Acute Phase Group Research Articles

Regulatory T cells and Th1/Th2 in peripheral blood and their roles in asthmatic children.

To determine the changes in CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) and the Th1/Th2 ratio in peripheral blood of children with asthma, in order to investigate its association with asthma. A total of 150 children with asthma were allocated into the acute phase group (n=94) and remission phase group (n=56) based on clinical manifestations. The acute phase group was subdivided into the mild group (n=54) and severe group (n=40). Flow cytometry was applied to determine CD4(+)CD25(+)Foxp3(+) Treg, CD4(+)IFN-γ(+) Th1 and CD4(+)IL-4(+) Th2 levels in peripheral blood of different groups, and the results were compared with normal children (control group, n=50). The Treg level was significantly lower in the asthma group than the control group (P<0.01): the Treg level was significantly lower in the acute phase group than the remission phase group and control group (P<0.01) and also significantly lower in the severe group than the mild group (P<0.01). The Th1/Th2 ratio was significantly lower in the asthma group than the control group (P<0.01) and also significantly lower in the acute phase group than the remission phase group and control group (P<0.01). The Treg level in peripheral blood of asthmatic children was negatively correlated with the severity of asthma (r=-0.737, P<0.01) and the Th1/Th2 ratio was also negatively correlated with the severity of asthma (r=-0.615, P<0.01), but the Treg level was positively correlated with the Th1/Th2 ratio (r=0.856, P<0.01). The significantly decreased level of Treg in peripheral blood and Th subset imbalance in asthmatic children suggest the important roles of Treg and Th immunity in pathogenesis of asthma. The Treg level and Th1/Th2 ratio in peripheral blood can be used to evaluate the severity asthma.

Selenium and leptin levels in febrile seizure: a case-control study in children

PurposeFebrile seizures (FS) are seizures that occur between the age of 6 and 60 months, but its pathophysiology still is not fully understood. There is limited information about the correlation between levels of selenium and leptin with FS. This study aimed to determine the relationship between serum levels of selenium and leptin in children with FS.MethodsThis case-control study was conducted in a University Hospital in Shahrekord, Iran, in 2011. The serum levels of selenium and leptin of 25 children with simple febrile seizure (case group) were compared with 25 febrile children without seizure (control group) in acute phase and after three months. The levels of serum selenium and leptin were measured by flame atomic absorption spectrophotometer and enzyme-linked immunosorbent assay method, respectively.ResultsIn acute phase, the mean serum level of selenium in case and control groups were 95.88±42.55 and 113.25±54.43 µg/dL, respectively, and difference was not significant (P=0.415), but after three months, this level had a significant increase in both groups (P<0.001). In acute phase, the mean serum leptin level in case and control groups were 0.94±0.5 and 0.98±0.84 ng/mL, respectively, but difference was not significant (P=0.405). After three months, serum leptin level had no significant change in both groups (P=0.882).ConclusionThese observations suggest that serum levels of selenium and leptin have not specific relation with FS but overllay is lower, however, further study is recommended. Also selenium level in stress and acute phase was significantly lower than recovery phase.

Comparison of the Changes in Thickness of the Abdominal Wall Muscles of Stroke Patients According to the Duration of Their Illness as Observed Using Ultrasonographic Images

[Purpose] This study was conducted in order to investigate the importance of trunk muscle strength in stroke patients. By comparing the thicknesses of the abdominal wall muscles through ultrasonography, relative to the duration of illness, the results of the objective data were applied. [Methods] Thirty stroke patients were divided into three groups including an acute phase group participating in the study within 1 month after the onset of a stroke (n=10), a subacute phase group participating less than 6 months (n=10) after a stroke, and a chronic phase group participating more than 6 months (n=10) after suffering a stroke. The thicknesses of the transversus abdominis muscles (TrA), internal oblique muscle (IO), and the external oblique muscle (EO) were measured at rest and during abdominal draw-in maneuver (ADIM) in a supine hook-lying position, and their differences were compared. [Results] The results showed that, in comparison of the thicknesses of the paretic and nonparetic sides, the TrA of the subacute phase and chronic phase groups showed significant differences. In addition, the IO of the subacute phase group and the EO of the chronic phase groups also showed significant differences. [Conclusion] According to the duration of illness in stroke patients, the abdominal wall muscles become noticeably infirm and asymmetric. By improving their symmetry, the functions of the trunk muscles can be recovered.

