-) T cells. Overexpression of IL-10 in patients with inherited apoptotic defects is strongly associated with the overt manifestations of ALPS.

Comparison of quantitations of viral load in varicella and zoster.

The pathogenesis of varicella and zoster and the effects of antiviral treatment were investigated using real-time PCR for varicella-zoster virus (VZV) DNA in skin lesions and peripheral blood. A higher occurrence of viremic VZV DNA was observed in varicella than in zoster. Acyclovir treatment resulted in marked suppression of viremia in varicella.

Quantitation of latent varicella-zoster virus and herpes simplex virus genomes in human trigeminal ganglia.

Using real-time fluorescence PCR, we quantitated the numbers of copies of latent varicella-zoster virus (VZV) and herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) genomes in 15 human trigeminal ganglia. Eight (53%) and 1 (7%) of 15 ganglia were PCR positive for HSV-1 or -2 glycoprotein G genes, with means of 2,902 +/- 1,082 (standard error of the mean) or 109 genomes/10(5) cells, respectively. Eleven of 14 (79%) to 13 of 15 (87%) of the ganglia were PCR positive for VZV gene 29, 31, or 62. Pooling of the results for the three VZV genes yielded a mean of 258 +/- 38 genomes/10(5) ganglion cells. These levels of latent viral genome loads have implications for virus distribution in and reactivation from human sensory ganglia.

Baculovirus expression, purification, and properties of varicella-zoster virus gE, gI, and the complex they form.

Varicella-zoster virus (VZV) expresses six known glycoproteins. High level expression of recombinant soluble forms of the VZV glycoproteins E and I (gE and gI) was achieved in the baculovirus system. gE and gI associate in VZV-infected cells to form an intermolecular complex. To purify large amounts of these glycoproteins, gE was produced with a C-terminal six-histidine (HIS-6) tag sequence, and gI was produced both with and without the HIS-6 sequence. The individual glycoproteins or the gE/gI complex were purified in their native forms by use of affinity chromatography. Recombinant soluble VZV gE and gI provided important tools in the biochemical analysis and may contribute further to the functional and immunologic studies of these VZV envelope components.

Recombinant varicella-zoster virus glycoproteins E and I: immunologic responses and clearance of virus in a guinea pig model of chronic uveitis.

Guinea pigs immunized with recombinant varicella-zoster virus (VZV) glycoproteins E (gE) and I (gI) developed antigen-specific antibodies in the sera, vitreous, and conjunctival washes. Sera from immunized animals neutralized both cell-free and cell-associated VZV, and peripheral blood lymphocytes proliferated in vitro in response to recombinant gE and gI and to antigens from VZV-infected cells. Immunized guinea pigs were inoculated intravitreally with VZV, which induces chronic uveitis. VZV DNA was more rapidly cleared and infectious VZV was isolated less frequently from the retinas of animals immunized with gE and gI compared with that in controls receiving adjuvant alone. Nonetheless, cellular infiltrates in the vitreous, retina, and choroid were prevalent 21 days after VZV inoculation in both the adjuvant-alone- and gE-gI-immunized animals. Immunization with VZV gE and gI induced potent humoral and cellular responses that accelerated the clearance of VZV DNA and may neutralize virus within the eye.

Purified, soluble recombinant mouse hepatitis virus receptor, Bgp1(b), and Bgp2 murine coronavirus receptors differ in mouse hepatitis virus binding and neutralizing activities.

Mouse hepatitis virus receptor (MHVR) is a murine biliary glycoprotein (Bgp1(a)). Purified, soluble MHVR expressed from a recombinant vaccinia virus neutralized the infectivity of the A59 strain of mouse hepatitis virus (MHV-A59) in a concentration-dependent manner. Several anchored murine Bgps in addition to MHVR can also function as MHV-A59 receptors when expressed at high levels in nonmurine cells. To investigate the interactions of these alternative MHVR glycoproteins with MHV, we expressed and purified to apparent homogeneity the extracellular domains of several murine Bgps as soluble, six-histidine-tagged glycoproteins, using a baculovirus expression system. These include MHVR isoforms containing four or two extracellular domains and the corresponding Bgp1(b) glycoproteins from MHV-resistant SJL/J mice, as well as Bgp2 and truncation mutants of MHVR and Bgp1(b) comprised of the first two immunoglobulin-like domains. The soluble four-domain MHVR glycoprotein (sMHVR[1-4]) had fourfold more MHV-A59 neutralizing activity than the corresponding soluble Bgp1(b) (sBgp1(b)) glycoprotein and at least 1,000-fold more neutralizing activity than sBgp2. Although virus binds to the N-terminal domain (domain 1), soluble truncation mutants of MHVR and Bgp1(b) containing only domains 1 and 2 bound virus poorly and had 10- and 300-fold less MHV-A59 neutralizing activity than the corresponding four-domain glycoproteins. In contrast, the soluble MHVR glycoprotein containing domains 1 and 4 (sMHVR[1,4]) had as much neutralizing activity as the four-domain glycoprotein, sMHVR[1-4]. Thus, the virus neutralizing activity of MHVR domain 1 appears to be enhanced by domain 4. The sBgp1(b)[1-4] glycoprotein had 500-fold less neutralizing activity for MHV-JHM than for MHV-A59. Thus, MHV strains with differences in S-glycoprotein sequence, tissue tropism, and virulence can differ in the ability to utilize the various murine Bgps as receptors.

