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91.
BackgroundIliotibial Band Syndrome (ITBS) is a common clinical condition likely caused by abnormal compressive forces to the iliotibial band (ITB). Stretching interventions are common in ITBS treatment and may predominantly affect tensor fascia latae (TFL). Another ITBS treatment is foam rolling, which may more directly affect the ITB. Shear wave ultrasound elastography (SWUE) measures real-time soft tissue stiffness, allowing tissue changes to be measured and compared.PurposeTo examine effects of foam rolling and iliotibial complex stretching on ITB stiffness at 0˚ and 10˚ of hip adduction and hip adduction passive range of motion (PROM).Study DesignRandomized controlled trial.MethodsData from 11 males (age = 30.5 ± 9.0 years, Body Mass Index (BMI) = 27.8 ± 4.0) and 19 females (age = 23.5 ± 4.9, BMI = 23.2 ± 2.1) were analyzed for this study. Subjects were randomly assigned to one of three groups: control, stretching, and foam rolling. Shear wave ultrasound elastography measurements included ITB Young’s modulus at the mid-thigh, the distal femur and the TFL muscle belly. ITB-to-femur depth was measured at mid-thigh level. Hip adduction PROM was measured from digital images taken during the movement.ResultsNo significant interactions or main effects were found for group or time differences in ITB Young’s modulus at the three measured locations. The ITB stiffness at the mid-thigh and distal femur increased with 10° adduction, but TFL stiffness did not increase. A main effect for adduction PROM was observed, where PROM increased 0.8˚ post-treatment (p = 0.02).ConclusionA single episode of stretching and foam rolling does not affect short-term ITB stiffness. The lack of ITB stiffness changes may be from an inadequate intervention stimulus or indicate that the interventions have no impact on ITB stiffness.Levels of Evidence1b  相似文献   
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A selective polyclonal antibody directed toward the C-terminal decapeptide common to the alpha subunits of Gq and G11 G proteins (G alpha q/G alpha 11) was prepared and used to investigate the subcellular distribution fo these proteins in WRK1 cells, a rat mammary tumor cell line. In immunoblots, the antibody recognized purified G alpha q and G alpha 11 proteins and labeled only two bands corresponding to these alpha subunits. Functional studies indicated that this antibody inhibited vasopressin- and guanosine 5'-[alpha-thio]triphosphate-sensitive phospholipase C activities. Immunofluorescence experiments done with this antibody revealed a filamentous labeling corresponding to intracytoplasmic and perimembranous actin-like filament structures. Colocalization of G alpha q/G alpha 11 and F-actin filaments (F-actin) was demonstrated by double-labeling experiments with anti-G alpha q/G alpha 11 and anti-actin antibodies. Immunoblot analysis of membrane, cytoskeletal, and F-actin-rich fractions confirmed the close association of G alpha q/G alpha 11 with actin. Large amounts of G alpha q/G alpha 11 were recovered in the desmin- and tubulin-free F-actin-rich fraction obtained by a double depolymerization-repolymerization cycle. Disorganization of F-actin filaments with cytochalasin D preserved G alpha q/G alpha 11 and F-actin colocalization but partially inhibited vasopressin- and fluoroaluminate-sensitive phospholipase C activity, suggesting that actin-associated G alpha q/G alpha 11 proteins play a role in signal transduction.  相似文献   
95.
