bluuebunny/crossref_metadata_2025_split huggingface dataset:
Causes of pleural exudates in a region with a high incidence of tuberculosis
Authors: Liam Chong‐Kin , Lim Kim‐Hatt , Wong Catherine Mee‐Ming 
Published: March 2003

Objective:To define the causes of exudative pleural effusions in our region. Methodology: A retrospective study was performed on consecutive patients with exudative pleural effusion seen in our hospital during a 4‐year period. Results: Of 186 patients with a mean age (± SD) of 51.2 (± 19.2) years with exudative pleural effusions, 131 (70.4%) were males and 55 (29.6%) were females. The most frequent cause of exudative pleural effusions was tuberculosis (44.1%), followed by malignancy (29.6%). The majority (94.5%) of malignant pleural effusions were due to lung cancer. Apart from a patient with bilateral pleural effusions due to cryptococcosis, patients with tuberculous pleural effusion (mean age ( ± SD), 39.7 (± 17.5)) were significantly younger than the rest (P < 0.05). Tuberculous effusions were most frequent in the first five decades (60/82, 73.2%) and were the most common type of pleural effusion, accounting for 60 (69.8%) of 86 cases, in this age range. Malignant effusions were more frequent among the older age groups, 74.5% (41/55) of patients with malignant effusions being older than 50 years. Most types of pleural effusions showed a preference for the right side. Of the 44 cases of large effusions, 28 (63.6%) were caused by malignancy. Conclusions: In our region with a high incidence of tuberculosis, the most frequent cause of pleural exudates is tuberculosis followed by malignancy, particularly lung cancer.
A case of pulmonary tumour embolism mimicking miliary tuberculosis
Authors: Chai Louis , Ong Kian Chung , Ng Siok Bian 
Published: March 2003

Abstract:Pulmonary metastases from choriocarcinoma can very rarely give rise to a ‘miliary’ pattern on the chest X‐ray. A 23‐year‐old woman with a diffuse nodular pattern on chest X‐ray died due to acute respiratory failure and cor pulmonale. At autopsy, choriocarcinoma of the uterus was found. In the lungs, multiple macrovascular tumour emboli within branches of pulmonary muscular arteries in the region of segmental/subsegmental bronchi were detected. There was no evidence of pulmonary parenchymal metastases, pneumonia or tuberculosis. The ‘miliary’ pattern of pulmonary metastases described in cases of choriocarcinoma may be due to large vessel intra‐arterial tumour emboli rather than disseminated parenchymal metastases.
Early unplanned readmission of patients with newly diagnosed tuberculosis discharged from acute hospital to ambulatory treatment
Authors: Chu Chung Ming , Yung Cho Yiu , Leung Wah Shing , Chan Veronica L. , Leung Edward M. F. 
Published: March 2003

Objective: The aim of this study was to examine whether patients with newly diagnosed tuberculosis (TB) discharged to ambulatory treatment are at risk of unplanned readmission through the emergency department within 28 days of discharge, and the risk factors associated with such readmission.Methodology: A cohort of 134 patients admitted to an acute medical department with TB, who were subsequently discharged to ambulatory treatment of TB, were studied by a retrospective record review for unplanned readmission in 28 days. Potential risk factors associated with the readmission were recorded during hospital stay and follow‐up visits, including age, sex, length of stay, substance abuse, need of assistance in the activities of daily living (ADL), comorbidities, non‐compliance, drug complications and use of non‐standard drug regimen.Results: Up to 20.1% of patients were readmitted. Factors independently associated with early unplanned readmission were need of assistance in ADL, drug complications, the need to use a non‐standard drug regimen and more than three non‐chest comorbidities.Conclusions: A significant readmission rate was found in these patients and potential risk factors were identified. Ambulatory treatment for TB may not be appropriate for selected patients. Local guidelines for the management of TB patients at high risk of readmission is needed.
Replication‐deficient adenovirus‐mediated transfer of B7‐1 (CD80) cDNA induces anti‐tumour immunity in isolated human lung cancer
Authors: Iwakami Shin‐Ichiro , Setoguchi Yasuhiro , Saijo Yasuo , Azuma Miyuki , Fukuchi Yoshinosuke 
Published: March 2003

