[Show abstract][Hide abstract] ABSTRACT: Monosodium urate (MSU) crystals, which are highly precipitated in the joint cartilage, increase the production of cartilage-degrading enzymes and pro-inflammatory mediators in cartilage, thereby leading to gouty inflammation and joint damage. In this study, we investigated the effect of MSU crystals on the viability of human articular chondrocytes and the mechanism of MSU crystal-induced chondrocyte death. MSU crystals significantly decreased the viability of primary chondrocytes in a time- and dose-dependent manner. DNA fragmentation was observed in a culture medium of MSU crystal-treated chondrocytes, but not in cell lysates. MSU crystals did not activate caspase-3, a marker of apoptosis, compared with actinomycin D and TNF-α-treated cells. MSU crystals did not directly affect the expression of endoplasmic reticulum (ER) stress markers at the mRNA and protein levels. However, MSU crystals significantly increased the LC3-II level in a time-dependent manner, indicating autophagy activation. Moreover, MSU crystal-induced autophagy and subsequent chondrocyte death were significantly inhibited by 3-methyladenine, a blocker of autophagosomes formation. MSU crystals activated autophagy via inhibition of phosporylation of the Akt/mTOR signaling pathway. These results demonstrate that MSU crystals may cause the death of chondrocytes through the activation of the autophagic process rather than apoptosis or ER stress.
Preview · Article · Dec 2015 · International Journal of Molecular Sciences
[Show abstract][Hide abstract] ABSTRACT: Introduction:
Fibronectin fragments (FN-fs) are increased in the cartilage of patients with osteoarthritis (OA) and have a potent chondrolytic effect. However, little is known about the cellular receptors and signaling mechanisms that are mediated by FN-fs. We investigated whether the 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) regulates cartilage catabolism via the Toll-like receptor (TLR)-2 signaling pathway in human chondrocytes.
Small interfering RNA was used to knock down TLR-2 and myeloid differentiation factor 88 (MyD88). TLR-2 was overexpressed in chondrocytes transfected with a TLR-2 expression plasmid. The expression levels of matrix metalloproteinase (MMP)-1, MMP-3, and MMP-13 were analyzed using quantitative real-time reverse transcription polymerase chain reactions, immunoblotting, or enzyme-linked immunosorbent assay. The effect of TLR-2 on 29-kDa FN-f-mediated signaling pathways was investigated by immunoblotting.
TLR-2, TLR-3, TLR-4, and TLR-5 mRNA were significantly overexpressed in OA cartilage compared with normal cartilage, whereas no significant difference of TLR-1 mRNA expression was found. 29-kDa FN-f significantly increased TLR-2 expression in human chondrocytes in a dose- and time-dependent manner. Knockdown of TLR-2 or MyD88, the latter a downstream adaptor of TLR-2, significantly inhibited 29-kDa FN-f-induced MMP production at the mRNA and protein levels. Conversely, TLR-2 overexpression led to enhanced MMP production by 29-kDa FN-f. In addition, TLR-2 knockdown apparently inhibited 29-kDa FN-f-mediated activation of phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha, and p38, but not of c-Jun N-terminal kinase or extracellular signal-regulated kinase. Exposure to synovial fluid (SF) from affected joints of patients with OA elevated MMP-1, MMP-3, and MMP-13 expression markedly in primary chondrocytes without reducing cell viability. However, TLR-2 knockdown in chondrocytes significantly suppressed SF-induced MMP induction.
Our data demonstrate that the MyD88-dependent TLR-2 signaling pathway may be responsible for 29-kDa FN-f-mediated cartilage catabolic responses. Our results will enhance understanding of cartilage catabolic mechanisms driven by cartilage degradation products, including FN-f. The modulation of TLR-2 signaling activated by damage-associated molecular patterns, including 29-kDa FN-f, is a potential therapeutic strategy for the prevention of cartilage degradation in OA.