Significance of serum neutrophil cell elastase and α 1-antitrypsin detection of COPD

Objective To select patients with chronic obstructive pulmonary disease(COPD)and healthy people for comparative study and analysis during the stabilization period of the patients with COPD exacerbation of neutrophil elastase and α 1-antitrypsin(α 1-AT)change status,and the changes,risk factors and lung function indicators of relevance,and to explore the significance of anti-proteases and protease imbalance in the pathogenesis of COPD.Methods We randomly collected 43 cases of COPD from February 2009 to January 2012 as acute exacerbation group,and 24 cases of healthy people as controls,taking their serum samples,patients with COPD including 21 cases of acute exacerbation with the stabilization period among 22 cases to detect serum α 1-AT,NE level,using the enzyme-linked immunosorbent assay.Results NE level in normal control group was significantly lower than that of the acute exacerbation group,the difference was statistically significant(P＜ 0.01).the NE level of stabilization period was less than that of acute exacerbation with statistical significant difference(P＜ 0.05);Independent samples T-test results,acute exacerbation phase group α 1-AT level was significantly lower than that of the control group,the difference was statistically significant(P＜ 0.01);acute exacerbation α 1-AT levels below the stabilization period,the difference was statistically significant(P＜ 0.05).Conclusion The imbalance of α 1-AT and the NE level plays an important role in the pathogenesis of COPD;the α 1-AT deficiency and increase of NE level are closely associated with airway obstruction and airway inflammation. Key words: Serum neutrophil cell elastase; α 1-antitrypsin detection(α 1-AT); Chronic obstructive pulmonary disease(COPD)

Investigation of cytokine levels and their association with SCORAD index in adults with acute atopic dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease with increasing frequency over the last decades, especially in adults. Cytokines orchestrate atopic skin inflammation. Objectives The aim of this study was to compare serum levels of cytokines in adult patients with acute AD (AD1) with other groups of AD patients and controls and investigate the possible association between such cytokines and disease severity. We measured cytokine levels using flow cytometry in 21 adult patients with acute AD, 12 adults with chronic AD, 10 children with acute AD and 10 healthy adults. Flow cytometry analysis of cytokines revealed that interleukin 10 (IL-10), IL-6, interferon γ (IFN-γ) and IL-4 levels were significantly decreased in AD1 group compared with controls, whereas IL-2 and tumour necrosis factor (TNF) did not differ. Comparison of AD1 group with adults chronic phase group showed that IgE, eosinophil and IL-2 levels remained unaltered, whereas IL-10, IL-6, IFN-γ, IL-4 and TNF were significantly decreased. SCORAD and IgE levels were significantly increased, IL-10, IL-6 and IFN-γ were decreased and TNF, IL-2, IL-4 and eosinophil levels remained unchanged in AD1 group compared with children acute phase group. Within AD1 group correlation analysis revealed that IgE and TNF levels were significantly associated with AD severity. Coefficient of determination analysis revealed that TNF and IgE levels could explain 49.14% and 35.28% of the variance of SCORAD. These data indicate that serum IgE and TNF levels correlate with AD severity and that serum cytokines are downregulated in AD1 group. Further studies are clearly needed to elucidate cytokines' role in adults with AD.

