In comparison, the rats underwent bariatric surgery had relatively higher proportions of smooth muscle fibers in the cavernosal 
tissue. This appears to indicate that bariatric surgery could potentially reduce cavernosal fibrosis in the setting of diabetes. Through these findings, bariatric surgery seems to improve glucose homeostasis with biochemical factors, thus leading to structural and functional improvements in the corpus cavernosum and resulting in improved erectile dysfunction. The limitations of this pilot study included firstly the relatively small sample size and lack of metabolic parameters. As the purpose of this experiment was to identify the structural and functional background of bariatric surgery in cases of diabetes, we did not perform metabolic evaluations such as testosterone and lipid Etidronate profiles. In future studies, evaluation of these metabolic parameters can be further investigated. Second, the lack of physical measurement, except that of body weight, means that the results of this study cannot be generalized to human studies because obesity is closely correlated to BMI and abdominal circumference. Further evaluation with a larger sample size and metabolic parameter evaluation would be needed. A conventional drug treatment model with a positive control would be needed to clarify the effect of bariatric surgery. Third, the baseline information of histological/expression study were not evaluated. With baseline information for evaluating the pre- and post-operative changes in histological and expression study, the exact effect of bariatric surgery on erectile tissue might be more elucidated. Though this experiment focused on the comparison of the effect of bariatric surgery on erectile dysfunction in a T2DM rat model, the lack of baseline information of histological and biochemical is limitation of this study. In a future study, the limitations including baseline data should be evaluated to understand the exact effect of bariatric surgery on erectile tissue. The gram-negative bacterium Bordetella pertussis, the causative agent of whooping cough, accounted for high mortality rates among infants in the pre-vaccine era. Whole cell and acellular Indinavir sulfate vaccines have drastically decreased the number of cases. However, recently resurgence of pertussis in the vaccinated population has been observed in the USA and in European countries. Currently pertussis is still endemic, ranking in the top-ten of vaccine preventable diseases worldwide, according to the WHO. Next to improved diagnostics and public awareness, also strain adaptation and waning immunity are thought to be responsible for this increase in disease cases. Thus, a call for vaccines with improved efficacy is evident. As a main feature of the innate immune response upon B. pertussis infection in mice the recognition of lipopolysaccharide by TLR4 has been acknowledged. This activation of TLR4 by B. pertussis leads to up-regulation of cytokine gene expression and recruitment of neutrophils into the lungs. It was found in animal models that B. pertussis infection results in formation of T-helper 1 and Th17 cells. Since immunity induced by natural infections provides faster clearance upon reinfection and is longer lasting compared to both acellular and whole cell pertussis vaccination, immune mechanisms induced upon infection or vaccination have been compared. In human and murine studies, immunization with whole cell or acellular pertussis vaccines results predominantly in a Th1 or a Th2 response, respectively.