Preview · Article · Nov 2015 · Arthritis research & therapy
[Show abstract][Hide abstract] ABSTRACT: In epidemiologic and animal studies, a high fat diet (HFD) has been shown to be associated with lower bone mineral density (BMD) and a higher risk of osteoporotic fractures. Meanwhile, consuming a HFD containing diacylglycerol (DAG) instead of triacylglycerol (TAG) is known to offer metabolically beneficial effects of reductions in body weight and abdominal fat. The purpose of this study was to investigate the effects of a HFD containing DAG (HFD-DAG) on bone in mice.
Four-week-old male C57BL/6J mice (n=39) were divided into three weight-matched groups based on diet type: a chow diet group, a HFD containing TAG (HFD-TAG) group, and a HFD-DAG group. After 20 weeks, body composition and bone microstructure were analyzed using dual energy X-ray absorptiometry and micro-computed tomography. Reverse transcription-polymerase chain reaction (PCR) and real-time PCR of bone marrow cells were performed to investigate the expressions of transcription factors for osteogenesis or adipogenesis.
The HFD-DAG group exhibited lower body weight, higher BMD, and superior microstructural bone parameters, compared to the HFD-TAG group. The HFD-DAG group showed increased expression of Runx2 and decreased expression of PPARgamma in bone marrow cells, compared to the HFD-TAG group. The HFD-DAG group also had lower levels of plasma glucose, insulin, total cholesterol, and triglyceride than the HFD-TAG group.
Compared to HFD-TAG, HFD-DAG showed beneficial effects on bone and bone metabolism in C57BL/6J mice.
Preview · Article · Jul 2015 · Yonsei medical journal
[Show abstract][Hide abstract] ABSTRACT: IFN-gamma releasing assays (IGRAs) such as T-SPOT.TB assay and QuantiFERON-TB In-Tube (QFT-GIT) have yielded promising results for the diagnosis of tuberculosis (TB). However, little is known about the usefulness of these assays for diagnosing disseminated TB. We therefore compared their usefulness with traditional tests in patients with disseminated TB. All adult patients with suspected disseminated TB were prospectively enrolled at a tertiary hospital in an intermediate TB-burden country during a 6-year period. Disseminated TB was defined as involvement of the bone marrow or ≥2 noncontiguous organs, or presence of miliary lung lesions. A total of 101 patients with confirmed and probable disseminated TB were finally analyzed. Of these 101 patients, 52 (52%) had miliary TB and the remaining 49 (48%) had nonmiliary disseminated TB. In addition, 63 (62%) had no underlying disease. Chronic granuloma with/without necrosis, acid-fast bacillus staining, Mycobacterium tuberculosis PCR, and culture for M tuberculosis were positive in 77% (41/53), 43% (43/101), 70% (67/96), and 72% (73/101), of the patients, respectively. The T-SPOT.TB assay was positive in 90% (91/101) of them. The sensitivity of the T-SPOT.TB assay in patients with miliary TB (90%) was similar to that in patients with nonmiliary TB (90%) (P > 0.99). In a subgroup analysis of the 58 patients in whom both QFT-GIT and the T-SPOT.TB results were available, the sensitivity of QFT-GIT (67%) was lower than that of T-SPOT.TB (95%) (P < 0.001).
In conclusion, T-SPOT.TB assay may be a helpful adjunct test for disseminated TB.