Role of CD4 +CD25 + T Cells in Children With Idiopathic Thrombocytopenic Purpura

CD4CD25 T cells play an important role in the induction and maintenance of peripheral self-tolerance. These professional regulatory cells prevent the activation and proliferation of potentially autoreactive T cells that have escaped thymic deletion. To investigate the role of CD4CD25 regulatory T cells in children with idiopathic thrombocytopenic purpura (ITP) and correlate their levels with different disease stages, this study was conducted in 45 children (15 controls and 30 cases with ITP); 10 of these patients were in the acute phase (Group I), 10 in the remission phase (Group II), and the remaining 10 in the chronic phase (Group III). Studied groups were subjected to the following investigations: complete blood count, erythrocyte sedimentation rate, Coombs test, and flow cytometric analysis of CD4CD25 T lymphocyte count. There was a highly significant decrease in platelet count and CD4CD25 count in patients of the acute group when compared with remission, chronic, and control groups. There was a significant decrease in CD4CD25 count in the chronic group when compared with remission group. In addition, a significant decrease in CD4CD25 count was found in remission group when compared with the control group. Moreover, there was a positive correlation between CD4CD25 count and platelet count in all the groups; this correlation was significant in the acute group and insignificant in the remission and chronic groups. Decreased number of CD4CD25 T cells might be one of the mechanisms that cause immune regulation dysfunction in ITP and the count of CD4CD25 T cells is considered to be related to the severity of ITP, as these cells were significantly decreased in the active phase of the disease and increased in the patients at the complete remission phase. Therefore, count of CD4CD25 T cells might be a helpful diagnostic predictor of onset and improvement of ITP in children. Finally, it is suggested that these cells may have therapeutic implications that need further clarification.

Diagnostic value of serum Cys-C, hs-CRP, and urine mALB for early renal injury in gonty patients

Objective To explore the diagnostic value of serum Cys-C,hs-CRP,and urine mALB for early renal injury in gonty patients.Methods A total of 100 gonty patients and 50 healthy volunteers were divided into 3 groups:acute phase group(n = 50),intermittent group(n = 50),and healthy control group(n = 50).The serum Cys C,hs-CRP,and urine creatinine were determined by automatic chemistry analyzer and urine mALB by immunofluorometer equipment,and the results were analyzed in each group.Results The results of mALB/Cr(mg/[g·Cr]),hs-CRP(mg/L),and Cys-C(mg/L) in acute phase group were 11.45 ± 3.55,5.15 ± 1.98,and 2.62 ± 0.83,in intermittent group were 8.96 ± 1.78,3.28 ± 1.23,and 0.93 ± 0.26,and in healthy volunteer group were 3.89 ± 0.76,1.91 ± 0.57,and 0.78 ± 0.22,respectively.The values of the above three parameters in the acute phase and intermittent groups were significantly higher than those in the healthy control group(P 0.05) ;and the values in the acute phase group were significantly higher than those in the intermittent group(P 0.05).The abnormal rate of hs-CRP + Cys-C + mALB/Cr was 87% in gonty patients.Conclusion Simultaneous determination of mALB/Cr,hs-CRP,and Cys-C can help to assess the early renal injury in gonty patients.

Distal Semitendinosus Ruptures in Elite-Level Athletes

Background: No case series of isolated complete rupture of the distal semitendinosus tendon have been reported previously. Purpose: This study was undertaken to increase awareness and report the authors’ treatment experience, particularly the less than favorable results of nonoperative initial treatment. Study Design: Case series; Level of evidence, 4. Methods: The authors identified 25 cases of distal semitendinosus tendon rupture over a 14-year period (1991-2005). All players were male professional (20), collegiate (4), or high-level amateur (1) athletes. Follow-up of 17 cases averaged 13 months (range, 4-55), and 8 patients were lost to follow-up. Eight Major League Baseball, 8 National Football League, and 1 National Hockey League athletes were included in this study. Early treatment experience always involved nonoperative treatment, including rest, modalities, and rehabilitation exercises, followed by functional progression. “Recovery” was defined by clinical criteria including clearance to return to play. Failure to improve with nonoperative treatment, and thus requiring surgical treatment, was deemed a failure of nonoperative treatment. There were 12 players who had initial nonoperative treatment. The authors had later experience with 5 players who had surgery early in the acute phase in hopes of speeding return to competition. Results: In the nonoperative treatment group (12), 7 players recovered at an average of 10.4 weeks (range, 3-35). Five of these players (42%) failed initial nonoperative treatment (mean, 16.8 weeks) and subsequently had surgery to resect the torn tendon and surrounding scar tissue. These 5 players recovered at an average of 12.8 weeks postoperatively. In the acute surgery group, 5players had surgery to resect the torn tendon and scar tissue within 4 weeks of injury. The acute-phase group had an average recovery of 6.8 weeks after surgery. Conclusion: Distal semitendinosus ruptures frequently (42%) do not recover after nonoperative treatment. Acute surgical resection of the completely ruptured semitendinosus tendon may speed recovery when the athlete has a tender mass and difficulty extending the knee fully in the stance phase of gate. Future investigation is warranted to compare the long-term outcome of nonoperative treatment with that after acute surgery.

