Three cases of posttransplant lymphoproliferative disorder in recipients of liver transplantation.
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Biomedical subjects
Publications and source records attributed to I S Choi.
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BACKGROUND: Poor perception of dyspnea in asthma may lead to a delay in starting appropriate treatment which is probably one of the factors contributing to death from asthma. OBJECTIVE: This study was carried out to determine whether impaired perception of dyspnea in patients with asthma of varying severity can be corrected by inhalation of short acting beta2 agonist treatment. METHODS: We enrolled 20 patients with asthma of varying severity. Forced expiratory volume in one second (FEV1) was measured before and 10 minutes after two puffs of salbutamol administered by metered dose inhaler. Perception of dyspnea was scored on the Borg scale during breathing through an inspiratory muscle trainer. RESULTS: After inhalation of short acting beta2 agonist treatment, the baseline Borg score was decreased significantly from 2.20 +/- 0.32 to 1.80 +/- 0.31 (P < .01). The Borg score during breathing with the highest resistance, on the contrary, was increased significantly from 6.25 +/- 0.35 to 6.90 +/- 0.35 after inhalation of short acting beta2 agonist treatment (P < .01). Highest resistance-induced score difference from the baseline value (highest resistance-load score) was increased significantly from 4.10 +/- 0.46 to 5.25 +/- 0.42 (P < .01). There was no relationship between the change of Borg score from baseline value at each resistive load and the % change of FEV1 after inhalation of short acting beta2 agonist treatment. CONCLUSION: These studies demonstrate that inhalation of short acting beta2 agonist treatment decrease dyspnea, but increase perception of dyspnea induced by a resistive load in patients with asthma, and the mechanism of the increased perception may not be related to the increased airflow rate. It may be due to some local or central effects of bronchodilator drug on perception of asthma.
Feline immunodeficiency virus (FIV) causes AIDS-like symptoms in infected cats. Concanavalin A (ConA)-stimulated peripheral blood mononuclear cells (PBMC) from chronically FIV strain PPR-infected cats readily expressed FIV. In contrast, when PBMC from these animals were stimulated with irradiated, autologous antigen-presenting cells (APC), at least a 10-fold drop in viral production was observed. In addition to FIV-specific cytotoxic T lymphocytes, anti-FIV activity was demonstrated in the cell-free supernatants of effector T lymphocytes stimulated with APC. The FIV-suppressive activity was induced from APC-stimulated PBMC of either FIV-infected or uninfected cats but not from ConA-stimulated PBMC. Suppression of FIV strain PPR replication was observed for both autologous and heterologous feline PBMC, was dose dependent, and demonstrated cross-reactivity and cell specificity. It was also demonstrated that the anti-FIV activity originated from CD8(+) T lymphocytes and was mediated by a noncytolytic mechanism.
BACKGROUND: Eosinophils play a pivotal role in asthmatic airway inflammation. Apoptosis is thought to be critically relevant in promoting the clearance of inflammatory cells and the resolution of inflammation. Bcl-2 inhibits apoptosis in cellular systems. A study was undertaken to determine whether bcl-2 expression in sputum reflects the clinical severity of patients with asthma. The relationship between bcl-2 expression in sputum eosinophils and eosinophil activation markers such as interleukin (IL)-5 and eosinophil cationic protein (ECP) levels in sputum supernatant was evaluated. METHODS: Sputum was obtained from 18 patients with asthma. Fresh expectorated sputum separated from saliva was treated with an equal volume of dithiothreitol 0.1%, cytospun for cell differentials and bcl-2 stain, and the supernatant was collected for biochemical assay. Bcl-2+ eosinophils were stained using immunocytochemistry, ECP was measured by fluoroimmunoassay, and IL-5 was detected by sandwich enzyme linked immunosorbant assay. RESULTS: Twelve patients with severe or life threatening asthma had more bcl-2+ eosinophils (mean difference 46.8% (95% CI 27.0 to 66.6), p<0.01) and a higher ECP level (p<0.01) in the sputum than those with mild to moderate asthma (n = 6). IL-5 was frequently detected in patients with severe or life threatening asthma (11/12 versus 1/6, p<0.01). There was a significant positive correlation between bcl-2+ eosinophils and ECP levels (r = 0.61, p<0.01) and between bcl-2+ eosinophils and IL-5 levels (r = 0.83, p<0.01). There was a significant negative correlation between bcl-2+ eosinophils and FEV(1)/FVC (r = -0.54, p<0.05). CONCLUSION: The increased expression of bcl-2 in eosinophils from sputum of subjects with severe asthma suggests that bcl-2 may prolong survival and decrease apoptosis of airway eosinophils in asthma.