Varicella-zoster virus glycoproteins E and I expressed in insect cells form a heterodimer that requires the N-terminal domain of glycoprotein I.

Varicella-zoster virus (VZV) glycoproteins E and I (gE and gI), which are major components of the virion envelope, form a noncovalently linked complex. To understand their properties and functions, we expressed and purified soluble forms of gE and gI in the baculovirus system. Extracellular domains of gE and gI were cloned into baculoviruses, using either native or insect-derived signal peptides. Each recombinant virus yielded soluble protein in culture medium although a higher level of secretion was achieved with insect-derived signal peptides in recombinant gE baculoviruses. A soluble gE-gI complex was formed by co-infecting insect cells with recombinant gE and gI baculoviruses and detected by immunoprecipitation followed by Western blotting analyses. By gel filtration and cross-linking studies, we showed that the VZV gE-gI complex expressed in insect cells is a heterodimer. Interestingly, two recombinant gI proteins in which signal peptides were replaced with insect-derived signal peptides did not associate with gE. Amino-terminal sequencing and site-specific mutational studies showed that the replacement of only the signal peptides did not prevent complex formation but alterations in the processed amino-terminus of gI abrogated its ability to complex with gE. These findings indicate that the mature amino-terminus of gI is required for gE-gI complex formation by the external domains of VZV gE and gI.

Combined spinal and epidural anaesthesia for major abdominal surgery in infants.

PURPOSE: Subarachnoid anaesthesia is becoming increasingly popular in neonates and infants. However, single dose spinal anaesthesia is of limited value for major abdominal surgery in infants due to its short duration of action and inability to provide analgesia in the post operative period. A new technique of combined spinal and epidural anaesthesia for major abdominal surgery in the infant is described. METHODS: Data were gathered prospectively from 19 infants presenting for upper and lower abdominal surgery. Anaesthesia was induced with a subarachnoid injection of tetracaine. After the subarachnoid block was established, an epidural catheter was placed for further intraoperative and postoperative management. Data collected included age and weight of the patients, type and duration of the surgical procedure. Doses of local anaesthetics as well as the need for intraoperative and postoperative supplements were recorded. An illustrative case report is provided. RESULTS: Infants studied represented a wide range of weights (1520-7840 g). Spinal anaesthesia was successful in all 19 patients. A variety of extensive surgical procedures including small bowel resections and various genitourinary procedures were successfully performed. In 17 patients a functioning epidural catheter was in place postoperatively. In these patients effective analgesia was maintained with dilute solutions of epidural bupivacaine. Only three doses of narcotic were required for pain control. No patient required postoperative mechanical ventilation or tracheal intubation. CONCLUSION: Combined spinal and epidural anaesthesia is a potential option to general anaesthesia for major abdominal surgery in infants.

Specificity and affinity of binding of herpes simplex virus type 2 glycoprotein B to glycosaminoglycans.

Herpes simplex virus type 2 (HSV-2) interacts with cell surface glycosaminoglycans during virus attachment. Glycoprotein B of HSV-2 can potentially mediate the interaction between the virion and cell surface glycosaminoglycans. To determine the specificity, kinetics, and affinity of these interactions, we used plasmon resonance-based biosensor technology to measure HSV-2 glycoprotein binding to glycosaminoglycans in real time. The recombinant soluble ectodomain of HSV-2 gB (gB2) but not the soluble ectodomain of HSV-2 gD bound readily to biosensor surfaces coated with heparin. The affinity constants (Kds) were determined for gB2 (Kd = 7.7 x 10(-7) M) and for gB2 deltaTM (Kd = 9.9 x 10(-7) M), a recombinant soluble form of HSV-2 gB in which only its transmembrane domain has been deleted. gB2 binding to the heparin surface was competitively inhibited by low concentrations of heparin (50% effective dose [ED50] = 0.08 microg/ml). Heparan sulfate and dermatan sulfate glycosaminoglycans have each been suggested as cell surface receptors for HSV. Our biosensor analyses showed that both heparan sulfate and dermatan sulfate inhibited gB2 binding (ED50 = 1 to 5 microg/ml), indicating that gB2 interacts with both heparin-like and dermatan sulfate glycosaminoglycans. Chondroitin sulfate A, in contrast, inhibited gB2 binding to heparin only at high levels (ED50 = 65 microg/ml). The affinity and specificity of gB2 binding to glycosaminoglycans demonstrated in these studies support its role in the initial binding of HSV-2 to cells bearing heparan sulfate or dermatan sulfate glycosaminoglycans.