Introduction and objectivesWe assessed the long-term hemodynamic performance of transcatheter heart valve (THV) by paired transthoracic echocardiography (TTE), and the incidence, characteristics and factors associated with THV structural valve degeneration (SVD).MethodsA total of 212 patients who underwent transcatheter aortic valve replacement and had a potential follow-up > 5 years with at least 1 TTE ≥ 1-year postprocedure were included. All patients had a TTE at 1 to 5 years and 36 had another one at 6 to 10 years. SVD was defined as subclinical (increase > 10 mmHg in mean transvalvular gradient +  decrease > 0.3 cm2 in valve area and/or new-onset mild or moderate aortic regurgitation) and clinically relevant (increase > 20 mmHg in mean transvalvular gradient + decrease > 0.6 cm2 in valve area and/or new-onset moderate-to-severe aortic regurgitation). Fifteen patients had a transesophageal echocardiography at the time of SVD diagnosis, and 85 an opportunistic computed tomography examination at 1 (0.5-2) years.ResultsTransvalvular mean gradient increased and valve area decreased over time (P < .01). At 8 years of follow-up, SVD occurred in 30.2% of patients (clinically relevant: 9.3%). Transesophageal echocardiography revealed thickened and reduced-mobility leaflets in 80% and 73% of SVD cases, respectively. No baseline or procedural factors were associated with SVD. THV underexpansion (3.5%) or eccentricity (8.2%) had no impact on valve hemodynamics/SVD at follow-up.ConclusionsA gradual THV hemodynamic deterioration occurred throughout a 10-year period, leading to SVD in ~30% of patients (clinically relevant in < 10%). Leaflet morphology/mobility were frequently impaired in SVD cases, but THV geometry did not influence valve hemodynamics or SVD.  相似文献   
96.
Empirical approaches have guided the development of bacterial cultures. The availability of sequenced genomes now provides opportunities to define culture media for growth of fastidious pathogens with computer modelling of metabolic networks. A key issue is the possibility of growing host-dependent bacteria in cell-free conditions. The sequenced Tropheryma whipplei genome was analysed to identify specific metabolic deficiencies. We used this information to design a comprehensive medium that allowed three established T whipplei strains from culture with human cells and one new strain from a clinical sample to grow axenically. Genomic information can, therefore, provide sufficient clues for designing axenic media for fastidious and uncultured pathogens.  相似文献   
97.
BACKGROUND: Both highly potent antiretroviral drug rescue therapy and treatment interruption have been suggested to be effective in patients with multiple treatment failure. OBJECTIVE: To assess both the benefits and risks of an 8-week treatment interruption associated with a six to nine-drug rescue regimen in patients with multiple treatment failures. DESIGN: A randomized comparative controlled trial in 19 university hospitals in France. PATIENTS: Sixty-eight HIV-infected patients with multiple previous treatment failures and CD4 cell counts less than 200 x 10(6) cells/l and plasma HIV-1-RNA levels of 50,000 copies/ml or greater. MEASUREMENTS: The primary efficacy outcome was the proportion of patients with at least a 1 log10 decrease (copies/ml) in the plasma HIV-1-RNA level after 12 weeks of therapy. RESULTS: Treatment interruption followed by multidrug salvage therapy led to a greater proportion of patients achieving virological success (i.e. 1 log10 decrease) at 12 weeks compared with patients receiving multidrug therapy alone (62 versus 26%, intent-to-treat analysis; P = 0.007). The median decrease in the HIV-1-RNA level was -1.91 and -0.37 log10 copies/ml (P = 0.008), respectively. Treatment interruption led to an increase in the number of sensitive drugs of the multidrug regimen (71 versus 35% of regimen with at least two sensitive drugs; P = 0.004). Factors associated with virological success were treatment interruption, the reversion of at least one mutation to wild type, adequate plasma drug concentration, and the use of lopinavir. CONCLUSION: Treatment interruption was beneficial for treatment-experienced HIV-infected patients with advanced HIV disease and multidrug-resistant virus.  相似文献   
98.
