Tuberculous splenic abscess: sonographic detection and follow-up.
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Biomedical subjects
Publications and source records attributed to S C Lin.
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Twenty-one patients with primary chronic pain received electroconvulsive therapy (ECT) for concurrent affective symptoms. Twenty of the 21 patients experienced improvement in the level of their pain. ECT can be an effective treatment modality for patients who have chronic pain complicated by affective symptoms.
Left main coronary artery (LMCA) disease is now uniformly treated with coronary artery bypass grafting (CABG). However, some patients with LMCA disease do not receive CABG because of high operative risks. The advent of stent implantation has permitted a non-operative improvement in myocardial blood flow in many patients with single- and multi-vessel coronary artery disease. However, the outcomes of stent implantation for unprotected LMCA disease are still unclear. Stent implantation was performed for unprotected LMCA disease in 13 patients; eight patients had high operative risk and five patients had refused CABG. The primary success rate was 100% (13/13 patients). One patient (8%) developed a non-Q-wave myocardial infarction after LMCA stenting. Repeat angiography was obtained in five patients (38%) with recurrent angina, and three patients (23%) received repeated percutaneous transluminal coronary angioplasty (PTCA) for LMCA restenosis. In the follow-up period of 18+/-3 months, 12 patients (92%) remained in satisfactory condition with no further need for surgical intervention. One patient (8%) ultimately required CABG, and she died after CABG at 3 months after LMCA stenting. In conclusion, although CABG remains the standard treatment for LMCA disease, the present study demonstrates that stent implantation is a safe and clinically beneficial revascularization procedure for unprotected LMCA disease in patients who have high operative risk as well as those who refuse CABG.
Phenanthrenequinone diimine (phi) complexes of rhodium(III) bearing appended peptides have been prepared using two complementary solid phase synthetic strategies. The first method involves the direct coupling of the coordinatively saturated rhodium complex containing a pendant carboxylate to the N-terminus of a resin-bound peptide, in a manner analogous to the chain-elongation step in solid phase peptide synthesis. The second involves coupling a bidentate chelator containing the pendant carboxylate to the resin-bound peptide, followed by coordination of [Rh(phi)2]3+ to the bidentate chelator attached to the peptide. Peptides of length 5-30 residues have been covalently attached to rhodium complexes in 5-18% yield using both methods. Despite the low overall yields, the regioselective modification of the peptide chain afforded by these strategies is a distinct advantage over solution phase methods. With coordination complexes which are stable to peptide deprotection and cleavage conditions from the resin, the solid phase synthetic strategies are convenient to apply. Amino acid analysis, electronic spectroscopy, and circular dichroism confirm the presence of the two components in the metal-peptide chimeras; the metal-peptide complexes exhibit the combined spectral properties of the parent metal complex and the appended peptide. Significantly, plasma desorption mass spectrometry reveals a novel pattern of peptide fragmentation for the metal-peptide chimeras that is not observed in the absence of the tethered metal complex; this fragmentation facilitates the sequence analysis of the appended peptide. Thus, metal-peptide chimeras may be conveniently prepared using solid phase methodologies, and features of coordination chemistry may be exploited for new peptide design and analysis.
In Snell (dw) and Jackson (dwJ) dwarf mice, mutations in the gene encoding Pit-1, a tissue-specific POU-domain transcription factor, lead to the absence of somatotroph, lactotroph and thyrotroph cells. Pre-somatotroph proliferation is stimulated by increased intracellular levels of cyclic AMP, normally induced by growth hormone releasing factor (GRF; refs 7-17). Here we report the cloning of mouse and rat complementary DNAs encoding a new member of the seven-transmembrane-helix, G-protein-coupled receptor family restricted to the pituitary gland, which mediates increases in intracellular cAMP and cAMP-dependent gene transcription in response to GRF. The receptor is expressed in a spatial and temporal pattern corresponding precisely to growth hormone gene expression, and neither is expressed in dw/dw mice. The pituitary hypoplasia in these mice thus appears to be due, at least in part, to the absence of GRF receptor, which is in turn due to the absence of functional Pit-1.
The indirect calorimetric system of measuring O2 consumption and CO2 production has been developed for energy expenditure estimation of premature infants. This apparatus requires an input room air mixing with pure oxygen to obtain a stable gas with definite oxygen concentration flowing into the hood for neonatal breath or supplemental oxygen treatments. In this paper, we propose an oxygen control system based on fuzzy control logic to automatically adjust the mixing ratio of room air to pure oxygen gas from the hospital's supply system, designed for premature infants. It is designed to reduce the risks of oxygenic toxicity and retinopathy of prematurity by lowering the overshoot of oxygen concentration. Its performance was evaluated and optimal membership functions were obtained. As a result, the system is quite robust with little effect caused by disturbance and has little or no overshoot when step changing the level of oxygen concentration in the mixed gas.