Expression profiling of cardiac genes in Tako-Tsubo cardiomyopathy: Insight into a new cardiac entity

Tako-Tsubo cardiomyopathy (TTC) is characterized by a transient contractile dysfunction, but its specific pathomechanism remains unknown. Thus, we performed a systematic expression profiling of genes by microarray analysis in the acute phase and after functional recovery. We studied 3 female patients presenting with TTC. Complementary RNA was isolated from left ventricular biopsies taken in the acute phase (group A) and after functional recovery (group B). It was profiled for gene expression using cDNA microarrays. Functionally related genes were determined with the Gene Set Enrichment Analysis (GSEA) bioinformatic tool. Validation of selected genes was performed by means of real-time PCR and immunohistochemistry. In group A, different functional gene sets, such as Nrf2-induced genes, triggered by oxidative stress, and protein biosynthesis were significantly overrepresented among the upregulated targets. Increased transcription of GPX1, CAT, RPS6, and eIF4E was confirmed by RT-PCR. The targets of the Akt/PKB signaling showed significant upregulation in both groups. Immunohistochemistry showed that the downstream targets NF-κB and BcL-XL are upregulated and activated. Gene sets involved in energy metabolism (oxidative phosphorylation, mitochondrial genes) showed no differences in group A but were overexpressed in group B. This study demonstrated a significant contribution of oxidative stress to the pathomechanism of TTC; it is possibly triggered by excess catecholamine. Increased protein biosynthesis and an activated cell survival cascade can be interpreted as potential compensatory mechanisms. After functional recovery, processes involved in energy metabolism play a pivotal role, thereby potentially contributing to the normalization of contractile function.

Clinical significance of serum vascular endothelial growth factor in Kawasaki disease

Purpose : Kawasaki disease is a systemic vasculitis, leading cause of pediatric acquired heart disease. Vascular endothelial growth factor (VEGF) has functions as vascular permeability factor, plays an important role in coronary artery lesion (CAL). We studied the clinical significance of serum VEGF in Kawasaki disease. Methods : Kawasaki group was 49 patients, and control group was 15 patients. Diagnosis followed AHA (American Heart Association) diagnostic criteria, with blood sampling in acute, subacute, and convalescent phase. Echocardiographic abnormalities were defined and the definition of intravenous gamma globulin (IVGG)-responsive and IVGG-resistant was determined. Results : Serum VEGF of Kawasaki group was significantly higher than of control group. Comparison of serum VEGF between CAL and non-CAL group, between carditis group and non-carditis group showed no significant differences. Subacute serum VEGF was statistically higher in IVGG-resistant group than in IVGG-responsive group, and serum VEGF of IVGG-resistant group in subacute phase was statistically higher than in the other phases. Serum VEGF of convalescent CAL and non-CAL group in acute and subacute phase had meaningful differences. Total fever duration and subacute serum VEGF had positive correlation. Acute serum VEGF had positive correlation with ESR and CRP, all phases serum VEGF had also positive correlation with WBC. Acute and subacute serum VEGF had negative correlations with hemoglobin and albumin. Conclusion : Serum VEGF can help to determine the severity of Kawasaki disease, especially subacute serum VEGF seems to be used as a prognostic factor of coronary complication. Afterward, further studies needed with more strict diagnostic criteria and more study groups.