High spinal anaesthesia for repair of patent ductus arteriosus in neonates.

General anaesthesia with high dose narcotics has traditionally been used for repair of patent ductus arteriosus (PDA) in high risk neonates. Spinal anaesthesia in infants has generally been limited to cases involving the lower abdomen and lower extremities. Regional anaesthesia for PDA repair could potentially offer a more rapid recovery and the possibility of blunting the stress response in this vulnerable group of patients. High spinal anaesthesia with tetracaine was utilized as an alternative to general anaesthesia in a series of fifteen consecutive patients. Patient demographics, medication dosages, level of anaesthesia, intraoperative and immediate postoperative data were obtained and recorded in a prospective fashion. Spinal anaesthesia was achieved in all patients. The average dose of tetracaine was 2.4 mg.kg-1. Two patients early in the series had an inadequate level and received supplemental isoflurane. The remainder of the patients received either no or minimal supplementation to the basic technique. Cardiovascular status of the group was very stable with minimal changes in blood pressure noted. Recovery was rapid. All three patients who were not intubated at the time of surgery were extubated soon after surgical repair was completed. No complications of the technique were noted. High spinal anaesthesia is a safe and effective alternative to general anaesthesia in high risk neonates. This technique may offer the advantage of a faster recovery time and a protective effect on the neonatal stress response. In addition the stability of this technique may encourage the use of higher levels of spinal anaesthesia in infants than has traditionally been used.

Down-regulation of glial fibrillary acidic protein expression during acute lytic varicella-zoster virus infection of cultured human astrocytes.

The effects of the varicella-zoster virus (VZV) OKA vaccine strain in producing morphologic and antigenic changes in dissociated cultures of human fetal brain was investigated. Cultures containing 80% glial acidic fibrillary protein (GFAP), GFAP+ (positive) astrocytes and 20% GFAP- (negative) fibroblastic-like cells were infected with cell-free VZV OKA at a multiplicity of infection of 0.1 plaque-forming units per cell. Cytopathic effects and significant viral antigen labeling with antibodies against VZV gpl and immediate-early (IE) protein 62 were first detected 6 to 7 days postinfection. Several observations indicated that astrocyte GFAP expression was altered and diminished as a result of VZV infection itself, thereby raising doubts about the utility of combining cell markers and viral antigenic labeling in assessing the susceptibility of neural cell types to viral infection. The down-regulation of GFAP expression by VZV appears to be mediated by early rather than late events in the viral replication cycle and may not be the result of virally induced global shut-off of host cell protein synthesis. Similar observations were made using VZV Ellen, a multipassaged, nonvaccine strain. These observations have potential in vivo implications related to histologic analysis of VZV-infected tissues and disease pathogenesis.

Human aminopeptidase N is a receptor for human coronavirus 229E.

Human coronaviruses (HCV) in two serogroups represented by HCV-229E and HCV-OC43 are an important cause of upper respiratory tract infections. Here we report that human aminopeptidase N, a cell-surface metalloprotease on intestinal, lung and kidney epithelial cells, is a receptor for human coronavirus strain HCV-229E, but not for HCV-OC43. A monoclonal antibody, RBS, blocked HCV-229E virus infection of human lung fibroblasts, immunoprecipitated aminopeptidase N and inhibited its enzymatic activity. HCV-229E-resistant murine fibroblasts became susceptible after transfection with complementary DNA encoding human aminopeptidase N. By contrast, infection of human cells with HCV-OC43 was not inhibited by antibody RBS and expression of aminopeptidase N did not enhance HCV-OC43 replication in mouse cells. A mutant aminopeptidase lacking the catalytic site of the enzyme did not bind HCV-229E or RBS and did not render murine cells susceptible to HCV-229E infection, suggesting that the virus-binding site may lie at or near the active site of the human aminopeptidase molecule.