Objective: Interaction between the co‐stimulatory molecule B7‐1 (CD80) on antigen‐presenting cells and its counter‐receptor CD28 on T lymphocytes plays a key role in the induction of cell‐mediated immune responses. Many tumours, including lung cancer, lack expression of B7‐1 and this has been suggested to contribute to the failure of immune recognition of these diseases. Based on this knowledge, we hypothesized that the co‐stimulatory signal delivered through the B7‐1 molecule expressed on lung cancer cells using replication deficient adenovirus vector would induce efficient tumour immunity in T lymphocytes.Methodology: To evaluate this hypothesis, we constructed two adenovirus vectors: AdCMVhB7 (an E1‐deleted‐Ad5‐based vector containing human B7‐1 cDNA driven by cytomegalovirus immediate early promoter and enhancer) and AdNull (same vector as above without expression of exogenous gene) as control. Using these adenovirus vectors, efficient generation of tumour immunity in T lymphocytes was studied using primary cultured lung cancer cells and peripheral blood lymphocytes (PBL) obtained from patients with lung cancer.Results: Inoculation of lung cancer cells with 10 multiplicity of infection of AdCMVhB7 resulted in rapid and efficient cell surface expression of B7‐1 molecule (> 90% of cells at 24 h). Cytolytic activity of PBL in 51Cr‐release assay (E/T = 40) demonstrated that effector lymphocytes induced by hB7‐1 (+) lung cancer cells treated with AdCMVhB7could lyse parental lung cancer cells hB7‐1 (–). In contrast, effector lymphocytes induced by lung cancer cells treated with AdNull as control virus or PBS as control could not lyse parental lung cancer cells at all. Furthermore, cytolytic activity of the effector lymphocytes induced by B7‐1‐transduced lung cancer cells was inhibited by addition of anti‐CD3 antibody.Conclusions: These data demonstrate that primary‐cultured lung cancer cells treated with AdCMVhB7 would efficiently generate tumour immunity in T lymphocytes. Adenovirus‐mediated‐hB7‐1 gene transfer may be a useful means for gene therapy of lung cancer using adoptive immunotherapy.
Comparing transforming growth factor beta‐2 and fibronectin as pleurodesing agents
Authors: LEE Y. C. GARY , MALKERNEKER DEE , DEVIN CLINTON J. , THOMPSON PHILIP J. , JOHNSON JOYCE E. , LANE KIRK B. , LIGHT RICHARD W. 
Published: March 2003

Background: We have recently demonstrated that transforming growth factor beta‐2 (TGF‐β2)
can produce effective pleurodesis. Whether this effect can be reproduced by the use
of its downstream proteins is not known. This study compared the effectiveness of
TGF‐β2 and fibronectin in inducing pleurodesis in rabbits.Methodology: New Zealand white rabbits (1.5–2.0 kg) were given 1.7 μg of TGF‐β2
(n = 5) or 2.0 mg of cellular fibronectin (n = 4) intrapleurally via a chest tube. The induced pleural fluid was collected and analyzed. The rabbits were sacrificed after 14 days. The pleurodesis was graded macroscopically from 1 (none) to 8 (symphysis > 50%).Results: All rabbits in the TGF‐β2 group developed effective pleurodesis
while none in the fibronectin group had scores > 2 (pleurodesis scores 7.0 ±
0.6 vs 1.3 ± 0.3, P < 0.001). Rabbits that received TGF‐β2
produced large amounts of pleural fluid initially (< 4 days). Microscopically,
the pleura of rabbits in the TGF‐β2 group showed prominent spindle
cell proliferation and collagen deposition, but no significant inflammation or mesothelial
proliferation. Pleural tissues of rabbits in the fibronectin group had occasional
thin collagen deposits only. The intrapleural administration of 2.0 mg of fibronectin,
a downstream product of TGF‐β, did not induce effective pleurodesis, as did the
intrapleural administration of TGF‐β2.Conclusions: The present study suggests that the mechanism by which TGF‐β2 induces pleurodesis is not predominantly dependent on the production of fibronectin.
Clinical, laboratory findings and microbiologic characterization of bronchiectasis in Thai patients
Authors: PALWATWICHAI APIRAK , CHAOPRASONG CHUTIMA , VATTANATHUM ANAN , WONGSA ADISORN , JATAKANON ANON 
Published: March 2003