The most consistently observed neurological deficits in the anterior choroidal artery (AChA) territory infarction are pure motor or sensorimotor syndromes. Visual field defects and higher cortical dysfunction are occasionally accompanied, but pure homonymous hemianopia without motor and sensory symptom has never been reported yet. We present 2 patients with pure homonymous hemianopia, whose MRI disclosed cerebral infarction in the well-known territory of the AChA. In most patients with ischemic stroke, pure homonymous hemianopia indicates infarction in the posterior circulation, particularly in the posterior cerebral artery territory. However, the present cases provide evidence that it can also be caused by infarction in the anterior circulation, i.e. the AChA.
Hypertrophic cranial pachymeningitis (HCP) is a rare inflammatory disease of unknown origin in which recurrence is frequently observed in spite of the initial response to steroid therapy. Three patients, 1 man and 2 women, aged 63, 66, and 67 years, with severe intractable headache were evaluated by brain MRI. All patients were initially given prednisolone (60 mg/day, oral) or dexamethasone (20 mg/day, i.v.), and followed by long-term (at least 1 year) azathioprine therapy. All patients were evaluated by follow-up laboratory tests and brain MRI study, and completed the 2-year follow-up period. Symptoms including headache were initially improved with corticosteroid therapy, but patients became steroid-dependent. Azathioprine administration in these steroid-dependent patients permitted the complete cessation of corticosteroid and led to the clinical and radiological recovery. In conclusion, initial high-dose corticosteroid administration followed by long-term azathioprine therapy may be the ideal treatment of HCP at present.
BACKGROUND: Eosinophils play an important role in asthmatic airway inflammation. Monoclonal antibody EG2 has been considered to identify activated eosinophils. OBJECTIVE: The present study was aimed to investigate whether immunohistochemically stained EG2+ eosinophils in sputum reflect the severity of asthma. METHODS: Sputum was obtained in 23 asthmatic patients, of whom 13 patients were examined before and after antiasthma treatment including steroid preparations. We used immunohistochemical staining to detect EG2+ (activation marker) eosinophils and fluoroimmunoassay to detect eosinophil cationic protein (ECP). RESULTS: Moderate to severe asthmatics had a significantly higher proportion of eosinophils and EG2+ eosinophils and higher levels of ECP compared to mild asthmatics (40.9 +/- 5.8 vs. 6.4 +/- 1.2%, 35.5 +/- 5.6 vs. 2.7 +/- 1.0%, 1.470.2 +/- 251.5 vs. 210.6 +/- 52.0 microgram/l, respectively; p < 0.01). Significant increases in proportions of eosinophils, EG2+ eosinophils and ECP in the sputum from patients with exacerbated asthma were evident. The proportions of eosinophils, EG2+ eosinophils, and the levels of ECP were reduced following treatment with antiasthmatic drugs. FEV(1) and FEV(1)/FVC were significantly correlated with EG2+ eosinophils. CONCLUSION: These findings demonstrate that EG2+ eosinophils in sputum are closely related to the clinical status in patients with asthma.