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Interictal or ictal events in partial epilepsies may project on scalp EEG contralaterally to the side of the epileptogenic lesion. Such paradoxical lateralization can be observed in case of para-sagittal generators, and is likely due to the spatial orientation of the generator, presenting an oblique projection towards the midline. We present here a case of medial occipital epilepsy investigated using EEG, MEG and stereoelectroencephalography (SEEG). MRI displayed a focal cortical dysplasia in the superior margin of the right calcarine fissure. SEEG demonstrated bilateral medial occipital interictal spikes, with an inversion of polarity at the level of the lesion and a contralateral propagation occurring in 10 ms. Interictal iterative EEG cartographies showed a large posterior field, with a maximum contralateral to the initial generator (EEG paradoxical lateralization). With the same number of channels, interictal iterative MEG cartographies were more precise and more complex than EEG ones, indicating an onset accurately lateralized. A few milliseconds later, MEG cartographies were quadripolar, thus indicating two homotopic active generators. These MEG and EEG cartographies have been reproduced using BESA dipole simulator. Relative merits of MEG and EEG are still debated. With 151 channels, MEG source localizations indicated the right medial occipital area, as demonstrated by SEEG. An investigation with a corresponding number of EEG channels was not performed. After a down sampling to 64 sensors, this precision was lost. MEG and EEG source localization results, both with 64 channels, were quite comparable, indicating both medial occipital areas. However, a careful analysis of MEG/EEG iterative cartographies, performed with the same number of channels in both modalities, demonstrated that, in this configuration, MEG sensitivity was superior to the EEG one, allowing separating two medial occipital sources, characterized in SEEG by a time delay of 10 ms.  相似文献   
100.
We studied cross-reactive antibodies against avian influenza H5N1 and 2009 pandemic (p) H1N1 in 200 serum samples from US military personnel collected before the H1N1 pandemic. Assays used to measure antibodies against viral proteins involved in protection included a hemagglutination inhibition (HI) assay and a neuraminidase inhibition (NI) assay. Viral neutralization by antibodies against avian influenza H5N1 and 2009 pH1N1 was assessed by influenza (H5) pseudotyped lentiviral particle-based and H1N1 microneutralization assays. Some US military personnel had cross-neutralizing antibodies against H5N1 (14%) and 2009 pH1N1 (16.5%). The odds of having cross-neutralizing antibodies against 2009 pH1N1 were 4.4 times higher in subjects receiving more than five inactivated whole influenza virus vaccinations than those subjects with no record of vaccination. Although unclear if the result of prior vaccination or disease exposure, these pre-existing antibodies may prevent or reduce disease severity.Outbreaks of 1997 avian influenza H5N1 and 2009 pandemic (p) H1N1 in humans have provided an opportunity to gain insight into cross-reactive immunity. The US military periodically collects and stores serum samples from service members linked to medical records.1 We measured cross-reactive antibodies in stored serum to avian influenza H5N1 and 2009 pH1N1 from US military personnel and identified factors associated with presence of neutralizing antibodies.Two hundred archived serum samples were obtained from the US Department