Integrating data that reside in different systems remains an often laborious process, requiring either manual steps or complicated programming. This paper describes a method for state-mandated reporting of childhood blood lead testing results that makes use of object linking and embedding technology and readily available software products to pull together information from different legacy systems. A terminal session emulator employs object linking and embedding automation to extract host data, and Visual Basic routines specify the user interface and database manipulation. This system has significantly increased the efficiency and accuracy with which blood lead testing reports are provided to the local state health department. The system provides a model for a relatively easy solution for laboratories and other groups that need a way to integrate standard data sets that are distributed across legacy systems.
Physiological knock-knee (PKK) was categorized by measuring intermalleolar distance (IMD), a clinically simple method, to evaluate the prevalence and correlating factors in 305 preschool children. The prevalence in this cross-sectional study was relatively high, and it was age related (p = 0.002; 64, 44, and 34% for ages 3-4, 4-5, and 5-6 years, respectively). The following factors were correlated with PKK: use of walking chair early (p = 0.0001), independently walked late (p = 0.0005), dependently walked longer (p = 0.0001), concurrence with flatfoot (p = 0.001), and angular deformity (toe in/out, p = 0.03). Gait analysis, with spatiotemporal, kinematics, and kinetics parameters, was performed to evaluate the ambulatory significance. Preschool children with PKK have a shorter stride length (p = 0.02) and a slower walking speed (p = 0.004). Dynamic hyperextension of the knee is noted for 8 degrees during the whole gait cycle (p < 0.05). We conclude that PKK is a variable that should be considered in the development of mature gait for preschool children.
A four month-old male infant was noted to have had severe corneal opacity since birth. Buphthalmos, increased intraocular pressure and corneal opacity with neovascularization were noted during physical examination. There was neither dysmorphic face nor hirsutism and the liver and spleen were impalpable. In addition, hypotonia, poor head control, and absence of Moro and grasping reflexes were also noted. There was no evidence of congenital infection by TORCH study. Tests of both urine and plasma amino acids were within normal limits. However, excessive urinary excretion of heparan sulfate was detected by thin-layer chromatography. Corneal transplantation was performed at 6 months old. Histopathological examination of the corneal button showed homogeneous thickening of Bowmen's membrane and intracytoplasmic pinkish substances in corneal stroma. The Alcian blue stain was positive, which was consistent with mucopolysaccharidosis of cornea. The manifestation of this case may be a clinical variant of Sanfilippo's syndrome (Mucopolysaccharidosis type III).
Primary immunodeficiency comprises a heterogeneous group of disorders. Autoimmune and/or rheumatic manifestations are not uncommon in these patients. It may be the first and/or sole sign before the underlying disease is established. This study focuses on the children of primary immunodeficiency with autoimmune disease to survey the clinical and laboratory finding retrospectively. From January 1985 to June 1998, ten patients (M:F = 9:1) of primary immunodeficiency with at least one well defined autoimmune disease were identified. The underlying immunodeficiency included three with Bruton's disease, three with common variable immunodeficiency, one with hyper-IgM, one with primary CD4 T-cell deficiency and two with Wiskott-Aldrich syndrome. The autoimmune manifestations include arthritis in six, ulcerative colitis in one, and autoimmune hemolytic anemia in three children. The major treatment was steroid and non-steroid anti-inflammatory drug. Infection could be controlled with antibiotics and intravenous immunoglobulin in all save one. The morbidity among these patients included bronchiectasis with pulmonary hypertension in three, joint stiffness, short stature, and delayed puberty in two. In conclusion, autoimmune diseases are frequently seen in patients with primary immunodeficiency. It could be the first and/or sole sign of disease. The possibility of immunodeficiency should be kept in mind when evaluating patients with autoimmune diseases.
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From September 1994 to April 1995, we encountered eight children, two boys and six girls, (aged 1 year 6 months to 9 years), presented with acute diarrhea followed by afebrile, generalized tonic-clonic seizures, or transient loss of consciousness with urine incontinence. Their biochemical data, including serum electrolyte levels, were within normal limits. The infective agent causing diarrhea was later proved by stool examination to be rotavirus, judged to be serotype G1 by reverse transcription - polymerase chain reaction (RT-PCR) typing. Cerebrospinal fluid (CSF) examinations performed in seven of the eight patients were within normal limits, and cultures for bacteria and virus were negative. The electroencephalograms (EEGs) performed from 1 to 13 days after seizure showed abnormal in six, and normal in two, patients. Follow-up EEGs, performed from 4 to 11 months after onset of seizure, were all normal. None had seizure recurrence despite the fact that no long-term anticonvulsant had been given. From observation here, the authors emphasize that there is a close relationship between rotavirus and afebrile seizure, and the course of afebrile seizure following rotavirus gastroenteritis is usually benign. Further studies are needed to elucidate the underlying pathogenesis.
