Bowing of one or both bones of the forearm in children following acute trauma was first recognized by Borden in 1974. Since then, a total of 30 cases have been reported in the English literature. The injury is a result of an acute plastic deformation of the tubular bones due to mainly a longitudinal compression force, and is charactcrized by: 1) a broad fixed curvature of the entire bone, 2) absence of periosteal new bone formation on later roentgenograms, and 3) partial correction of the curvature through cortical remodeling in young children. In this paper, three cases of traumatic bowing of the tubular bone in children are presented: one traumatic bowing of both forearm bones in 15 years old girl and two traumatic bowing of fibulae in combination with fractures of diaphysis of the tibiae of the same legs in 6 years old girl and 6 years old boy respectively. Manipulative reduction for the bowing of the both forearm bones corrected remarkably the plastic curvature, whereas manipulation for the bent fibulae with fractures of the tibiae failed to reduce the curvature, causing no delay in fracturt healing. These three cases are of special interest from two points of view. The first case was caused by tangential force instead of a longitudinal one and was associated with ulnar nerve paralysis which has eventually been recovered. The other two cases occurred in the lower leg in which plastic deformation, according to previous report, would not develop because of the lack of intrinsic curvature of the tibia and fibula.
Child ; Diaphyses ; Female ; Fibula ; Forearm ; Humans ; Leg ; Male ; Osteogenesis ; Paralysis ; Plastics ; Tibia ; Ulnar Nerve

No abstract available.
Acute Lung Injury* ; Animals ; Hydroxyl Radical* ; Rats*

No abstract available.

BACKGROUND: Monocytes/macrophages play a central role in determining the host response during Gram-negative infection through secretion of a variety of mediators after stimulation of LPS. Even though cytokine production has been shown to play an important role in host defense during sepsis cytokine release may also lead to tissue injury. Thus, regulation of macrophage response to LPS is critical for host survival during Gram-neg-alive sepsis. In animals exposed to nonlethal doses of endotoxin a characteristic hyporesponsiveness to subsequent administration of endotoxin has been observed. This phenomenon was knowm as 'LPS tolerance'. However, little information is availavble regarding the underlying mechanism of U)S tolerance. METHOD: Peripheral blood monocyte(PBMC) was isolated from peripheral blood of normal volunteers by adhesion purification method. To evaluate conditions to obtain LPS tolerance. preculture was carried out with LPS at 10ng/ml for 24 hours. For stimulation culture plates were washed two times and were stimulated with LPS at 1ng/ml for 4, 6 and 26 hours. To assess the underlying mechanisms of LPS tolerance, autologous serum, PMA, anti-CD14 Ab, Indomethacin or PGF2 were added to preculture solution respectively. Cytokine concentrations in culture supernatants were measured using ELISA for TNF-α and IL-8 and mRNA of TNF-α and IL-8 were determined by Northern blot analysis. RESULTS: The exposure of PBMC to low dose of LPS suppressed the cytokine production and mRNA expression of TNF-α, but not IL-8. Anti-CDl4 Ab partially recovered production of TNF-α which was suppressed by preculture with low dose LPS. The preculture with PMA induces US tolerance, as preculture with low dose LPS. CONCLUSION: LPS tolerance to TNF-α is regulated pretranslationally and is influenced by protein kinase C pathway and CD14.
Animals ; Blotting, Northern ; Dinoprost ; Enzyme-Linked Immunosorbent Assay ; Healthy Volunteers ; Indomethacin ; Interleukin-8* ; Macrophages ; Monocytes* ; Protein Kinase C ; RNA, Messenger ; Sepsis ; Tumor Necrosis Factor-alpha*

BACKGROUND: Tumor necrosis factor(TNF) has been considered as an important candidate for cancer gene therapy based on it9 potent anti-tumor activity. However, since the efficiency of current techniques of gene transfer is not satisfactory, the majorities of current protocols is aiming the in vitro gene transfer to cancer cells and re-introducing genetically modified cancer cells to host In previous study, it was shown that TNF-sensitive cancer cells transfected with TNF-α CDNA would become highly resistant to TNF. Understanding the mechanisms of TNF-resistance in TNF-α gene transfected cancer cells would be an important step for improving the efficacy of cancer gene therapy as we]1 as for better understandings of tumor biology. This study was designed to evaluate the role of new protective protein synthesis in the acquired resistance to TNF of TNF-α gene transfected cancer cells. METHOD: We transfected TNF-α c-DNA to WEHI l64, a murine fibrosarcoma cell line, using retroviral vector (pLT12SN(TNF)) and confirm the expression of TNF with PCRf ELISA, MTT assay. Then we determined the TNF resistance of TNF gene transfected cells(WEHI 164-TNF) and the changes of TNF sensitivities after treatments with actinomycin D(transcription inhibitor) and cycloheximide(translation inhibitor). RESULTS: WEHI 164 which was sensitive to TNF became resistant to TNF after being trsnsfected with TNF-α gene and the resistance to TNF was partially reversed after treatment with actinomycin D, but not with cycloheximide. CONCLUSION: The acquired resistance to TNF after TNF-α gene transfection may be associated with synthesis of some protective proteins.
Biology ; Cell Line ; Cycloheximide ; Dactinomycin ; DNA, Complementary ; Enzyme-Linked Immunosorbent Assay ; Fibrosarcoma ; Genes, Neoplasm ; Necrosis ; Transfection ; Tumor Necrosis Factor-alpha* ; Zidovudine*