Approche thérapeutique d’une population de patients présentant des troubles psychotiques aigus ou chroniques : enquête RÉALITÉ (Recherche Épidémiologique sur l’Activité de la Loxapine et ses Indications en Thérapeutique quotidiennE)

A retrospective observational pharmaco-epidemiological survey was conducted during 24 weeks between October 2004 and March 2005 in metropolitan France (384 investigators) to more clearly define the use of loxapine in acute and chronic psychotic states. The objective of this national survey was to specify the clinical and therapeutic profile of patients managed by this antipsychotic in two cohorts of adult patients: one in "acute phase" (prescription of loxapine during the previous 4 weeks), the other in "maintenance phase" (prescription of loxapine for more than 8 weeks). The two groups of the recruited population (1,511 patients) presented identical sociodemographic data. Selection criteria were adapted to the data collected to ensure statistically relevant analysis: 696 patients in acute phase and 633 patients in maintenance phase. The acute phase group was predominantly composed of known patients (82% of patients had a psychotic history) with schizophrenia (47%) or mood disorders (57%) who had already presented acute episodes (an average of 5.4). The current episode consisted of a state of agitation (88%) lasting an average of two weeks, requiring hospitalization (87%), scheduled admission [HDT (admission at the request of another person) in 47.5% of cases and HO (statutory admission) in 40.8% of cases] and prescription of loxapine monotherapy (56%) at a mean daily dose of 177,3 mg. The maintenance phase group comprised a population of known patients (87.5%), schizophrenics (63%), presenting psychotic symptoms (dissociation 82%, delusions 74%) or mood disorders (71%) requiring voluntary hospitalization (78%) for a mean duration of 180 days and a prescription of loxapine monotherapy in 28% of cases at a mean daily dose of 131.6 mg. The loxapine-haloperidol combination (21%) was prescribed more frequently in the second group in the case of chronic disorders; in the other cases, loxapine was coprescribed with the main second generation antipsychotics: risperidone (16%), olanzapine (16%), amisulpride (11%). CGI assessment of the overall study population revealed a marked or very marked clinical improvement with no significant adverse effects in more than 80% of cases.

P1-131: Acute phase and following phase in transient global amnesia

Transient global amnesia is a reversible memory disorder characterized by episodic dysfunction of declarative memory. The purpose of this study is to investigate the change on clinical aspect and functional imaging during and after attack of TGA. Six patients were included in this study with amnestic episodes which fulfilled the criteria for TGA, as published by Hodges and Warlow. The patients were divided into two subgroups according to encoding failure on episodic memory. Acute phase group was defined as patients having encoding failure on episodic memory. Following phase group was defined as patients recovering from amnestic period. Two patients belonged to the acute phase group and the remaining four patients to following phase group. All the subjects underwent brain perfusion SPECT. Clinical aspect in memory disturbance was rated with full neuropsychological test. It consists of many tests in five domains (attention, language and related functions, visuospatial function, memory and frontal executive function). Two patients, who were evaluated during the attack of TGA, showed encoding failure on verbal and visuospatial memory. Brain perfusion SPECT ,however, revealed no perfusion defect. In following phase group (n=4), neuropsychological test demonstrated frontal lobe dysfunction involving retrieval difficulty in verbal and visuospatial memory, decreased semantic word fluency and decreased inhibition ability on stroop test in three patients. The remaining one patient showed encoding failure in visuospatial memory. Brain perfusion SPECT demonstrated variable abnormality on cortical areas; hypoperfusion on right medial temporal and basal ganglia (n=1), bilateral temporal lobe (n=1), left post. sup. parietal lobe (n=1) and normal perfusion with decreased vascular reserve on right basal ganglia (n=1). No perfusion defect in SPECT was exhibited in the two patients evaluated during the attack of TGA, who showed bilateral temporal dysfunction in neuropsychological studies at the same time. Hypoperfusion in the variable cortical area was revealed in the following phase group, but perfusion defect was not found in the frontal lobe. Three patients showed frontal lobe dysfunction in neuropsychological test at that time. These findings suggested that hypoperfusion is not a primary event in TGA. It probably represents the secondary response to decreased metabolism.