[Show abstract][Hide abstract] ABSTRACT: Asthma and atopic dermatitis are common allergic diseases, and their prevalence has increased in urban children. Recently, it is becoming understood that forest environment has favorable health effects in patients with chronic diseases. To investigate favorable clinical and immunologic effects of forest, we examined changes in clinical symptoms, indirect airway inflammatory marker, and serum chemokines before and after a short-term forest trip. The forest trips were performed with 21 children with asthma and 27 children with atopic dermatitis. All participating children were living in air polluted urban inner-city. We measured spirometry and fractional exhaled nitric oxide (FeNO) in children with asthma and measured scoring atopic dermatitis (SCORAD) index and Thymus and Activation-Regulated Chemokine (TARC)/CCL17 and Macrophage-Derived Chemokine (MDC)/CCL22 levels in children with atopic dermatitis before and after the forest trip. Indoor air pollutants such as indoor mold, particulate matter 10 (PM10) and total volatile organic compounds (TVOCs) of each child's home and the accommodations within forest were measured. A significant increase in forced vital capacity (FVC) and a significant decrease in FeNO were observed after the forest trip in children with asthma. SCORAD indices and MDC/CCL22 levels were significantly decreased after the forest trip in children with atopic dermatitis. Airborne mold and PM10 levels in indoor were significantly lower in the forest accommodations than those of children's homes; however, TVOC levels were not different between the two measured sites. Short-term exposure to forest environment may have clinical and immunological effects in children with allergic diseases who were living in the urban community.
No preview · Article · Feb 2015 · Iranian journal of allergy, asthma, and immunology
[Show abstract][Hide abstract] ABSTRACT: There have been many suggestions and much debate about climate variability during the Holocene. However, their complex forcing factors and mechanisms have not yet been clearly identified. In this paper, we have examined the Holocene climate cycles and features based on the wavelet analyses of 14C, 10Be, and 18O records. The wavelet results of the 14C and 10Be data show that the cycles of ~2180-2310, ~970, ~500-520, ~350-360, and ~210-220 years are dominant, and the ~1720 and ~1500 year cycles are relatively weak and subdominant. In particular, the ~2180-2310 year periodicity corresponding to the Hallstatt cycle is constantly significant throughout the Holocene, while the ~970 year cycle corresponding to the Eddy cycle is mainly prominent in the early half of the Holocene. In addition, distinctive signals of the ~210-220 year period corresponding to the de Vries cycle appear recurrently in the wavelet distribution of 14C and 10Be, which coincide with the grand solar minima periods. These de Vries cycle events occurred every ~2270 years on average, implying a connection with the Hallstatt cycle. In contrast, the wavelet results of 18O data show that the cycles of ~1900-2000, ~900-1000, and ~550-560 years are dominant, while the ~2750 and ~2500 year cycles are subdominant. The periods of ~2750, ~2500, and ~1900 years being derived from the 18O records of NGRIP, GRIP and GISP2 ice cores, respectively, are rather longer or shorter than the Hallstatt cycle derived from the 14C and 10Be records. The records of these three sites all show the ~900-1000 year periodicity corresponding to the Eddy cycle in the early half of the Holocene.
No preview · Article · Dec 2014 · Journal of Astronomy and Space Science
[Show abstract][Hide abstract] ABSTRACT: Limited data are available on which factors are associated with strong immunologic responses to T-SPOT.TB. We investigated the factors associated with strong positive responses in patients with extrapulmonary tuberculosis (E-TB). Of 173 patients with E-TB who gave positive results on T-SPOT.TB, 26 (15%) with a strong positive response (defined as ≥1,000 spot-forming units (SFU)/2.5×10(5) PBMC to ESAT-6 or CFP-10) and 71 (41%) with a low positive response (≤ 99 SFU (6-99 SFU)/2.5×10(5) PBMC) were further analyzed. Miliary TB was independently associated with a strong positive response to T-SPOT.TB, while advanced age and immunosuppression were independently associated with weak positive T-SPOT.TB responses.
[Show abstract][Hide abstract] ABSTRACT: Many of duplicated genes are enriched in signaling pathways. Recently, gene duplication of kinases has been shown to provide genetic buffering and functional diversification in cellular signaling. Transcription factors (TFs) are also often duplicated. However, how duplication of TFs affects their regulatory structures and functions of target genes has not been explored at the systems level. Here, we examined regulatory and functional roles of duplication of three major ARR TFs (ARR1, 10, and 12) in Arabidopsis cytokinin signaling using wild-type and single, double, and triple deletion mutants of the TFs. Comparative analysis of gene expression profiles obtained from Arabidopsis roots in wild-type and these mutants showed that duplication of ARR TFs systematically extended their transcriptional regulatory structures, leading to enhanced robustness and diversification in functions of target genes, as well as in regulation of cellular networks of target genes. Therefore, our results suggest that duplication of TFs contributes to robustness and diversification in functions of target genes by extending transcriptional regulatory structures.