BACKGROUND: Phagocytosis is probably the first step for mycobacteria to be virulent in host because virulent strains are more readily phagocytosed by macrophage than attenuated strains. According 13 the traditional concept, multi-drug resistant strains have been regarded as less virulent. However, this concept has been challenged, since recent studies(reported) showed that the degree of virulence and drug-resistance is not related. The purpose of this study is to evaluate whether the phagocytic activity of M. tuberculosis by peripheral blood mononuclear cells(PBMC) is different according to drug-resistance or host factor. To evaluate this, we estimated the difference of phagocytic activity of drug-resistant and drug-sensitive M. tuberculosis and also estimated the phagocytic activity of PBMC from intractable tuberculosis patients and healthy controls. METHODS: PBMC from ten intractable tuberculosis patients and twelve healthy control and three different strains of heat-killed M. tuberculosis, ie, ADS(all drug sensitive), MDR(multi-drug resistant), and ADR(all drug resistant) were used. After incubation of various strains of M. tuberculosis with PBMC, the phagocytic activity was evaluated by estimating proportion of PBMC which have phagocytosed M. tuberculosis. RESULTS: Drug-resistant strains of M. tuberculosis were phagocylosed easily than drug sensitive strains(Percentage of PBMC phagocytosed M. tuberculosis in healthy control : ADS : 32.3α2.9%, ADR : 49.6α3.4%, p=0.0022, Percentage of PBMC phagocytosed M. tuberculosis in intractable tuberculosis patients : ADS : 34.9α3.6%, ADR : 50.7α4.5%), p=0.0069). However, there was no difference in phagocytic activity of PBMC from healthy control and intractable tuberculosis patients. CONCLUSION: Drug-resistant strains of M. tuberculosis were phagocytosed easily than drug sensitive strains and host factors does not seems to influence the phagocytosis of M. tuberculosis.
Humans ; Macrophages ; Monocytes* ; Mycobacterium tuberculosis* ; Mycobacterium* ; Phagocytosis* ; Tuberculosis ; Virulence

No abstract available.
Acute Lung Injury* ; Capillaries* ; Oxygen*

No abstract available.
Lung Neoplasms* ; Lung* ; Mass Screening* ; Seoul*

No abstract available.

BACKGROUND: The percutaneous pleural needle biopsy have been regarded as cornerstone in the diagnosis of lymphocyte dominant pleural effusions of which acid fast bacilli smear and cytologic exam was negative. However, the complications of percutaneous pleural needle biopsy is not rare arid its diagnostic efficacy is not always satisfactory. Recently, pleural fluid adenosine deaminase (ADA) and carcinoembryonic antigen (CEA) are widely accepted as markers of tuberculous pleurisy arid malignant pleural effusion respectively. We designed this study to re-evaluate the role of percutaneous pleural needle biopsy in the diagnosis of lymphocyte dominant exudative pleural effusions whose APE smear, cytologic exam was negative. METHODS: Retrospective analysis of 73 cases of percutaneous pleural needle biopsy in case of lymphocyte dominant exudative pleural effusions whose AFB smear and cytoloic exam was negative from Jan 1994 to Feb 1996 was done. RESULT: In 35 cases, specific diagnosis was obtained(all cases were tuberculous pleurisy), arid in 3(1 cases specific diagnosis was not obtained in spite of getting adequate pleural tissues, and in the other 8 cases, percutaneous pleural biopsy failed to get pleural tissues. In 9 cases, complications were combined including pneuomothorax and hemothorax. All 49 cases of pleural effusions whose ADA value was higher than 40IU/L and satisfying other categories were finally diagnosed as tuberculous pleurisy, however, the pleural biopsy confirmed only 28 cases as tuberculous pleurisy. In 6 cases of pleural effusions of which CEA value is higher than l0ng/ml, the pleural biopsy made specific diagnosis n no case. Final diagnosis of above 6 cases consisted of 4 malignant of fusions, I malignancy associated effusion and I tuberculous pleurisy. CONCLUSION: In the diagnosis of 73 cases of lymphocyte dominant pleural effusions of which acid fast bacilli smear and cytologic exam was negative, percutaneous pleural biopsy diagnosed only in 35 cases. In the diagnosis of tuberculous pleurisy, the positive predictive value of higher ADA than 40 IU/L in lymphocyte dominant pleural effusion with negative AFB smear and negative cytologic exam was l00%. And the diagnostic efficacy of pleural biopsy was 57%. In cases of effusions with high CEA than 10ng/ml 83% and 0% respectively. Finally, we concluded that percutaneous pleural needle biopsy in the diagnosis of APE smear negative and cytologic exam negative lymphocyte dominant exudative pleural effusion was not obligatory especially in effusions with high ADA and low CEA value.
Adenosine Deaminase ; Biopsy ; Biopsy, Needle* ; Carcinoembryonic Antigen ; Diagnosis* ; Hemothorax ; Hominidae ; Humans ; Lymphocytes* ; Needles* ; Pleural Effusion* ; Pleural Effusion, Malignant ; Retrospective Studies ; Tuberculosis, Pleural