of Defense Serum Repository. They were representative of a wide cross-section of active military personnel at the times of collection, whereas specific geographic information was not available on the individual selected; the cohort represents the general US military population, which is deployed throughout the United States and globally. Fifty samples each were selected from four birth cohorts: (1) < 1949, (2) 1960–1965, (3) 1966–1971, and (4) 1972–1977. Within each cohort, 25 samples were collected in the year 2000 (before the introduction of intranasal live attenuated influenza vaccine [LAIV]), and 25 samples were collected in 2008 (where 51% of donors had received LAIV). It has been suggested that LAIV elicits cross-reactive immunity.2,3 The samples were all collected before the outbreak of 2009 pH1N1, and there have not been any reported outbreaks of H5N1 in US military personnel.Assays used to measure antibodies included a hemagglutination inhibition (HI) assay and a neuraminidase inhibition (NI) assay.4 Viral neutralization by antibodies against H5N1 and 2009 pH1N1 was assessed by influenza (H5) pseudotyped lentiviral particle-based (H5pp)5 and microneutralization assays, respectively. Electronic medical and vaccination records from the Defense Medical Surveillance System (DMSS), which captured records before the serum sample date, were linked to samples and compared with the in vitro results.1The odds ratios (ORs) and 95% confidence intervals (95% CIs) of univariate and multivariate binary logistic regression analyses were used to determine the association between donor characteristics and positive antibody responses. A multiple logistic regression model was constructed, and it included independent variables with a P value of < 0.05 in univariate logistic regression. A P value of < 0.05 was considered to indicate statistical significance. SPSS 12.0 for Windows (SPSS Inc., Chicago, IL) was used to perform all statistical analysis.Cross-reactivity is summarized in 5 and 22.5% for the NI assay. H5pp and NI antibody titers to H5N1 were evenly distributed among birth cohorts and did not differ substantially based on history of vaccination or prior respiratory infections. Of those individuals with neutralizing antibodies to H5N1 (N = 28), 32.1% also had neutralizing antibodies to pH1N1, whereas 19.3% of those individuals with any H5N1-specific antibody response also had neutralizing antibodies to pH1N1 (
Characteristics (n)H5N12009 pH1N1§
HI assay* % positive (GM titer)H5pp % positive (GM titer)NI assay % positive (GM titer)HI assay % positive (GM titer)Neutralization % positive (GM titer)NI assay % positive (GM titer)
Total
 2000.5 (5.1)14.0 (21.4)22.5 (121.6)5.5 (7.1)16.5 (20.4)9.0 (92.8)
Birth cohort
 1936–1949 (50)2.0 (5.3)18.0 (22.0)24.0 (126.0)6.0 (7.3)16.0 (19.5)12.0 (97.6)
 1960–1965 (50)0.0 (5.0)16.0 (20.3)26.0 (129.6)6.0 (7.7)30.0 (27.5)6.0 (90.3)
 1966–1971 (50)0.0 (5.0)12.0 (23.3)20.0 (117.9)10.0 (8.0)16.0 (23.6)10.0 (92.2)
 1972–1977 (50)0.0 (5.3)10.0 (20.0)20.0 (113.7)0.0 (5.7)4.0 (13.6)8.0 (91.5)
Serum collection year
 Y2000 (100)0.0 (5.1)15.0 (21.7)21.0 (120.3)7.0 (7.3)16.0 (20.6)11.0 (94.5)
 Y2008 (100)1.0 (5.2)13.0 (21.1)24.0 (123.0)4.0 (7.0)17.0 (20.1)7.0 (91.2)
Sex
 Female (32)3.1 (5.7)21.9 (26.3)12.5 (102.4)3.1 (6.9)12.5 (19.2)6.3 (96.7)
 Male (168)0.0 (5.0)12.5 (20.5)24.4 (125.7)6.0 (7.2)17.3 (20.6)9.5 (92.1)
Any cross-reactive antibody to
 H5N1 (57)8.8 (8.9)19.3 (25.2)22.8 (119.9)
 pH1N1 (45)2.2 (5.3)28.9 (31.2)37.8 (165.2)
Neutralizing antibodies to
 H5N1 H5pp (28)10.7 (9.5)32.1 (33.6)25.0 (116.9)