Full-text · Article · Nov 2014 · Scientific Reports
[Show abstract][Hide abstract] ABSTRACT: In Pseudomonas aeruginosa, quorum sensing (QS) plays an essential role in pathogenesis and the QS response controls many virulence factors. Using a mealworm, Tenebrio molitor as a host model, we found that Protease IV, a QS-regulated exoprotease of P. aeruginosa functions as a key virulence effector causing the melanization and death of T. molitor larvae. Protease IV was able to degrade zymogens of spätzle processing enzyme (SPE) and SPE-activating enzyme (SAE) without the activation of the antimicrobial peptide (AMP) production. Since SPE and SAE function to activate spätzle, a ligand of Toll receptor in the innate immune system of T. molitor, we suggest that Protease IV may interfere with the activation of the Toll signaling. Independently of the Toll pathway, the melanization response, another innate immunity was still generated, since Protease IV directly converted Tenebrio prophenoloxidase into active phenoloxidase. Protease IV also worked as an important factor in the virulence to brine shrimp and nematode. These results suggest that Protease IV provides P. aeruginosa with a sophisticated way to escape the immune attack of host by interfering with the production of AMPs.
No preview · Article · Oct 2014 · Molecular Microbiology
[Show abstract][Hide abstract] ABSTRACT: The profile of infective endocarditis (IE) has changed and is now showing an increasing prevalence of IE among congenital heart disease (CHD) patients. We studied the change of clinical profiles of IE over the past 25 years in patients with CHD at a single institution.
We reviewed medical records retrospectively for 325 patients diagnosed with IE between January 1, 1987, and March 31, 2012. We analyzed and compared the differences in patient characteristics and outcomes between 1987-2000 (group A) and 2001-2012 (group B).
Over the 25-year period, 93 cases of IE in CHD patients were diagnosed (59 cases in group A and 34 cases in group B). Ventricular septal defect was the most common underlying cardiac disease observed during the entire period. The most common causative pathogen was Streptococcus in both groups. Group A contained 16 cases (27.1%) that had undergone cardiac surgery, whereas this number was 19 (55.8%) in group B. The number of patients who had undergone palliative care or surgery using prosthetic materials was higher among group B patients (p<0.001). Surgical procedures due to uncontrolled infection were performed in three cases in group A and 10 cases in group B.
Infective endocarditis and CHD show a close correlation, and the profile of IE patients can change in line with an increase in the survival rate of patients with complex CHD and the improvement of surgical techniques. Ongoing reassessment and the systematic management of these patients is crucial in the prevention and treatment of IE.
Full-text · Article · Jan 2014 · Korean Circulation Journal
[Show abstract][Hide abstract] ABSTRACT: Objective:
MicroRNAs (miRNAs), small noncoding RNA molecules, are involved in the pathogenesis of various diseases such as cancer and arthritis. The aim of this study was to determine whether miR-127-5p regulates interleukin-1β (IL-1β)-induced expression of matrix metalloproteinase 13 (MMP-13) and other catabolic factors in human chondrocytes.
Expression of miR-127-5p and MMP-13 by normal and osteoarthritic (OA) human cartilage was determined using real-time polymerase chain reaction. The effect of miR-127-5p on MMP-13 expression was evaluated using transient transfection of human chondrocytes or chondrogenic SW-1353 cells with miR-127-5p or its antisense inhibitor (anti-miR-127-5p). MMP-13 protein production was quantified by enzyme-linked immunosorbent assay, and the involvement of miR-127-5p in IL-1β-mediated catabolic effects was examined by immunoblotting. MicroRNA-127-5p binding with the putative site in the 3'-untranslated region (3'-UTR) of MMP-13 messenger RNA (mRNA) was validated by luciferase reporter assay.