On the increase of portal pressure during the acute and chronic phases of murine schistosomiasis mansoni and its reversibility after treatment with oxamniquine

The purpose of the present study was to evaluate the effect of treatment with oxamniquine on the portal pressure of mice infected with Schistosoma mansoni. The animals were infected with 30 cercariae and portal pressure was measured with a polygraph at 70 (acute phase) and 160 (chronic phase) days after infection. On days 70 and 160 two other groups of infected mice were treated with 400 mg/kg of oxamniquine and portal pressure was measured 90 days later (160 and 250 days after infection). A group of uninfected mice was used as control. The measured portal pressures, in mmHg, were: matched uninfected control mice 8.7±2.1 and acute phase group, measured at day 70, 13.4±3.5. Matched uninfected control 7.5±0.6 and chronic phase group, measured at day 160 post-infection, 11.6±1.5. Matched uninfected mice 6.9±0.9 and chronic phase group, measured at day 250, 10.4±1.8. Oxamniquine-treated at day 70 and measured at day 160 7.9±0.4; oxamniquine-treated at day 160 and measured at day 250, 7.6±1.7. The infection of mice with 30 cercariae of S. mansoni induced portal hypertension, both during the acute and chronic phases and treatment with oxamniquine caused portal pressure to return to normal levels.

Expression of Apoptosis Inhibitor Genes and Resistance of T Cells to Apoptosis in the Early Acute Phase of Kawasaki Disease

Objective. The acute phase of Kawasaki disease (KD) is characterized by the deregulated production of proinflammatory cytokines and chemokines by PBMC. We studied the activation induced cell death of the peripheral blood T cells and the expression of the apoptosis-related genes during the course of the disease. Methods. Heparinized blood was obtained from 63 patients, 2-4d (Group A, n=25), 5-7d (Group B, n=29), 8-11d (Group C, n=9), 12-14d (Group D, n=9), and >15d (Group E, n=13) after the onset of fever. PBMC were isolated 24h after blood drawing and stained with anti-CD3 antibody and Annexin V followed by the flow cytometry analysis. The expression of the apoptosis-related genes was studied on PBMC obtained during the acute (<6d) and convalescent (>11d) phase of KD by RT-PCR. Results. The percentage of apoptotic T cells was not increased in the early acute phase (Group A, 13.3%), but gradually increased during the subacute phase with the peak value in the Group C (26.2%, p=0.0002 by Fisher's PLSD). After IVGG therapy, the percentage of apoptotic T cells was significantly increased (15.2% vs. 20.2%, p=0.02 by unpaired t test). The expression of the anti-apoptotic protein genes such as FLICE-like inhibitory protein (FLIP), X-linked inhibitor of apoptosis protein (XIAP), and Bcl-XL was significantly elevated during the acute phase compared with the convalescent phase of KD. Conclusion. The enhanced expression of the apoptosis inhibitory proteins during the early acute phase of KD may prevent the induction of activation induced cell death of PBMC and contribute to the sustained production of proinflammatory cytokines during the acute illness.

Ureteral ischemia model: an explanation of ureteral dysfunction after chronic obstruction.