Objective: The aim of the present study was to characterize the clinical features, underlying disease states, laboratory findings and microbiological characterization of bronchiectasis in Thai patients.Methodology: For a 2‐year period all consecutive patients diagnosed with bronchiectasis at Phramongkutklao Hospital, Bangkok, Thailand, were recruited. Data including history, physical examination, underlying disease and laboratory studies were carefully reviewed and recorded.Results: Fifty patients diagnosed with bronchiectasis were enrolled. Their mean age was
58 years. The most common background aetiology was tuberculosis. Six per cent of
the patients were diagnosed as having diffuse panbronchiolitis. Normal chest radiographs
were found in 10%. The common organisms isolated were Pseudomonas aeruginosa
(20%), Haemophilus influenzae (14%), Klebsiella pneumoniae
(14%) and Streptococcus pneumoniae (6%). Non‐tuberculous mycobacteria
which included Mycobacterium kansasii and Mycobacterium chelonae were found in 6%.Conclusion: We report the characteristics of bronchiectasis in Thai patients. The most common identifiable aetiology was tuberculosis.
What is the optimal approach for using a direct amplification test in the routine diagnosis of pulmonary tuberculosis? A preliminary assessment
Authors: LIM T. K. , ZHU DAVID , GOUGH ANNIE , LEE KANG‐HOE , KUMARASINGHE GAMINI 
Published: March 2003

Objective: The aim of this study was to determine the most appropriate strategy for the rapid diagnosis of pulmonary tuberculosis (PTB) using a nucleic acid amplification (NAA) test.Methodology: This was a prospective study of 128 adult patients in whom respiratory secretions were tested for Mycobacterium tuberculosis by the AMPLICOR assay. The basis for starting PTB treatment was noted for each patient. The optimal approach was determined by using Bayes’ theorem to compare different combinations of pretest probability, smear results with the AMPLICOR test.Results: The incidence of PTB was 15.6%. In only one patient was treatment for PTB commenced because of a positive AMPLICOR result. The rest were managed according to the conventional approach which relied upon clinical judgment and direct smear. The optimal approach was to treat patients with high or intermediate pretest risk for PTB who returned positive AMPLICOR tests. The overall accuracies of the conventional approach, AMPLICOR test and optimal approach were 89.8, 95.3 and 96.1%, respectively.Conclusion: This small study suggests that NAA testing be limited to patients with high or intermediate pretest risk of PTB. In this group, positive results demand treatment while the management of those with negative results still relies on clinical judgment.
Preliminary evaluation of soluble IL‐2 receptor and type III procollagen N‐terminal aminopeptide in pleural fluid for differentiating tuberculous, carcinomatous and parapneumonic pleural effusions
Authors: HARITA SHINGO , NOGAMI NAOYUKI , KIKUCHI TAKESHI , KIBATA MASAYOSHI 
Published: March 2003

Objective: The aim of the study was to clarify the possibility of using pleural fluid levels of soluble IL‐2 receptor (sIL‐2R) and type III procollagen N‐terminal aminopeptide (PIIIP) for differentiating tuberculous, carcinomatous and parapneumonic pleural effusions.Methodology: Fifty patients with pleural effusions were investigated retrospectively. The pleural effusions were due to tuberculosis (n = 11), carcinoma (n = 22), pneumonia (n = 9) and heart failure (n = 8). The concentrations of sIL‐2R and PIIIP were measured in pleural effusion using commercially available kits.Results: Soluble IL‐2 receptor concentrations were highest in the patients with tuberculosis (6856 ± 3212 U/mL), followed by those with carcinoma (4680 ± 1872 U/mL), pneumonia (2227 ± 525 U/mL) and heart failure (1439 ± 244 U/mL). Significant differences were found between tuberculosis and carcinoma (P = 0.023), carcinoma and pneumonia (P = 0.015), and pneumonia and heart failure (P = 0.002) groups. Type III procollagen N‐terminal aminopeptide concentrations were higher in the patients with tuberculosis (262.5 ± 157.9 U/mL) and pneumonia (257.0 ± 96.7 U/mL) than in those with carcinoma (48.0 ± 27.7 U/mL) and heart failure (10.9 ± 5.6 U/mL). Significant differences were found between tuberculosis and carcinoma (P < 0.001) and pneumonia and carcinoma (P < 0.001). To differentiate effusions, the cutoff points of sIL‐2R (2980 U/mL) and PIIIP (110.0 U/mL) were obtained from the highest concentration in the pneumonia group and in the carcinoma group, respectively. Using these criteria, the sensitivities for differentiating tuberculous, carcinomatous, and parapneumonic effusions were 90.9, 86.4 and 88.9%, respectively, with 100, 95 and 100% specificity, respectively.Conclusions: The simultaneous determination of sIL‐2R and PIIIP concentrations in pleural effusions may be clinically useful in differentiating tuberculous, carcinomatous, and parapneumonic effusions. Further assessments are required to determine the broad clinical application of this assay.
Agreement in surfactant measurements of sputum induced with hypertonic and normal saline
Authors: CHANG Anne B. , HILLS Yvette , HARRHY Veronica A. , HILLS Brian A. 
Published: March 2003