There was a significant reduction in miR-127-5p expression in OA cartilage compared with normal cartilage. Up-regulation of MMP-13 expression by IL-1β was correlated with down-regulation of miR-127-5p expression in human chondrocytes. MicroRNA-127-5p suppressed IL-1β-induced MMP-13 production as well as the activity of a reporter construct containing the 3'-UTR of human MMP-13 mRNA. In addition, mutation of the miR-127-5p binding site in the 3'-UTR of MMP-13 mRNA abolished miR-127-5p-mediated repression of reporter activity. Conversely, treatment with anti-miR-127-5p remarkably increased reporter activity and MMP-13 production. Interestingly, the IL-1β-induced activation of JNK, p38, and NF-κB and expression of MMP-1 and cyclooxygenase 2 were significantly inhibited by miR-127-5p.
MicroRNA-127-5p is an important regulator of MMP-13 in human chondrocytes and may contribute to the development of OA.
No preview · Article · Dec 2013 · Arthritis & Rheumatology
[Show abstract][Hide abstract] ABSTRACT: Aims:
The collagen-stimulated generation of reactive oxygen species (ROS) regulates signal transduction in platelets, although the mechanism is unclear. The major targets of ROS include protein tyrosine phosphatases (PTPs). ROS-mediated oxidation of the active cysteine site in PTPs abrogates the PTP catalytic activity. The aim of this study was to elucidate whether collagen-induced ROS generation leads to PTP oxidation, which promotes platelet stimulation.
SH2 domain-containing PTP-2 (SHP-2) is oxidized in platelets by ROS produced upon collagen stimulation. The oxidative inactivation of SHP-2 leads to the enhanced tyrosine phosphorylation of spleen tyrosine kinase (Syk), Vav1, and Bruton's tyrosine kinase (Btk) in the linker for the activation of T cells signaling complex, which promotes the tyrosine phosphorylation-mediated activation of phospholipase Cγ2 (PLCγ2). Moreover, we found that, relative to wild-type platelets, platelets derived from glutathione peroxidase 1 (GPx1)/catalase double-deficient mice showed enhanced cellular ROS levels, oxidative inactivation of SHP-2, and tyrosine phosphorylation of Syk, Vav1, Btk, and PLCγ2 in response to collagen, which subsequently led to increased intracellular calcium levels, degranulation, and integrin αIIbβ3 activation. Consistent with these findings, GPx1/catalase double-deficiency accelerated the thrombotic response in FeCl3-injured carotid arteries.
The present study is the first to demonstrate that SHP-2 is targeted by ROS produced in collagen-stimulated platelets and suggests that a novel mechanism for the regulation of platelet activation by ROS is due to oxidative inactivation of SHP-2.
We conclude that collagen-induced ROS production leads to SHP-2 oxidation, which promotes platelet activation by upregulating tyrosine phosphorylation-based signal transduction.
No preview · Article · Oct 2013 · Antioxidants & Redox Signaling
[Show abstract][Hide abstract] ABSTRACT: Background: T-SPOT.TB, a recently developed T-cell based assay, has shown promising results in diagnosing tuberculosis (TB). It is hypothesized that the magnitude of response to early secretory antigenic target-6 (ESAT-6) and culture filtrate protein-10 (CFP-10), which are encoded by genes in the region of difference-1 (RD-1), is influenced by difference of disease status or host condition. Although strong responses of T-SPOT.TB occasionally occur, limited data are available on which factors are associated with these strong immunologic responses. We thus investigated the factors associated with extremely high response of T-SPOT.TB in patients with extrapulmonary TB (E-TB).