 2009 pH1N1 neutralization (33)3.0 (5.4)27.3 (28.9)30.3 (140.3)
Lifetime seasonal vaccinations
 No record (66)0.0 (5.1)10.6 (20.2)27.7 (128.1)7.6 (7.4)15.2 (20.6)12.1 (96.5)
 1–5 vaccinations (88)1.1 (5.2)15.9 (21.5)17.0 (109.2)5.7 (7.1)17.0 (20.5)6.8 (89.1)
  > 5 vaccinations (46)0.0 (5.1)15.2 (22.2)32.6 (138.8)2.2 (6.8)17.4 (19.7)8.7 (95.0)
Time since last vaccine
 No record (66)0.0 (5.1)10.6 (20.2)22.7 (128.1)7.6 (7.4)15.2 (20.6)12.1 (96.5)
  ≤ 1 year (96)0.0 (5.1)15.6 (21.5)24.0 (120.7)4.2 (7.1)19.8 (21.0)8.3 (91.2)
 > 1 year (38)2.6 (5.3)15.8 (22.4)18.4 (113.4)5.2 (6.8)10.5 (18.3)5.3 (90.6)
Vaccination history lifetime (at least one dose)
 No record of vaccination (66)0.0 (5.1)10.6 (20.2)22.7 (128.1)7.6 (7.4)15.2 (20.6)12.1 (96.5)
 Inactivated whole virus (71)0.0 (5.0)14.1 (20.4)22.5 (115.7)2.8 (6.4)15.5 (19.6)5.6 (87.1)
 Split type (102)1.0 (5.0)15.7 (20.4)21.6 (115.7)4.9 (6.4)19.6 (19.6)6.9 (87.1)
 Influenza vaccine not otherwise specified (16)0.0 (5.2)12.5 (27.9)37.5 (166.4)0.0 (6.2)6.3 (16.1)12.5 (102.3)
 Live attenuated intranasal (50)0.0 (5.1)10.0 (18.8)20.0 (112.2)4.0 (7.0)18.0 (20.3)4.0 (85.2)
History of respiratory illness
 No record of illness (119)0.0 (5.0)10.1 (18.5)18.5 (112.6)4.2 (7.0)15.1 (20.5)8.4 (90.7)
 Influenza-like illness (4)0.0 (5.0)25.0 (20.7)0.0 (80.0)0.0 (8.4)25.0 (28.3)25.0 (100.2)
 Upper respiratory infection (65)1.5 (5.4)23.1 (29.3)27.7 (135.0)7.7 (7.3)18.5 (20.7)9.2 (93.1)
 Lower respiratory infection (37)2.7 (5.6)18.9 (30.2)35.1 (157.6)8.1 (8.1)21.6 (22.4)13.5 (108.4)
 Respiratory illness past year (28)0 (5.1)25.0 (25.1)32.1 (154.9)7.1 (8.0)28.6 (24.4)3.6 (86.3)
Open in a separate windowTiters with a value of zero (below the detection limit) were assigned a value of five for calculation of geometric means (GMs).*H5N1, A/Vietnam/1203/2004; positive titer ≥ 40.H5 hemagglutinin (A/Cambodia/408008/05) pseudotyped lentiviral particle; positive titer ≥ 160.Reassortant H1N1 (HA, PB1, PB2, PA, NP, and M from H1N1 [A/PR/8/34]; N1 from H5N1 [A/Vietnam/DT-036/2005]); positive titer ≥ 160.§2009 H1N1, A/California/04/2009; same positive titer cutoffs as for H5N1.As with H5N1, samples with positive HI titers were low for 2009 pH1N1 at 5.5%, whereas neutralizing antibody titers were higher, with 16.5% positive in the microneutralization assay but only 9% positive in the NI assay. Positive neutralization titers were less evenly distributed among birth cohorts, with only 4% positive in the 1972–1977 birth cohort, whereas 30% were positive in the 1960–1965 cohort. Like H5N1, positive antibody titers to 2009 pH1N1 did not differ substantially based on history of vaccination or prior respiratory infections. Of those individuals with neutralizing antibodies to pH1N1 (N = 33), 27.3% also had neutralizing antibodies to H5N1, whereas 28.9% of those individuals with any pH1N1-specific antibody response also had neutralizing antibodies to H5N1.Univariate associations between the prevalence of cross-reactive antibodies to H5N1 and 2009 pH1N1 and independent variables, including year of birth, serum collection year, sex, and seasonal influenza vaccination history, are shown in Characteristic (n)2009 pH1N1H5N1PrevalenceOR (95% CI)Adjusted OR (95% CI)PrevalenceOR (95% CI)Positive neutralizing antibody33 (16.5%)28 (14.0%)Serum collection year 2000 (100)16 (16.0%)ReferenceReference15 (15.0%)Reference 2008 (100)17 (17.0%)1.1 (0.5–2.3)0.7 (0.3–1.8)13 (13.0%)0.9 (0.4–1.9)Birth cohort 1936–1949 (50)8 (16.0%)4.6 (0.9–22.7)5.3 (1.0–27.0)9 (18.0%)2.0 (0.6–6.4) 1960–1965 (50)15 (30.0%)10.3 (2.2–47.9)11.0 (2.3–52.9)8 (16.0%)1.7 (0.5–5.7) 1966–1971 (50)8 (16.0%)4.6 (0.9–22.7)5.1 (1.0–26.2)6 (12.0%)1.2 (0.4–4.3) 1972–1977 (50)2 (4.0%)ReferenceReference5 (10.0%)ReferenceSex Female (32)4 (12.5%)Reference7 (21.9%)Reference Male (168)29 (17.3%)1.5 (0.5–4.5)21 (12.5%)0.5 (0.2–1.3)Positive neutralizing antibody titers H5pp (57)11 (19.3%)1.3 (0.6–2.9) pH1N1 (45)13 (28.9%)3.8 (1.6–8.7)Vaccination record Number of seasonal influenza vaccinations  No record (66)10 (15.2%)Reference7 (10.6%)Reference  1–5 vaccinations (88)15 (17.0%)1.2 (0.5–2.8)14 (15.9%)1.6 (0.6–4.2)  > 5 vaccinations (46)8 (17.4%)1.2 (0.4–3.3)7 (15.2%)1.5 (0.5–4.7) Time since last vaccination  No record (66)10 (15.2%)Reference7 (10.61%)Reference   ≤ 1 year (96)19 (19.8%)1.4 (0.6–3.2)15 (15.6%)1.6 (0.6–4.1)  > 1 year (33)4 (10.5%)0.7 (0.2–2.3)6 (15.8%)1.6 (0.5–5.1) Number of inactivated whole virus vaccinations  No record (129)22 (17.1%)ReferenceReference18 (14.0%)Reference  1–5 vaccinations (53)4 (7.5%)0.4 (0.1–1.2)0.4 (0.1–1.4)7 (13.2%)0.9 (0.4–2.4)  > 5 vaccinations (18)7 (38.9%)3.1 (1.1–8.9)4.4 (1.3–15.6)3 (16.7%)1.2 (0.3–4.7) Time since last inactivated whole virus vaccination  No record (129)22 (17.1%)Reference18 (14.0%)Reference   ≤ 1 year (19)4 (21.1%)1.3 (0.4–4.3)3 (15.8%)1.2 (0.3–4.4)  > 1 year (52)7 (13.5%)0.8 (0.3–1.9)7 (13.5%)1.0 (0.4–2.5) Number of split type vaccinations  No record (98)13 (13.3%)Reference12 (12.2%)Reference  1–5 vaccinations (94)19 (20.2%)1.7 (0.8–3.6)14 (14.9%)1.3 (0.6–2.9)  > 5 vaccinations (8)1 (12.5%)0.9 (0.1–8.2)2 (25.0%)2.4 (0.4–13.2) Time since last split type vaccination  No record (98)13 (13.3%)Reference12 (12.2%)Reference   ≤ 1 year (44)10 (22.7%)1.9 (0.8–4.8)10 (22.7%)2.1 (0.8–5.3)  > 1 year (58)10 (17.2%)1.4 (0.6–3.3)6 (10.3%)0.8 (0.3–2.3) Number of intranasal LAIV vaccinations  No record (150)24 (16.0%)Reference23 (15.3%)Reference  1–5 vaccinations (50)9 (18.0%)1.2 (0.5–2.7)5 (10%)0.6 (0.2–1.7) Time since last intranasal LAIV vaccination  No record (150)24 (16.0%)Reference23 (15.3%)Reference   ≤ 1 year (34)7 (20.6%)1.4 (0.5–3.5)3 (8.8%)0.5 (0.2–1.9)  > 1 year (16)2 (12.5%)0.8 (0.2–3.5)2 (12.5%)0.8 (0.2–3.7)Open in a separate windowTo the best of our knowledge, the present study is the first report of cross-reactive antibodies to both H5N1 and 2009 pH1N1 in a US military population. Cross-reactive antibodies to both influenza viruses were common in this population. Most serum samples (86%) positive in the H5N1 neutralization assay had no detectable HI activity (titer ≥ 10), whereas 94% of samples that neutralized 2009 pH1N1 also had detectable HI activity (titer ≥ 10; data not shown). In addition, cross-reactive antibodies to avian influenza H5N1 were not necessarily accompanied by cross-reactive antibodies to 2009 pH1N1. Taken together, these findings suggest that the observed cross-reactive neutralization against the two influenza viruses was caused by different antibodies in serum samples.This report is also the first report to associate history of receiving more than five doses of inactivated whole influenza virus vaccine with neutralizing antibodies against 2009 pH1N1. This finding suggests a protective advantage of repeated vaccination with seasonal whole virus vaccine, generating cross-reactive antibodies against previously unencountered strains. It has been suggested that the high immunogenicity of the inactivated whole virus vaccine is partly caused by the adjuvant effect of the viral RNA presented, stimulating innate immunity through the Toll-like receptor (TLR) 7-dependent pathway.6 We hypothesize that the combined effect of