The objective of this study is to investigate whether BCG infection before, during or after sensitization suppresses allergen-induced airway hyperresponsiveness and eosinophilic inflammation in allergic asthma rats, and to determine the required dose of BCG to induce such an inhibition. Eighty-seven Sprague-Dawley (SD) rats were sensitized and provoked with ovalbumin (OA). A pretreatment of 6 x 10(4) or 6 x 10(5) colony forming units (CFUs) of BCG or saline was done at four different times: 3 days before sensitization, at sensitization, 3 days before provocation, or at provocation. The assessment of tracheal smooth muscle (TSM) responsiveness to electrical field stimulation or acetylcholine (ACh) and bronchoalveolar lavage (BAL) were performed 1 day after OA provocation. Doses of 6 x 10(4) CFUs inhibited TSM sensitivity of rats infected 3 days before sensitization or at sensitization, but not 3 days before provocation or at provocation. However, doses of 6 x 10(5) CFUs significantly inhibited not only the airway eosinophilia of rats infected 3 days before sensitization or at sensitization, but also the TSM sensitivity of rats infected 3 days before provocation or at provocation. In conclusion, BCG infection suppresses the development of sensitivity of airway smooth muscle and airway eosinophilic inflammation in allergic asthma rats. Furthermore, a relatively high dose of BCG infection inhibits airway sensitivity, even after allergen sensitization.
Corticosteroids are considered to be one of the most effective medicine for asthma by suppressing airway inflammation. This study was carried out to investigate the effects of prednisolone in the sputum of exacerbated asthmatics. Clinical severity, cell differentials, levels of interleukin (IL)-5, eosinophil cationic protein (ECP), EG2+ eosinophils, and nitric oxide (NO) metabolites were measured. Sputum was examined 2 weeks apart in 13 exacerbated asthmatics before and after prednisolone treatment, and once in 12 stable asthmatics. We used a sandwich ELISA for IL-5, fluoroimmunoassay for ECP, immunohistochemical staining for EG2+ eosinophils, a NO metabolites assay using modified Griess reaction. Exacerbated asthmatics, in comparison with stable asthmatics, had significantly higher proportion of eosinophils, higher level of ECP, higher percentage of EG2+ eosinophils, and NO metabolites. Exacerbated asthmatics after treatment with prednisolone had reduced the proportions of eosinophils, reduced level of IL-5, ECP and percentage of EG2+ eosinophils. FEV1 was correlated with the proportion of eosinophils, ECP, and IL-5 respectively. These findings suggest that prednisolone is considered to be effective medicine for asthma by suppressing eosinophil activation through IL-5.
OBJECTIVES: Eosinophils play an important role in asthmatic airway inflammation collaborately with other inflammatory cells. The present study was aimed to determine whether the eosinophil activation markers in induced sputum reflect the clinical status in asthmatics. METHODS: The clinical severity and FEV1 were measured. Hypertonic saline induced sputum was obtained from 25 asthmatics and ten control subjects. We processed freshly expectorated sputum separated from saliva by treatment with an equal volume of dithiothreitol 0.1%, cytospins for cell count and special stain, and a collection of the supernatant for biochemical assay. We used a fluoroimmunoassay to detect eosinophil cationic protein (ECP), and a sandwich ELISA to detect interleukin (IL)-5. RESULTS: Asthmatics, compared with control subjects, had a significantly higher proportion of eosinophils (25.6 +/- 4.6% vs 1.7 +/- 0.2%, p < 0.01) and higher levels of ECP (1117.8 +/- 213.9 micrograms/L vs 154.6 +/- 47.4 micrograms/L, p < 0.01) in their sputum. IL-5 was detected more frequently in asthmatics than in control subjects [11/25 (44%) vs 1/10 (10%), p < 0.05]. Moderate to severe asthmatics had a significantly higher proportion of eosinophils, higher levels of ECP and IL-5 compared to mild asthmatics. FEV1, FEV1/FVC were significantly correlated with the proportion of eosinophils and the levels of ECP and IL-5. Significant positive correlations were noted between the proportion of eosinophils and the level of ECP and IL-5. Sputum ECP level showed a significant positive correlation with IL-5 level. CONCLUSION: These findings demonstrate that eosinophils and the eosinophil activation markers, such as ECP and IL-5 in induced sputum, are closely related to the clinical status in asthmatics. Induced sputum study may thus be useful in clinically measuring indices of airway inflammation in asthma.
