Effect of allergic rhinitis on the expression of human β-defensin 2 in tonsils

BackgroundHuman β-defensins (HBDs) are a newly identified family of antimicrobial peptides that are expressed by epithelia on mucosal surfaces. Exposure of airway epithelial cells to T_H2-type cytokines results in a significant decrease in the antimicrobial activity of the cells.ObjectiveTo investigate the effect of allergic rhinitis on the expression of HBD-2 in tonsils and adenoids.MethodsPalatine tonsils and adenoids were obtained from 30 patients with no history of recurrent tonsillitis. The patients were divided into 2 groups: allergic rhinitis and nonallergic rhinitis groups. Real-time polymerase chain reaction analysis was used to measure messenger RNA (mRNA) levels of HBD-2 mRNA in tonsil and adenoid tissue samples from the 2 patient groups. Immunofluorescent staining and enzyme-linked immunosorbent assay (ELISA) were used to evaluate the expression of HBD-2 protein in tonsil and adenoid tissues. The concentration of the cytokines interleukin (IL) 4, IL-5, and interferon γ (IFN-γ) in tissue homogenates was measured by ELISA.ResultsImmunofluorescent staining data demonstrated the expression of HBD-2 protein in the surface epithelia of tonsils, and a marked difference in the staining intensity was observed the between 2 groups. HBD-2 mRNA and protein levels in the tonsils were significantly lower in the allergic rhinitis group than that in the nonallergic rhinitis group (P = .03 and P = .04, respectively). IL-5 and IFN-γ were not detected, and no significant difference was found in IL-4 concentrations in tonsil homogenates between the 2 groups.ConclusionAllergic rhinitis suppresses HBD-2, an epithelial antimicrobial peptide, in the tonsils.     

Magnetic resonance appearance of bioabsorbable anchor screws for double row arthroscopic rotator cuff repairs

Background:

Little is known about the bioabsorbable, anchor related postoperative changes in rotator cuff surgery, which has become more popular recently. The purpose of the present study was to use magnetic resonance imaging (MRI) to analyze the degradation of bioabsorbable anchors and to determine the incidences and characteristics of early postoperative reactions around the anchors and their mechanical failures.

Materials and Methods:

Postoperative MRIs of 200 patients who underwent arthroscopic rotator cuff repair were retrospectively analyzed. The tissue reactions around the bioanchors included fluid accumulations around the anchor, granulation tissue formation and changes in the condition of the surrounding osseous structure. The condition of the bioanchor itself was also examined, including whether the bioanchor failed mechanically. In the case of mechanical failure, the location of the failure was noted. Serial MRIs of 18 patients were available for analysis.

Results:

The total number of medial row bioanchors was 124, while that of the lateral row was 338. A low signal intensity rim suggestive of sclerosis surrounded all lateral row bioanchors. Ninety three lateral row bioanchors (27%) showed a rim with signal intensity similar to or less than that of surrounding bone, which was granulation tissue or foreign body reaction (FBR). Similar signal intensity was seen around nine medial row bioanchors (7%). Fluid accumulation was seen around 4 lateral row bioanchors (1%) and around 14 medial row bioanchors (11%). Five lateral row bioanchors showed the breakage, while there was none in the medial row bioanchors. There were nine cases with a cuff re-tear (4.5%). There was no evidence of affection of glenohumeral articular surfaces or of osteolysis around any bioanchor. In serial MRI, there was no change in appearance of the bioanchors, but the granulation tissue or FBR around four bioanchors and the fluid around one bioanchor showed a decrease in successive MRI.

Conclusion:

This study highlights the normal and adverse reactions to Bioabsorbable anchors that surgeons can expect to see on MRI after rotator cuff repairs.     

A viral protease-mediated cleavage of the transmembrane glycoprotein of Mason-Pfizer monkey virus can be suppressed by mutations within the matrix protein.

The envelope glycoprotein precursor of retroviruses undergoes proteolytic cleavage in the Golgi complex to yield the mature surface and transmembrane (TM) glycoproteins of the virus. We report here that the TM glycoprotein of Mason-Pfizer monkey virus undergoes a second proteolytic processing event during a late maturation step that can follow virus release and Gag polyprotein cleavage. Cleavage results in the conversion of the cell-associated TM glycoprotein (gp22) to a virus-associated gp20. Processing continues after virus release and yields virions that contain predominantly gp20. A mutation within the active site of the Mason-Pfizer monkey virus aspartyl protease was shown to block both TM glycoprotein cleavage and the processing of the Gag polyprotein precursor. The role of the viral protease in cleavage of the TM glycoprotein localizes the cleavage site to the cytoplasmic domain of this protein. Surprisingly, point mutations within the matrix (MA) coding region of the gag gene can affect the extent to which gp22 is processed to gp20 and in one case [p10(MA)-A79V] results in greater than 90% inhibition of gp22 cleavage. The data provide genetic evidence of a specific interaction between the capsid proteins and the cytoplasmic domain of the TM glycoprotein of a retrovirus. This interaction is required for cytoplasmic domain cleavage to occur and may play a critical role in virus assembly and viral infectivity.     

Atrial flutter. Electrocardiographic,vectorcardiographic and echocardiographic correlation

The duration, contour, and amplitude of atrial flutter wave (f) was studied by electrocardiogram (ECG) and vectorcardiogram (VCG) in 32 patients and was related to the size of the left atrium (LA) measured by the echocardiogram (E). The following ECG parameters were analyzed: (1) the duration of left atrial depolarization, i.e., LA wave; (2) the amplitude of LA wave; (3) the surface area of LA wave; (4) maximum amplitude (A) of f in Leads 2 and V₁. There was good correlation between LA size and the duration of depolarization and surface area (p < 0.01), but the maximum amplitude of the f wave in Leads 2 and V₁ failed to predict LA size.The post-conversion sinus P wave showed abnormal LA depolarization time (P > 0.12 sec.) in 62 per cent of patients with enlarged left atrium (ELA) and in 43 per cent of patients with normal size LA (NLA).The VCG of the flutter wave revealed two patterns, (1) an eliptical smooth fsÊ loop in 63 per cent of patients with NLA, and (2) distorted fsÊ loop in 67 per cent of patients with ELA.Both VCG patterns were subdivided in two subgroups according to the number and location of conduction delays. The VCG of post-conversion P wave confirmed conduction delays in both groups.We conclude that both the size of the left atrium and conduction delays play a basic role in the duration and contour of left atrial wave.