Association Between Pet Ownership and the Sensitization to Pet Allergens in Adults With Various Allergic Diseases

Purpose

As pet ownership increases, sensitization to animal allergens due to domestic exposure is a concern. Sensitization to animal allergens may occur from indirect exposure, as well as direct ownership of animals. However, there have been conflicting results regarding the association between pet ownership and sensitization to animal allergens in adults.

Methods

In total, 401 patients with various allergic diseases were enrolled in this study. We performed skin prick tests with 55 common inhalant and food allergens, including dog, cat, and rabbit allergens. A mean wheal diameter of 3 mm or greater was considered a positive reaction. The exposure modality to each animal allergen was investigated using a questionnaire and included present ownership, past ownership, occupational exposure, occasional exposure, contact with pet owner, and no contact. Present ownership, past ownership, occupational, and occasional exposure were regarded as direct exposure.

Results

The sensitization rate for animal allergens was 20.4% for dog, 15.0% for cat, and 9.0% for rabbit. Direct exposure to dogs (72.0%) was significantly higher than that of other animals (18.4% for cats and 16.7% for rabbits), whereas ''no contact'' with cats (78.3%) and rabbits (83.3%) was significantly higher than with dogs (26.8%; P<0.0001). Independent risk factors for sensitization to animal allergens were sensitization to Dermatophagoides pteronyssinus (OR=2.4, P=0.052), Dermatophagoides farinae (OR=5.1, P<0.001), cat (OR=4.4, P<0.0001), and direct exposure to dogs (OR=1.5, P=0.029) for dog, and sensitization to dog (OR=4.4, P<0.0001) and rabbit (OR=2.6, P=0.036) for cats. Finally, for rabbits, the independent risk factor was sensitization to Alternaria (OR=6.0, P<0.002).

Conclusions

These results suggest that direct exposure to dogs contributes to the sensitization to dog allergens in patients with allergic diseases, whereas indirect exposure to cats and rabbits may induce sensitization to each animal''s allergen.     

Three-dimensional changes of the hyoid bone and airway volumes related to its relationship with horizontal anatomic planes after bimaxillary surgery in skeletal Class III patients

Objective:To evaluate longitudinal changes of the hyoid bone position and pharyngeal airway space after bimaxillary surgery in mandibular prognathism patients.Materials and Methods:Cone-beam computed tomography scans were taken for 25 mandibular prognathism patients before surgery (T0), 2 months after surgery (T1), and 6 months after surgery (T2). The positional displacement of the hyoid bone was assessed using the coordinates at T0, T1, and T2. Additionally, the volume of each subject''s pharyngeal airway was measured.Results:The mean amount of posterior maxilla impaction was 3.76 ± 1.33 mm as the palatal plane rotated 2.04° ± 2.28° in a clockwise direction as a result of bimaxillary surgery. The hyoid bone moved backward (P < .05, P < .001) and downward (P > .05, P < .05) at 2 months and 6 months after surgery, while the total volume of the pharyngeal airway significantly decreased at the same time points (P < .001, P < .001). There was significant relationship between the changes of the hyoid bone position and airway volume at 2 months after surgery (P < .05). The change of the palatal plane angle was positively correlated to the decrease in the total airway volume (P < .001).Conclusions:The null hypothesis was rejected. The hyoid bone moved inferoposteriorly, and the pharyngeal airway volume decreased for up to 6 months after bimaxillary surgery. The decrease in the pharyngeal airway volume was correlated to the changes in the palatal plane inclination and the positional change of the hyoid bone.     

Kaempferol Inhibits P. intermedia Lipopolysaccharide‐Induced Production of Nitric Oxide Through Translational Regulation in Murine Macrophages: Critical Role of Heme Oxygenase‐1‐Mediated ROS Reduction