Methods: Between April 2008 and November 2012, adult patients with suspected E-TB were prospectively enrolled at a tertiary hospital in an intermediate TB-burden country. Patients with extremely high response of T-SPOT.TB, defined as results of >= 1000 spot forming units (SFU)/2.5 x105 PBMC to ESAT-6 or CFP-10, were compared with control patients with low response of T-SPOT.TB, <= 99 SFU (6-99 SFU)/2.5 x 105 PBMC to ESAT-6 or CFP-10.
Results: Of the 350 patients with suspected E-TB, 208 (59%) patients with 153 (74%) confirmed and 55 (26%) probable E-TB were included in this study. Of these 208, 173 (49%) patients showed positive results of T-SPOT.TB. Of these 173 patients, 26 (15%), 76 (44%), and 71 (41%) revealed >= 1000 SFU, 100-999 SFU, and 6-99 SFU/2.5 x 105 PBMC to RD-1 in T-SPOT.TB assay, respectively. Thus, 26 (15%) patients with extremely high response and 71 (41%) with low response were finally included for further analysis. Univariate and multivariate analyses are shown in Table 1. Univariate analysis revealed that young age, confirmed TB, and miliary TB were significantly associated with extremely high response results of T-SPOT.TB. In a multivariate analysis, miliary TB (OR=14.5; 95% CI 3.9-53.8) was significantly associated with extremely high response results of T-SPOT.TB, while advanced age (OR=0.9; 95% CI 0.9-1.0), and immunosuppression (OR=0.2; 95% CI 0.02-0.9) was associated with low response T-SPOT.TB results.
Conclusion: Our data suggest that mycobacterial burden and host immune status may contribute to the strong responsiveness of T-SPOT.TB assay.
[Show abstract][Hide abstract] ABSTRACT: Objective:
Cyclooxygenase-2 (COX-2) is a major prostaglandin E2 (PGE2) synthetic enzyme and is involved in the pathogenesis of chronic inflammation and pain in osteoarthritis (OA). The objective of this study was to directly address whether microRNA (miR)-558 can control the interleukin (IL)-1β-mediated induction of COX-2 and catabolic effects in human articular chondrocytes.
Materials and methods:
Total RNA was extracted from the cartilage tissues of normal and OA donors or cultured human articular chondrocytes. The expression of miR-558 was quantified by TaqMan assay. To investigate the repressive effect of miR-558 on COX-2 expression, human chondrocytes and chondrogenic SW1353 cells were transfected with mature miR-558 or an antisense inhibitor (anti-miR-558). The expression of COX-2 protein was determined by Western blot analysis and the involvement of miR-558 in IL-1β-induced catabolic effects was examined by Western blot analysis and enzyme-linked immunosorbent assay (ELISA). Direct interaction between miR-558 and the putative site in the 3'-untranslated region (UTR) of COX-2 messenger RNA (mRNA) was validated by luciferase reporter assay.
Normal human articular cartilage expressed miR-558, and its expression was significantly lower in OA cartilage. Stimulation with IL-1β led to a significant reduction in miR-558 expression in normal and OA chondrocytes. IL-1β-induced activation of MAP kinase (MAPK) and nuclear factor-κB (NF-κB) decreased miR-558 expression and induced COX-2 expression in chondrocytes. The overexpression of miR-558 directly suppressed the luciferase activity of a reporter construct containing the 3'-UTR of human COX-2 mRNA and significantly inhibited IL-1β-induced upregulation of COX-2, while treatment with anti-miR-558 enhanced IL-1β-induced COX-2 expression and reporter activity in chondrocytes. Interestingly, IL-1β-induced activation of NF-κB and expression of matrix metalloproteinase (MMP)-1 and MMP-13 was significantly inhibited by miR-558 overexpression.
These findings demonstrated that cartilage homeostasis is influenced by miR-558, which directly targets COX-2 and regulates IL-1β-stimulated catabolic effects in human chondrocytes.