The benefits of preoperative embolization have been known and reported on since the 1970s. With embolization of hypervascular tumors, surgical morbidity can be reduced with decreasing blood loss, thereby shortening operating time, and the chances for complete resection are increased. Superselective catheterization of feeding vessels close to a tumor of the CNS and head and neck is possible, resulting in more effective embolization. Endovascular management with embolization is now standard preoperative procedure. This article discusses the processes of neuroendovascular management of hypervascular intracranial and spinal tumors.
It is known that CD28, a positive costimulatory receptor, plays a very important role in inducing the optimal stimulation of T lymphocytes. CTLA-4 (CD152), however, acts as a negative regulator in T lymphocyte activation. The effect of an feline immunodeficiency virus (FIV) infection on the expression of feline CD28 and CTLA-4 was studied with FIV-infected and uninfected peripheral blood mononuclear cells (PBMC) using a competitive PCR assay. The nature of CD28 and CTLA-4 expression was also examined with fresh and antigen-stimulated PBMC. FIV infection induced a lower expression of CD28, but a higher expression of CTLA-4 in the infected PBMC than in the uninfected PBMC. Relatively high levels of CD28 expression were demonstrated in both the fresh and the antigen-stimulated PBMC. The expression level of CTLA-4 in the freshly isolated PBMC was rather low, however, FIV antigen stimulation induced a relatively high expression of CTLA-4 in feline PBMC.
Fas ligand (FasL) and Fas are mediators of apoptosis, which are implicated in the peripheral deletion of autoimmune cells, activation-induced T cell death, and cytotoxicity mediated by CD8+ T cells. Fas is also believed to be involved in several central nervous system diseases, but until now, the effector cells expressing FasL in the brain have not been identified. We investigated the expression levels of Fas and FasL with the stimulation of cytokines and the possible effector cells targeting Fas-bearing cells. Our data demonstrated that: 1) FasL is expressed constitutively on astrocytes taken from a fetus or an adult and that its expression increases when these cells are treated with IL-1, IL-6, or TNF-alpha in which the pretreatment of IFN-gamma triggers astrocytes to express more FasL; 2) astrocytes induce apoptosis in MOLT-4 cells through FasL; 3) Fas is also expressed constitutively and is up-regulated by IL-1, IL-6, or TNF-alpha in which the pretreatment of IFN-gamma triggers astrocytes to express more Fas; 4) apoptosis occurs when fetal astrocytes are treated with agonistic anti-Fas IgM Ab after culture with IFN-gamma and TNF-alpha; and 5) TNF-related apoptosis inducing ligand is up-regulated in fetal astrocytes with stimuli of IL-1 or TNF-alpha. These findings suggest a possible role of astrocytes in the induction of apoptosis in central nervous system diseases.
Nitric oxide (NO) plays an important role in physiological regulation of the airways. The monitoring of airway inflammation has being observed in bronchial asthma directly, by sputum examination, and indirectly, by measurements in peripheral blood. To investigate the diagnostic value of these two methods, we compared NO metabolites in induced sputum and serum obtained in patients with asthma and control subjects. Hypertonic saline induced sputum and serum were obtained in 13 patients with asthma and 10 control subjects. NO metabolite level was assayed by using modified Griess reaction. Eosinophil cationic protein (ECP) was measured by fluoroimmunoassay, and detected interleukin (IL)-5 by a sandwich ELISA. The accuracy of the tests was measured by plotting the data in receiver operating characteristic (ROC) curves and comparing the area under the curve for NO metabolites. Asthmatic patients, compared with control subjects, had significantly higher NO metabolites in induced sputum (1252.5+/-203.3 mol l(-1) vs. 557.2+/-101.5 mol l(-1), P<0.01) but not in serum. IL-5 in induced sputum was detected more frequently in patients with asthma than in control subjects [11/13 (84.6%) vs. 1/10 (10%), P<0.01]. Asthmatic patients, compared with control subjects, had significantly higher ECP concentration in induced sputum (1270.0+/-197.9 g l vs. 154.6+/-47.4 g l(-1), P<0.01). There were significant positive correlations between NO metabolites in induced sputum and eosinophils, ECP in induced sputum (r=0.58 P<0.05; r=0.64, P<0.01) in patients with asthma but not in serum. The area under the ROC curve showed that NO metabolites in induced sputum (0.78) are more accurate marker than NO metabolites in serum (0.53) (P<0.05). These findings suggest that NO metabolites in induced sputum is a more valuable indicator to monitor asthmatic airway inflammation than those in serum.