Background: Nitric oxide (NO) could be a potential target for the development of new therapeutic approaches to the treatment of periodontal disease because this molecule plays a significant role in the tissue destruction observed in periodontitis. In this study, the authors investigate the effect of kaempferol on the production of NO by murine macrophage‐like RAW264.7 cells stimulated with lipopolysaccharide (LPS) from Prevotella intermedia, a pathogen implicated in periodontal disease, and try to determine the underlying mechanisms of action. Methods: NO production was assayed by measuring the accumulation of nitrite in culture supernatants. Real‐time polymerase chain reaction was performed to quantify inducible NO synthase (iNOS) and heme oxygenase‐1 (HO‐1) mRNA expression. iNOS and HO‐1 protein expression and phosphorylation of c‐Jun N‐terminal kinase and p38 were characterized via immunoblot analysis. Reactive oxygen species (ROS) production was measured using the redox‐sensitive fluorescent probe 2′,7′‐dichlorodihydrofluorescein diacetate. Results: Kaempferol significantly inhibited NO production and expression of iNOS protein in P. intermedia LPS‐stimulated RAW246.7 cells without affecting iNOS mRNA expression. Kaempferol upregulated HO‐1 expression in LPS‐activated cells. Inhibition of HO‐1 activity by tin protoporphyrin IX (SnPP) abolished the suppressive effect of kaempferol on NO production. In addition, kaempferol significantly attenuated P. intermedia LPS‐induced increase of intracellular ROS, and SnPP blocked this reduction. Treatment with antioxidants downregulated the production of LPS‐induced NO. Conclusions: Kaempferol inhibits NO production and iNOS protein expression in P. intermedia LPS‐stimulated RAW264.7 cells at the translational level via HO‐1‐mediated ROS reduction and could be an efficient modulator of host response in the treatment of periodontal disease.     

Immunohistochemical Localization and Distribution of Proliferating Cell Nuclear Antigen in the Rabbit Mandibular Condyle Following Experimental Induction of Anterior Disk Displacement

The purpose of the present study was to identify proliferating cells in control versus experimental condyles two weeks following experimental Induction of anterior disk displacement (ADD) in the rabbit craniomandibular joint (CMJ). The right joint of 15 rabbits was exposed surgically and all diskal attachments were severed except for the posterior attachment. The disk was then repositioned anteriorly and sutured to the zygomatic arch. The left joint served as a sham-operated control. Ten additional joints were used as nonoperated controls. Mandibular condyles were excised two weeks following surgery and processed for proliferating cell nuclear antigen (PCNA) immunostaining. In control and sham operated condyles, PCNA was localized in the nuclei of chondroblasts of the reserve cell layer, chondrocytes of the upper hypertrophic layer and bone marrow cells of the subchondral bone. In contrast to control joints, the PCNA positive cells of the experimental joints were located throughout the osteoarthritic condylar cartilage. In addition, the percentage of PCNA positive cells of the osteoarthritic condylar cartilage was statistically significantly higher when compared to the control group, p < 0.05. It was concluded that surgical induction of ADD in the rabbit CMJ leads to an increase in mitosis of chondrocytes, which lead to cell proliferation and subsequent hyperplasia of the condylar cartilage.     

Perfusion Defects Detected After Liver Transplantation on Multidetector Computerized Tomography: Short- and Long-Term Follow-up

Background

Perfusion defects are sometimes found during the follow-up computerized tomography (CT) after liver transplantation (OLT). This study sought to determine the short- and long-term outcomes of perfusion defects observed after OLT with the use of multidetector CT.

Methods

From February 4, 2004, to December 8, 2011, a total 46 LTs were performed in our hospital owing to end-stage liver cirrhosis (n = 43), liver cirrhosis with hepatocellular carcinoma (HCC; n = 1), combined HCC with cholangiocellular carcinoma (CCC; n = 1), or hepatic failure from acute hepatitis A (n = 1). The transplanted livers were procured from cadaveric (n = 24) or living related donors (n = 22). The average age of the recipient was 53.3 ± 10.4 years. The male-female ratio was 30:16. Postoperative multidetector CT was performed with a dynamic sequence in 203 examinations and with a portal phase in 46 examinations. The contrast media was Radisense. The rate of injection of 120 mL was 3 mL/s with a power injector; the iodine concentration was 300 or 370 mg/dL. Follow-up ranged from 3 months 3 days to 7 years 363 days. We classified perfusion defects as chronic segmental or subsegmental benign ischemia, transient focal perfusion defects, benign subcapsular ischemia, or fatal whole liver perfusion defects.

Results

There were 3 cases of chronic segmental or subsegmental benign ischemia, 8 focal transient perfusion defects, 1 benign subcapsular ischemia, and 4 fatal whole liver perfusion defects. Except the fatal cases, all other perfusion defects occurred in the courses of benign conditions without resection or reoperation.

Conclusions

Most perfusion defects were benign and uneventful, requiring no treatment, with the exception of fatal whole liver perfusion defects, which resulted in death after detection.