Preview · Article · Apr 2013 · Osteoarthritis and Cartilage
[Show abstract][Hide abstract] ABSTRACT: The two interferon-γ release assays such as QuantiFERON-TB Gold / In-Tube (QFT-TB) and T-SPOT.TB-are useful tools for the rapid diagnosis of tuberculosis (TB) but can yield indeterminate test results (ITRs). While some studies have identified risk factors for ITRs in the QFT-TB test, there have been few such studies for the T-SPOT.TB test. The aim of this study was to investigate the risk factors associated with ITRs in the T-SPOT.TB test.
From April 2008 to August 2010, all patients with suspected extrapulmonary tuberculosis (E-TB) were enrolled in a tertiary hospital in Korea. ITR was defined as < 20 spots in the positive control well or > 10 spots in the negative control well.
Out of a total of 368 patients, 32 (8.7%, 95% CI, 6.0% to 11.7%) had ITRs in their T-SPOT.TB tests. The ITRs were due to a low mitogen response in 13 (40.6%) patients and to a high nil response in the other 19 (59.4%) patients. Statistical analysis revealed that old age, underlying diseases, immunosuppressive treatment, lymphopenia, and clinical manifestations of E-TB were not significantly associated with ITRs.
Indeterminate results in the T-SPOT.TB test are not affected by age, underlying disease, immunosuppressive treatment, lymphopenia, or clinical manifestations of E-TB, which are known risk factors for indeterminate results in the QFT-TB test.
[Show abstract][Hide abstract] ABSTRACT: Hemolytic disease in a newborn that causes early jaundice is common. It is often due to the Rh (D) and ABO incompatibility, but rarely due to unexpected antibodies. Among these unexpected antibodies, the anti-Dia antibody rarely occurs. The anti-Dia antibody was observed in the serum and red-cell eluate of an infant, and in the serum of his mother. The frequency of the appearance of the Dia antigen in the Korean population is estimated to be 6.4-14.5%. This paper reports a case of hemolytic disease in a newborn associated with the anti-Dia antibody. A full-term male infant was transferred to the authors' hospital due to hyperbilirubinemia the day after his birth. The laboratory data indicated a hemoglobin value of 11.6 g/dL, a reticulocyte count of 10.6%, a total bilirubin count of 14.4 mg/dL, a direct bilirubin count of 0.6 mg/dL, and a positive result in the direct Coombs' test. Due to the identification of an irregular antibody from the maternal serum, an anti-Dia antibody was detected, which was also found in the eluate made from the infant's blood. The infant had been treated with phototherapy and intravenous immunoglobulin since the second day after his birth and was discharged due to an improved condition without exchange transfusion. Therefore, in cases of iso-immune hemolytic disease in a newborn within 24 hours from birth who had a negative result in an antibody screening test, the conduct of an anti-Dia antibody identification test is recommended due to the suspicion of an anti-Dia antigen, followed by early administration of intravenous immunoglobulin.
[Show abstract][Hide abstract] ABSTRACT: Forty-three patients with miliary tuberculosis were evaluated for diagnostic usefulness of enzyme-linked immunospot (ELISPOT)
assay. Among noninvasive rapid tests available within 3–5 days, ELISPOT had the highest sensitivity (93%), compared with acid-fast
bacilli stain (sputum, 32% and bronchoalveolar lavage, 7%), Mycobacterium tuberculosis polymerase chain reaction (sputum, 53% and bronchoalveolar lavage, 36%), and tuberculin skin test (22%). In comparison with
44 patients with lymph node tuberculosis, the sensitivity of the ELISPOT assay in patients with miliary tuberculosis (93%)
was as high as in those with lymph node tuberculosis (95%, P = .63), whereas the sensitivity of the tuberculin skin test was substantially lower in patients with miliary tuberculosis
(22%) than in those with lymph node tuberculosis (73%, P < .001).
Full-text · Article · Oct 2012 · Clinical Infectious Diseases