BACKGROUND AND OBJECTIVE: The role of nitric oxide (NO) needs to be further clarified in allergic inflammation. This study was designed to investigate the relationships between NO metabolites and eosinophil count, eosinophil cationic protein (ECP), interleukin (IL)-5 in induced sputum from asthmatics. METHODS: Hypertonic saline-induced sputum was obtained in 25 asthmatic subjects, among which 13 patients were examined before and after anti-asthmatic medications including steroid preparations. Ten normal subjects were enrolled as controls. Fresh expectorated sputum separated from saliva was treated with equal volume of dithiothreitol 0.1%, cytospinned for cell count, and the supernatant was collected for biochemical assay. NO metabolites were assayed by using modified Griess reaction. ECP was measured by fluoroimmunoassay, and detected IL-5 by a sandwich ELISA. RESULTS: Asthmatic subjects, compared with controls, had significantly higher concentration of NO metabolites (1035.4 +/- 125.3 vs 557.2 +/- 101.5 micromol/L, P < 0.01), higher percentage of eosinophils (25.6 +/- 4.6 vs 1.7 +/- 0.2%, P < 0.01), and higher levels of ECP (1117.8 +/- 213.9 vs 154.6 +/- 47.4 microg/L, P < 0.01) in the induced sputum. IL-5 was detected more frequently in asthmatic subjects than in control subjects (11/25 [44%] vs 1/10 [10%], P < 0.05). According to asthma severity, moderate to severe asthmatic subjects (n = 18) had higher level of NO metabolites (1143.8 +/- 156.3 vs 575.5 +/- 89.5 micromol/L, P < 0. 01), higher levels of ECP and IL-5 (P < 0.01, respectively) in the induced sputum than in those of mild asthmatic subjects (n = 7). NO metabolites, the percentage of eosinophils, the levels of ECP, and IL-5 were reduced following treatment with anti-asthmatic drugs (P < 0.01, respectively). There were significant positive correlations between NO metabolites and percentage of eosinophils or ECP (r = 0. 34, P < 0.05; r = 0.28, P < 0.05). Negative correlations were noted between FEV1, FEV1/FVC and proportion of eosinophils, ECP, or IL-5 levels. CONCLUSION: These findings confirmed that the level of NO metabolites was increased in the tracheobronchial secretion of asthmatic subjects and was paralleled with severity of asthma. Measurement of NO metabolites in induced sputum may be used for monitoring the degree of airway inflammation in asthmatics.
Gastric diverticulum is a rare disorder. The laparoscopic approach may be ideal for the resection of gastric diverticulum in some cases. The authors believe this to be the first reported case of gastric diverticulum resected laparoscopically. A 59-year-old woman was admitted with indigestion and epigastric pain. Upper gastrointestinal series showed a single diverticulum (3 x 2 cm) on the posterior wall of the upper part of the stomach. The neck of the diverticulum was relatively narrow. Gastroduodenoscopy revealed that food residues were impacted within the diverticular pouch. Other areas of the stomach and the duodenum were normal. Abdominal ultrasonography showed no other pathologic conditions in the upper part of abdomen. On operation, the lesser sac was entered by division of the greater omentum along the avascular plane of the transverse colonic attachment. The location of the diverticulum was confirmed by intraoperative gastroscopy. Using a 5-cannula techniques, the diverticulum was resected with an endoscopic linear stapler device. Pathologic examination of the resected specimen demonstrated chronic superficial gastritis. Flatus was passed out on the first postoperative day, diet was started from the second day, and the patient was discharged on the fifth day without problems.