Objective:  The contribution of surfactant to the airway epithelial barrier is increasingly being recognized. Dipalmitoyl phosphatidycholine (DPPC), the major constituent of surfactant, is affected by lung injury. Hypertonic saline‐induced sputum is a convenient and reliable method of assessing airway cells and mediators. However, the influence of hypertonic saline on DPPC content of sputum is unknown. In this study the level of DPPC in induced sputum obtained using hypertonic saline is examined and compared with that obtained using normal saline.Methodology:  Sputum was induced on two occasions using nebulized hypertonic saline and normal saline, in 15 well non‐smoking adults, in random order on different days. DPPC content (µg/mL of sputum) was measured using a standard spectrophotometric method.Results:  The mean of log10 DPPC level in sputum obtained using hypertonic saline was 1.88 µg/mL sputum (95% CI 1.53, 2.13) and that obtained using normal saline was 1.83 (95% CI 1.62, 2.14). The mean difference of the two methods was −0.03 (95%CI −0.27, 0.33). Bland and Altman plot showed an equal distribution around the mean and all points were within the mean ± 2 SD.Conclusion:  We conclude that DPPC concentration of sputum can be easily measured in induced sputum and that the use of hypertonic saline does not influence the DPPC levels.
Anti‐interleukin‐8 auto‐antibodies in cerebrospinal fluid of children with purulent meningitis
Authors: Takasaki Jiro , Ogawa Yunosuke 
Published: March 2003

Abstract

Background
: Cerebrospinal fluid (CSF) of patients with purulent meningitis contains a high concentration of interleukin (IL)‐8. Recently, the presence of anti‐IL‐8 auto‐antibodies was noted in blood and alveolar fluid. Therefore, measurement of the concentration of anti‐IL‐8 auto‐antibodies was attempted in CSF of children with and without meningitis.
Methods and Results
: We measured the concentration of anti‐IL‐8 auto‐antibodies in CSF of children with purulent or aseptic meningitis and those without meningitis. The CSF obtained on admission showed a significantly higher concentration of anti‐IL‐8 IgG and IgM auto‐antibodies in children with purulent meningitis, compared with those with aseptic meningitis or without meningitis. Among the three groups of children, the concentration of IL‐8 was also significantly higher in CSF of children with purulent meningitis.
Conclusion
: Because the anti‐IL‐8 IgG auto‐antibody binds to IL‐8 and inhibits IL‐8 interaction with specific receptors on neutrophils, the presence of anti‐IL‐8 auto‐antibodies seems to provide a mechanism that limits the bioavailability of free IL‐8 in CSF.
Adult survivors of children’s cancer and their offspring
Authors: Bessho Fumio , Kobayashi Miyuki 
Published: March 2003