Many models of smooth muscle ischemia have been developed to explain organ insufficiency or failure. Ureteral decompensation may also be described in these terms. We anticipate that ureteral ischemia will result from overdistention brought about by obstruction. A preliminary model to create an ischemic ureter is described herein. Six white New Zealand female rabbits were used for this study. All had their left ureters surgically ligated at the level of the urinary bladder. The right ureters served as controls. In the acute-phase group, the ureters were all reexplored 2 weeks postobstruction. Exploration of the other rabbits was delayed for 3 more weeks. A laser Doppler needle (Transonics Inc.) was used to measure tissue perfusion in the rental artery, renal vein, renal parenchyma, renal pelvis, ureteropelvic junction, upper ureter, mid ureter, lower ureter, and lateral wall of the bladder. Baseline and postobstructive measurements of tissue perfusion were collected and compared. In both the acute and the chronic obstruction groups, there was a demonstrable drop-off in perfusion of the ureteral sidewall. A more notable loss of perfusion was seen in the distal ureter. The increased wall tension in the obstructed ureter results in a significant decrease in smooth muscle perfusion. This ischemia may result in the same functional and histologic changes that occur in other smooth muscle organs. Ultimately, the poor outcomes of some restorative/reconstructive procedures on the ureter may be explained in terms of smooth muscle ischemia.

Ureteral ischemia model: an explanation of ureteral dysfunction after chronic obstruction.

Many models of smooth muscle ischemia have been developed to explain organ insufficiency or failure. Ureteral decompensation may also be described in these terms. We anticipate that ureteral ischemia will result from overdistention brought about by obstruction. A preliminary model of an ischemic ureter is described herein. Six female New Zealand rabbits were used for this study. All had their left ureters surgically ligated at the level of the urinary bladder. The right ureters served as controls. In the acute-phase group, the ureters were reexplored 2 weeks after creation of obstruction. The other three rabbits were explored 3 weeks later. A laser Doppler needle was used to measure tissue perfusion with bilateral measurements of the renal artery and vein; renal parenchyma; renal pelvis; ureteropelvic junction; upper, mid, and lower ureter; and the lateral wall of the bladder. Baseline and postobstructive measurements of tissue perfusion were collected. In both the acute and chronic obstruction groups, there was a demonstrable drop-off in perfusion of the ureteral wall. The increased wall tension in the obstructed ureter results in a significant decrease in smooth muscle perfusion. This ischemia may result in the same functional and histologic changes that occur in other smooth muscle organs deprived of normal blood flow. Ultimately, poor outcomes of some restorative/reconstructive operations on the ureter may be explainable in terms of smooth muscle ischemia.

Immune response induced by airway sensitization after influenza A virus infection depends on timing of antigen exposure in mice.

To study which phase of viral infection promotes antigen sensitization via the airway and which type of antigen-presenting cells contributes to antigen sensitization, BALB/c mice were sensitized by inhalation of ovalbumin (OA) during the acute phase or the recovery phase of influenza A virus infection, and then 3 weeks later animals were challenged with OA. The numbers of eosinophils and lymphocytes, the amounts of interleukin-4 (IL-4) and IL-5 in the bronchoalveolar lavage fluid, and the serum levels of OA-specific immunoglobulin G1 (IgG1) and IgE increased in mice sensitized during the acute phase (acute phase group), while a high level of gamma interferon production was detected in those sensitized during the recovery phase (recovery phase group). In the acute phase group, both major histocompatibility complex class II molecules and CD11c were strongly stained on the bronchial epithelium; in the recovery phase group, however, neither molecule was detected. OA-capturing dendritic cells (DCs) migrated to the regional lymph nodes, and a small number of OA-capturing macrophages were also observed in the lymph nodes of the acute phase group. In the recovery group, however, no OA-capturing DCs were detected in either the lungs or the lymph nodes, while OA-capturing macrophages were observed in the lymph nodes. These results indicate that the timing of antigen sensitization after viral infection determines the type of immune response.

