The impact of psychological support on weight loss post weight loss surgery: a randomised control trial

Background The purpose of the present study is to evaluate the impact of a health psychology-led bariatric rehabilitation service (BRS) on patient weight loss following bariatric surgery at 1 year. Methods A single-site open-randomised parallel group control trial based at St. Richard’s Hospital in Chichester in the UK. Patients (n=162) were recruited immediately prior to Roux-en-Y gastric bypass and randomly allocated to receive either treatment as usual (n=80) or the BRS (n=82). The BRS involved three 50-min one-to-one sessions with a health psychologist and provided information, support and mentoring pre and post surgery addressing psychological issues such as dietary control, self esteem, coping and emotional eating. Weight loss was assessed at 1 year. The key outcome variable was BMI and change in BMI. Results Follow-up weight was available for 145 patients. Intention-to-treat analysis (n=162) using last measured weights showed that mean change in BMI by 1 year post surgery was −16.49. There was no significant difference between the two groups (control group=−16.37, 95 % CI= 15.15–17.57; intervention=−16.6, 95 % CI=15.42–17.81; ηp 2=0.001). Similarly, explanatory analysis (n=145) showed a mean change inBMI of −17.17. The difference between the two groups was not significant (control group=−16.9, 95 % CI=15.78–18.18; intervention=−17.35, 95 % CI=18.5– 16.16; ηp 2=0.001). Conclusions Psychological support pre and post bariatric surgery had no impact on weight loss as measured by BMI and change in BMI by 1 year. It is argued that psychological support should be targeted to patients who start to demonstrate weight regain at a later stage

Incidence of Respiratory Virus-Associated Pneumonia in Urban Poor Young Children of Dhaka, Bangladesh, 2009–2011

Pneumonia is the leading cause of childhood death in Bangladesh. We conducted a longitudinal study to estimate the incidence of virus-associated pneumonia in children aged <2 years in a low-income urban community in Dhaka, Bangladesh.We followed a cohort of children for two years. We collected nasal washes when children presented with respiratory symptoms. Study physicians diagnosed children with cough and age-specific tachypnea and positive lung findings as pneumonia case-patients. We tested respiratory samples for respiratory syncytial virus (RSV), rhinoviruses, human metapneumovirus (HMPV), influenza viruses, human parainfluenza viruses (HPIV 1, 2, 3), and adenoviruses using real-time reverse transcription polymerase chain reaction assays.Between April 2009-March 2011, we followed 515 children for 730 child-years. We identified a total of 378 pneumonia episodes, 77% of the episodes were associated with a respiratory viral pathogen. The overall incidence of pneumonia associated with a respiratory virus infection was 40/100 child-years. The annual incidence of pneumonia/100 child-years associated with a specific respiratory virus in children aged < 2 years was 12.5 for RSV, 6 for rhinoviruses, 6 for HMPV, 4 for influenza viruses, 3 for HPIV and 2 for adenoviruses.Young children in Dhaka are at high risk of childhood pneumonia and the majority of these episodes are associated with viral pathogens. Developing effective low-cost strategies for prevention are a high priority

Induction of Influenza-Specific Mucosal Immunity by an Attenuated Recombinant Sendai Virus

Background: Many pathogens initiate infection at the mucosal surfaces; therefore, induction of mucosal immune responses is a first level of defense against infection and is the most powerful means of protection. Although intramuscular injection is widely used for vaccination and is effective at inducing circulating antibodies, it is less effective at inducing mucosal antibodies. Methodology/Principal Findings: Here we report a novel recombinant, attenuated Sendai virus vector (GP42-H1) in which the hemagglutinin (HA) gene of influenza A virus was introduced into the Sendai virus genome as an additional gene. Infection of CV-1 cells by GP42-H1 resulted in cell surface expression of the HA protein. Intranasal immunization of mice with 1,000 plaque forming units (pfu) of GP42-H1 induced HA-specific IgG and IgA antibodies in the blood, brochoalveolar lavage fluid, fecal pellet extracts and saliva. The HA-specific antibody titer induced by GP42-H1 closely resembles the titer induced by sublethal infection by live influenza virus; however, in contrast to infection by influenza virus, immunization with GP42-H1 did not result in disease symptoms or the loss of body weight. In mice that were immunized with GP42-H1 and then challenged with 5LD50 (1250 pfu) of influenza virus, no significant weight loss was observed and other visual signs of morbidity were not detected. Conclusions: These results demonstrate that the GP42-H1 Sendai virus recombinant is able to confer full protection fro

Subcapsular sinus macrophages prevent CNS invasion on peripheral infection with a neurotropic virus

Lymph nodes (LNs) capture microorganisms that breach the body’s external barriers and enter draining lymphatics, limiting the systemic spread of pathogens1. Recent work has shown that CD11b(+)CD169(+) macrophages, which populate the subcapsular sinus (SCS) of LNs, are critical for clearance of viruses from the lymph and for initiating antiviral humoral immune responses2,3,4. Using vesicular stomatitis virus (VSV), a relative of rabies virus transmitted by insect bites, we show here that SCS macrophages perform a third vital function: they prevent lymph-borne neurotropic viruses from infecting the CNS. Upon local depletion of LN macrophages, ~60% of mice developed ascending paralysis and died 7–10 days after subcutaneous infection with a small dose of VSV, while macrophage-sufficient animals remained asymptomatic and cleared the virus. VSV gained access to the nervous system via peripheral nerves in macrophage-depleted LNs. In contrast, within macrophage-sufficient LNs VSV replicated preferentially within SCS macrophages but not in adjacent nerves. Removal of SCS macrophages did not compromise adaptive immune responses against VSV, but reduced type I interferon (IFN-I) production within infected LNs. VSV-infected macrophages recruited IFN-I producing plasmacytoid dendritic cells to the SCS and additionally were a major source of IFN-I themselves. Experiments in bone marrow chimeric mice revealed that IFN-I must act on both hematopoietic and stromal compartments, including the intranodal nerves, to prevent lethal VSV infection. These results identify SCS macrophages as crucial gatekeepers to the CNS that prevent fatal viral neuroinvasion upon peripheral infection