adjuvant activity and the heterogenous mix of flu strains that an individual would be exposed to over the course of multiple seasonal vaccinations may enhance the breadth of antibody response and promote the generation of cross-reactive antibodies.A retrospective case-control study conducted in US military personnel after the outbreak of 2009 pH1N1 showed that both 2008–2009 seasonal influenza vaccine and history of seasonal vaccine in the prior 4 years afforded some protection against pH1N1. Vaccine effectiveness (VE) was high in persons ≥ 40 (55%) or < 25 (50%) years of age but very low in persons 25–39 years of age (< 10%).7 These findings correlate with the high levels of cross-reactive 2009 pH1N1 antibodies reported here, with 30% in the 1960–1965 cohort (age range = 35–48) but only 4% in the 1972–1977 cohort (age range = 23–36). Our findings are similar to the results found recently in an elderly population in the United States.8 The exception is in those individuals born before 1950, in whom antibody responses were much higher in this cohort. Both our study and the US study differ from two recent seroprevalence studies in Singapore and China, where cross-reactive antibodies were rare in various age groups.9,10 High seasonal influenza vaccination rates in US military personnel found here and prior studies11 may explain the differences observed in these populations, although results from small retrospective seroprevalence studies should be interpreted cautiously. Possible alternative explanations include differences in laboratory assay methods, natural influenza exposure in the sampled populations, and/or use of convenience sampling methods.Studies in humans suggest that the antibody to influenza neuraminidase is associated with resistance to influenza.12 A recent serological study in a small number of human serum samples showed that 24% had cross-reactive antibodies to avian N1,13 similar to our findings (22.5%). In addition, we observed that 9% of serum samples had cross-reactive antibodies to pH1N1.Like pH1N1, persons < 40 years old seem to be most affected by H5N1 infection, with infection rarer in older individuals.14 However, we did not find a difference in cross-reactive antibody prevalence to either neuraminidase or neutralizing antibodies (H5pp) with year of birth or other immunologic markers of exposure, including vaccination history or prior respiratory illness.A possible limitation of our study is that the DMSS may not have captured all relevant medical encounter and/or vaccination data, particularly for encounters that were not entered into the system electronically or coded accurately. Data in the DMSS are provider-dependent, and the DMSS captures data from various historical time periods, dating back to 1980 for immunization data, 1985 for Department of Defense Serum Repository specimens, 1990 for demographic data, and only 1996 for outpatient data. Interpretation of data presented on history of respiratory illness, which is entirely dependent on voluntary provider reporting and International Classification of Diseases (ICD-9) coding, is particularly limited by lack of virologic confirmation.Cross-reactive immunity to pathogenic influenza strains was found in a subset of US military service members, and it may serve to prevent or reduce the severity of influenza. A better understanding of the mechanisms underlying the development of cross-reactive antibodies will aid in the development of more effective preventive and therapeutic measures.  相似文献   
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