El cepillado protegido bacteriológico en pacientes con EPOC severa

To determine the presence of germs and their concentration in a group of patients with severe chronic obstructive pulmonary disease (COPD) (FEV1 < 50%), some of whom were in stable condition and others of whom were in acute phase. Twenty-six patients with severe COPD (14 stable and 12 acute phase) were enrolled. None had received prior antibiotic or corticoid treatment. The stable patients had no signs or symptoms of exacerbation, whereas the acute-phase patients had increased dyspnea, sputum volume and purulence. The patients received aerosol rather than liquid anesthesia when PSB sampling was performed. A PSB finding was considered positive at a level > or = 10(3) CFU/ml. There were no significant differences between the groups with respect to age, sex, proportion of smokers and ex-smokers or packs per year. The only spirometric measure that was significantly different was (FEV1/FVC, which was lower in the acute-phase group (p < 0.05). Positive PSB findings were recorded for 57.1% of the stable patients and for 66.7% of the acute-phase patients (p = NS). H. influenzae was the microorganism found most often in both groups. The mean CFU/ml level was 8,625 in stable patients and 17,375 in acute-phase patients (p = NS). A large proportion of stable patients (57.1%) with severe COPD harbor significant concentrations of germs as revealed by PSB sampling. Germ concentrations were found in a non significantly greater number of acute-phase patients, confirming the lack of congruence between clinical status and bacteriological condition.

Experimental rat model representing both acute and chronic heart failure related to autoimmune myocarditis.

The most important clinical manifestation of myocarditis is congestive heart failure. The precise mechanisms of heart failure during myocarditis have not been elucidated because no animal model that would permit in vivo study of hemodynamics in severe active myocarditis has been available. We monitored hemodynamics and left ventricular function in a rat model of experimental autoimmune myocarditis to determine if this model could be useful for the study of in vivo hemodynamics in severe active myocarditis. Lewis rats were immunized with human cardiac myosin suspended in complete Freund's adjuvant. Baseline hemodynamics were measured using an ultraminiature catheter pressure transducer via the right internal carotid artery, 4 weeks after immunization in one group of rats (acute phase) and 3 months after immunization in another group (chronic phase). Untreated rats served as the control group. Hemodynamic measurements were also obtained after infusion of dobutamine in the acute-phase and chronic-phase groups. The heart weight-to-body weight ratios were significantly higher in both the acute-phase group and the chronic-phase group compared with normal control rats. The baseline left ventricular systolic pressure was significantly lower in the chronic phase group than in the control group. Peak dP/dt and peak -dP/dt were significantly lower in both the acute-phase group and the chronic-phase group compared with the control group. Dobutamine significantly increased left ventricular systolic pressure, peak dP/dt, and peak -dP/dt in the chronic-phase group but caused only minor changes in hemodynamic variables in the acute-phase group. In vivo measurements of hemodynamic variables indicated the presence of left ventricular dysfunction in rats with experimental autoimmune myocarditis. This animal model may be useful for the study of both acute heart failure related to acute myocarditis and chronic heart failure due to diffuse myocardial fibrosis.

Differential Regulation of α and β Chains of C4b-Binding Protein During Acute-Phase Response Resulting in Stable Plasma Levels of FreeAnticoagulant Protein S

Regulation of C4b-binding protein (C4BP) isoforms during acute phase and its relationship to the plasma concentration of free protein S was elucidated. An assay for beta chain containing C4BP (C4BP beta+) was developed and the concentrations of total C4BP, C4BP beta+, total, free, and bound protein S were measured in patients with acute-phase response. Even though total C4BP was increased to 162% (mean value) of controls, the corresponding value of C4BP beta+ was only 122%. In the acute-phase group, total protein S was increased to the same extent as C4BP beta+ (mean value of 124%), whereas free protein S was not decreased. In controls, total and bound protein S correlated with total C4BP and C4BP beta+. However, in the acute-phase group, the correlation between bound protein S and total C4BP was lost, although the correlation between C4BP beta+ and protein S remained. The present results suggest stable levels of free protein S during acute phase to be the result of differential regulation of C4BP alpha- and beta-chain expression, and the concentration of free protein S to be the resulting molar excess of protein S over C4BP beta+. This mechanism ensures functional levels of free anticoagulant protein S despite high levels of C4BP.