To investigate the effects of intravenous immunoglobulin (IVIG) on patients of juvenile dermatomyositis (JDM), seven children with JDM were given monthly IVIG in conjunction with other treatments. The indications included disease exacerbation, inability to reduce dose of steroid, replacing cytotoxic drug because of complication and remission-induction for those with severe initial manifestations. Two patients were reported to improve slowly and maintained improved status while on a markedly reduced dose of steroid. One patient responded favorably to the first three courses only. Three patients had evident and quick responses, which could be seen as early as two or three days after the infusion. One patient failed to experience any beneficial effect by IVIG. Four initial responders had an aggravation some time after discontinuing the monthly regimen. The untoward reactions included only two occasions of fever, and another two occasions of fever associated with transient proteinuria. In conclusion, IVIG may be of value in terms of its quick, pulsatile effect and the adjuvant potential to reduce the side effect resulting from exposure to steroid or other immunosuppressive agents as well. However, its long-term efficacy is doubtful, based on this observation.
Anaphylactoid purpura is a small-vessel, vasculitic disease of unknown etiology, but it is thought to be caused by an immunoglobulin-mediated inflammatory process. To study the immunological profiles of local anaphylactoid purpura patients, during the period from October 1996 to October 1997 with 17 patients, (6 boys and 11 girls), (aged 3 years to 17 years, mean age: 7.9 years), with anaphylactoid purpura who visited National Taiwan University Hospital. Immunological studies were performed in 17 patients and 20 age-matched healthy controls. Higher C3 was noted in patients (126.2 +/- 26.7 mg/dL) than in the control group (116.1 +/- 16.7 mg/dL), although without statistical significance (P = 0.307). C4 levels of patients were significantly higher in patients than control group (38.6 +/- 13.4 v.s. 23.7 +/- 6.9 mg/dL), P < 0.001). There were no significant differences in the IgG and IgM levels between patient and control groups. In contrast, the IgA levels of patient were significantly higher than that control groups (293.1 +/- 102.9 v.s. 179.8 +/- 71.0 mg/dL, P = 0.001). The serum level of TGF-beta 1 of patients was higher than that of the control group although not statistically significant (44.1 +/- 27.3 v.s. 29.9 +/- 19.0 ng/mL, p = 0.067). A significantly higher percentage of T cells was noted in anaphylactoid purpura patients than controls (71.5 +/- 9.2% v.s. 65.0 +/- 6.3%, P = 0.016). However, no significant difference was found in other subpopulations of lymphocytes. These basic immunological profiles may be helpful for further work on the pathogenesis of anaphylactoid purpura.
Cytokines that transduce their signals either through glycoprotein 130 (gp130) homodimers or gp 130/leukemia inhibitory factor (LIF) receptor beta heterodimers are potent inducers of osteoclast development in vitro as well as in vivo; and interleukin (IL)-6 has been recognized as an important pathogenic factor in diseases characterized by increased bone remodeling, such as the osteoporosis of sex steroid deficiency. Based on evidence that the same cytokines can also promote committed osteoblast differentiation and stimulate bone formation in vitro and in vivo and that mesenchymal cell differentiation toward the osteoblast lineage may be a prerequisite for osteoclastogenesis, we have investigated whether gp130 activation can affect the differentiation of uncommitted mesenchymal progenitors. Using as our model murine embryonic fibroblasts (EF), we found that IL-6 or IL-11 in combination with their soluble receptors (sIL-6R or sIL-11R) increased dose-dependently the number of alkaline phosphatase (AP)-positive cells in 3-6-day-long cultures. Moreover, EF cells maintained with IL-6/sIL-6R in the presence of ascorbic acid and beta-glycerophosphate expressed osteocalcin messenger RNA (mRNA) by 2 weeks and formed a matrix containing mineralized collagen fibers by 3 weeks. This prodifferentiation effect was specific for the osteoblastic lineage, as we found no evidence for increased differentiation of chondrocytes, adipocytes, or muscle cells. Unlike IL-6/sIL-6R, LIF, oncostatin M (OSM), and ciliary neurotrophic factor (CNTF) did not promote osteoblastic differentiation of EF cells. This pattern of specificity was accounted for by the finding that EF cells express gp130, but not the ligand-binding subunit of the IL-6 receptor (gp80) nor the LIF receptor beta. These observations add credence to the contention that increased production of gp130-utilizing cytokines and their receptors in pathological conditions like sex steroid deficiency is indeed responsible for not only the increased osteoclastogenesis, but also the increased osteoblastogenesis, and thereby for the increased rate of bone remodeling.