Cloning of the mouse hepatitis virus (MHV) receptor: expression in human and hamster cell lines confers susceptibility to MHV.

The cellular receptor for murine coronavirus mouse hepatitis virus (MHV)-A59 is a member of the carcinoembryonic antigen (CEA) family of glycoproteins in the immunoglobulin superfamily. We isolated a cDNA clone (MHVR1) encoding the MHV receptor. The sequence of this clone predicts a 424-amino-acid glycoprotein with four immunoglobulinlike domains, a transmembrane domain, and a short intracytoplasmic tail, MHVR1 is closely related to the murine CEA-related clone mmCGM1 (Mus musculus carcinoembryonic antigen gene family member). Western blot (immunoblot) analysis performed with antireceptor antibodies detected a glycoprotein of 120 kDa in BHK cells stably transfected with MHVR1. This corresponds to the size of the MHV receptor expressed in mouse intestine and liver. Human and hamster fibroblasts transfected with MHVR1 became susceptible to infection with MHV-A59. Like MHV-susceptible mouse fibroblasts, the MHVR1-transfected human and hamster cells were protected from MHV infection by pretreatment with monoclonal antireceptor antibody CC1. Thus, the 110- to 120-kDa CEA-related glycoprotein encoded by MHVR1 is a functional receptor for murine coronavirus MHV-A59.

Receptor for mouse hepatitis virus is a member of the carcinoembryonic antigen family of glycoproteins.

The receptor for mouse hepatitis virus (MHV), a murine coronavirus, is a 110- to 120-kDa glycoprotein on intestinal brush border membranes and hepatocyte membranes. The N-terminal 25-amino acid sequence of immunoaffinity-purified MHV receptor was identical to the predicted mature N termini of two mouse genes related to human carcinoembryonic antigen (CEA) and was strongly homologous to the N termini of members of the CEA family in humans and rats. Polyclonal antibodies to human CEA recognized the immunoaffinity-purified MHV receptor and the MHV receptor in liver membranes and intestinal brush border membranes from MHV-susceptible mouse strains. In membranes from MHV-resistant SJL/J mice, the anti-CEA antibodies recognized a homologous glycoprotein that failed to bind MHV. The MHV receptor glycoprotein was detected in membranes of BALB/c colon, small intestine, and liver, which are the principal targets for MHV replication in vivo. The MHV receptor glycoprotein resembled members of the human CEA family in molecular weight, acidic pI, extensive glycosylation, solubility in perchloric acid, and tissue distribution. Thus, the MHV receptor is, to our knowledge, the first member of the CEA family of glycoproteins to be identified as a virus receptor.

Purification of the 110-kilodalton glycoprotein receptor for mouse hepatitis virus (MHV)-A59 from mouse liver and identification of a nonfunctional, homologous protein in MHV-resistant SJL/J mice.

The receptor for mouse hepatitis virus strain A59 (MHV-A59) is a 110- to 120-kilodalton (kDa) glycoprotein which is expressed in MHV-susceptible mouse strains on the membranes of hepatocytes, intestinal epithelial cells, and macrophages. SJL/J mice, which are highly resistant to MHV-A59, were previously shown to lack detectable levels of receptor by using either solid-phase virus receptor assays or binding of a monoclonal anti-receptor antibody (MAb) which blocks infection of MHV-susceptible mouse cells. This MAb was used for affinity purification of the receptor glycoprotein from livers of MHV-susceptible Swiss Webster mice. The MHV receptor and an antigenically related protein of 48 to 58 kDa were copurified and then separated by preparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The first 15 amino acids of the receptor were sequenced, and a synthetic peptide of this amino acid sequence was prepared. Rabbit antiserum made against this peptide bound to the MHV receptor glycoprotein and the 48- to 58-kDa protein from livers of MHV-susceptible BALB/c mice and Swiss Webster mice and from the intestinal brush border of BALB/c mice. In immunoblots of intestinal brush border and hepatocyte membranes of MHV-resistant SJL/J mice, the antibody against the amino terminus of the receptor identified proteins that are 5 to 10 kDa smaller than the MHV receptor and the 48- to 58-kDa related protein from Swiss Webster or BALB/c mice. Thus, SJL/J mice express a protein which shares some sequence homology with the MHV receptor but which lacks virus-binding activity and is not recognized by the blocking anti-receptor MAb. These results suggest that resistance of SJL/J mice to MHV-A59 may be due to absence or mutation of the virus-binding domain in the nonfunctional receptor homolog in SJL/J mice.