Abstract

Background
: Although it is anticipated in Japan that the number of long‐term survivors of children’s cancer will rapidly increase and that they will have children, reports of studies concerning the offspring of such survivors have come mainly from western countries. For this reason, it seems that the results of this study will be important.
Methods
: Ninety‐seven survivors of children’s cancer, who were diagnosed between 1962 and 1989 and are now older than 20 years old, and their offspring were studied.
Results
: Of 97 survivors, 30 have married and 23 survivors or their spouses had been pregnant (33 total pregnancies). Twenty‐five babies were born and seven pregnancies ended in spontaneous abortion. The abortion rate was not different from that of the Japanese general population. The birthweights of babies born to survivors tended to be lower than those of control subjects. The proportion of babies with birthweights under 2500 g was significantly greater for babies born to survivors than to the control subjects. None of the 25 babies born had congenital anomalies. Subsequent development of these children has been uneventful with no malignancies after a median follow‐up period of 4 years 10 months (range: 10 months to 16 years, 3 months).
Conclusions
: The reproductive activity of children’s cancer survivors and the health status of their offspring seem to be satisfactory. However, the sample size of the present study is too small to draw any definite conclusions. Because it is anticipated that the number of long‐term survivors of children’s cancer will rapidly increase in Japan, it is important to establish an effective system of following up these survivors and their offspring in order to provide them with appropriate suggestions for a better quality of life.
Angiotensin‐converting enzyme gene insertion/deletion polymorphism and renal damage in childhood uropathies
Authors: Al‐Eisa Amal , Haider Mohammad Z , Srivastva Braham S 
Published: March 2003

Abstract Background: The activation of the renin–angiotensin system in various renal disorders is well established. Congenital urological abnormalities, such as obstruction and reflux, are common causes of renal failure in children contributing to approximately 25% of chronic renal failure in this age group. While the outlook relates to the severity of initial renal damage, there is considerable heterogeneity in renal parenchymal destruction among individuals and the reasons for this heterogeneity are not fully understood. A polymorphism within intron 16 of the angiostensin‐converting enzyme (ACE) gene has been shown to influence the activity of the renin–angiotensin system, thus, it may also have an impact on the expression of renal disorders. We have determined the incidence of this ID polymorphism of the ACE gene in 47 Kuwaiti children with different urological abnormalities leading to variable degrees of renal impairment and in 48 healthy control subjects with a similar ethnic background.
Methods
: Blood samples were collected from the patients (n=47) and controls (n=48), total genomic DNA extracted and the ACE genotypes were determined using a polymerase chain reaction‐based method.
Results
: The DD genotype was detected in 27/47 (57%) cases compared with 25/48 (52%) controls (P=0.439). The heterozygous genotype ID was found in 14/47 (29%) cases compared with 22/48 (46%) controls (P=0.0138). The homozygous II genotype was detected in 6/47 (13%) cases compared with 1/48 (2%) controls (P=0.0247). The D allele of ACE gene was detected in 41/47 (87%) uropathy cases when individuals with homozygous DD and heterozygous ID genotypes were considered collectively. The incidence of parenchymal damage was considerably higher in uropathy cases with DD genotype (62%) compared with those having ID (26%) and II (12%) genotypes.
Conclusions
: Our data suggest an association of D allele of the ACE gene insertion/deletion polymorphism and congenital urological abnormalities, which result in parenchymal damage in Kuwaiti Arab children.
Restenosis after balloon angioplasty of coarctation: Relationship with ductus arteriosus
Authors: Takahashi Ken , Ino Toshihiro , Ohkubo Mataichi , Akimoto Katsumi , Kishirou Masahiko 
Published: March 2003

Abstract

Background
: Recently, balloon angioplasty (BA) has been used for the treatment of coarctation of the aorta (CoA) and the effectiveness of this treatment has been reported. However, the restenosis rate following BA in native CoA in the infant is high and the cause may be related to tissue properties at the origin of the ductus arteriosus (DA). However, the mechanisms responsible for restenosis remain uncertain.
Methods/Results
: The present study was designed to examine transformation of the smooth muscle cell (SMC) phenotypes using immunohistologic studies and to investigate the cause of restenosis of CoA following BA. A CoA model was surgically created in 15 newborn pigs (10–14‐days‐old; 2.4–4.1 kg). Balloon angioplasty was performed 1 month after the initial operation. One or 3 months after BA, animals were killed and immunohistologic studies on smooth muscle cell (SMC) antibodies against SM1, SM2 and SMemb of the myosin heavy chain (MHC) isoform were performed in the aorta at the CoA and DA. In the neointima, only SMemb was positive. In the SMC layer of the DA, only SM2 was positive. One month after BA, the external layer of the tunica media was strongly positive for SM2 only in the area around the origin of the DA.
Conclusions
: The first cause of restenosis is obstructive neointimal formation caused by the proliferation of undifferentiated SMC into the subendothelial tissue. This proliferation seems to be triggered by BA. The distribution of SM2 1 month after balloon angioplasty showed a similar pattern of proliferation of SMC in the external layer around the DA. This may represent a second mechanism of restenosis.